sodium-bicarbonate and Alkalosis

Sodium bicarbonate (NaHCO3) is a buffering agent that is suggested to improve performance by promoting the efflux of hydrogen ions from working cells and tissues. Research surrounding its efficacy as an ergogenic aid is conflicting, making it difficult to draw conclusions as to its effectiveness for training and competition. This study performed a meta-analysis of relevant research articles to allow the development of concise practical recommendations for coaches and athletes. The overall effect size for the influence of NaHCO3 on performance was moderate, and was significantly lower for specifically trained as opposed to recreationally trained participants.

Topics: Acidosis; Alkalosis; Athletic Performance; Buffers; Humans; Sodium Bicarbonate

Ingestion of agents that modify blood buffering action may affect high-intensity performance. Here we present a meta-analysis of the effects of acute ingestion of three such agents - sodium bicarbonate, sodium citrate and ammonium chloride - on performance and related physiological variables (blood bicarbonate, pH and lactate). A literature search yielded 59 useable studies with 188 observations of performance effects. To perform the mixed-model meta-analysis, all performance effects were converted into a percentage change in mean power and were weighted using standard errors derived from exact p-values, confidence limits (CLs) or estimated errors of measurement. The fixed effects in the meta-analytic model included the number of performance-test bouts (linear), test duration (log linear), blinding (yes/no), competitive status (athlete/nonathlete) and sex (male/female). Dose expressed as buffering mmoL/kg/body mass (BM) was included as a strictly proportional linear effect interacted with all effects except blinding. Probabilistic inferences were derived with reference to thresholds for small and moderate effects on performance of 0.5% and 1.5%, respectively. Publication bias was reduced by excluding study estimates with a standard error >2.7%. The remaining 38 studies and 137 estimates for sodium bicarbonate produced a possibly moderate performance enhancement of 1.7% (90% CL ± 2.0%) with a typical dose of 3.5 mmoL/kg/BM (∼0.3 g/kg/BM) in a single 1-minute sprint, following blinded consumption by male athletes. In the 16 studies and 45 estimates for sodium citrate, a typical dose of 1.5 mmoL/kg/BM (∼0.5 g/kg/BM) had an unclear effect on performance of 0.0% (±1.3%), while the five studies and six estimates for ammonium chloride produced a possibly moderate impairment of 1.6% (±1.9%) with a typical dose of 5.5 mmoL/kg/BM (∼0.3 g/kg/BM). Study and subject characteristics had the following modifying small effects on the enhancement of performance with sodium bicarbonate: an increase of 0.5% (±0.6%) with a 1 mmoL/kg/BM increase in dose; an increase of 0.6% (±0.4%) with five extra sprint bouts; a reduction of 0.6% (±0.9%) for each 10-fold increase in test duration (e.g. 1-10 minutes); reductions of 1.1% (±1.1%) with nonathletes and 0.7% (±1.4%) with females. Unexplained variation in effects between research settings was typically ±1.2%. The only noteworthy effects involving physiological variables were a small correlation between performance and pre-exercise i

Topics: Acidosis; Alkalosis; Ammonium Chloride; Athletes; Athletic Performance; Buffers; Citrates; Female; Humans; Lactic Acid; Male; Running; Sodium Bicarbonate; Sodium Citrate

The objective of this teaching session with Professor McCance is to develop an approach to the management of patients with a very low plasma potassium (K(+)) concentration (P(K)). The session begins with a quiz based on six recent medical consultations for a P(K) < 2 mmol/l. Professor McCance outlined how he would proceed with his diagnosis and therapy, using the synopsis that described each patient. This approach was then applied to a new patient, a 69-year-old woman who had a large volume of dependent oedema and developed a severe degree of weakness and hypokalaemia during more aggressive diuretic therapy that included a K(+)-sparing diuretic. The initial challenge for Professor McCance was to deduce why the K(+)-sparing diuretic was not effective in this patient. He also needed to explain why the P(K) was so low on admission.

Topics: Acidosis; Adult; Aged; Alkalosis; Cell Physiological Phenomena; Creatinine; Diuretics; Female; Humans; Hypokalemia; Kidney; Male; Middle Aged; Paralysis; Potassium; Sodium Bicarbonate

Renal and electrolyte problems are common in patients in the ICU. Several advances that occurred in the recent past have been incorporated in the diagnosis and management of these disorders and were reviewed in this article. Unfortunately, many important questions remain unanswered, especially in the area of ARF, where new therapies are anxiously awaited to make the transition from bench to bedside. Better studies are sorely needed to define the best approach to dialysis in patients who have ARF.

Topics: Acid-Base Imbalance; Acute Kidney Injury; Alkalosis; Amphotericin B; Antifungal Agents; Cardiotonic Agents; Critical Care; Critical Illness; Dopamine; Humans; Kidney Diseases; Renal Dialysis; Sodium Bicarbonate

Topics: Acid-Base Imbalance; Acidosis; Alkalosis; Carbonates; Drug Combinations; Humans; Sodium Bicarbonate; Tromethamine

The rare congenital lactic acidosis is a consequence of enzyme defects. The acquired form is relatively common in critically ill patients. The altered metabolism of pyruvate and the imbalance between lactate production and utilization have a central role in the pathogenesis of this disease. The physiologic compensating mechanisms are generally not sufficient for complete correction of acidosis. In most of the cases the basic disease is the one that should be treated. The correction of the acidosis must be careful, because overtreatment may worsen acidosis, or may cause severe post-treatment alkalosis.

Topics: Acidosis, Lactic; Alkalosis; Bicarbonates; Dose-Response Relationship, Drug; Humans; Insulin; Nitroprusside; Sodium; Sodium Bicarbonate

Mechanisms of renal potassium excretion and internal potassium balance as the main determinants of serum and/or total body potassium are discussed. Renal handling of potassium is reviewed, with particular attention to the effects of diuretics, acid-base disturbances and aldosterone-deficient states. Among the regulatory processes of internal potassium balance, the importance of adrenergic stimuli/drugs, of acid-base balance, and of magnesium and insulin is stressed. Physiologic and pathophysiologic evidence provides the basis for discussion of relevant clinical implications.

Topics: Acid-Base Equilibrium; Adult; Aged; Alkalosis; Bicarbonates; Biological Transport; Catecholamines; Chlorides; Diuretics; Female; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney; Kidney Tubules; Magnesium Deficiency; Male; Middle Aged; Potassium; Renin-Angiotensin System; Sodium; Sodium Bicarbonate; Stress, Physiological

Current concepts hold that volume expansion is essential to the correction of chloride-depletion alkalosis (CDA) with chloride repletion in a permissive role. In this scheme, intranephronal fluid reabsorption would be redistributed with increased delivery to the distal nephron where the provided chloride is readily reabsorbed and the limited capacity for bicarbonate reabsorption would promote bicarbonate excretion and correction of CDA. In a model of CDA produced by peritoneal dialysis against 0.15 M NaHCO3, we have shown complete correction of CDA within 24 h without volume expansion by either oral isotonic sodium or chloride salts with 70 mM chloride and despite an obligatory bicarbonate load and negative sodium and potassium balance. During correction of CDA without volume expansion in rats by intravenous isotonic fluids containing 80 mM chloride, fractional fluid and chloride reabsorptions in the proximal convoluted tubule and in the loop segment of superficial nephrons were not different from controls but chloride reabsorption was enhanced in the collecting duct segment and probably within the distal convolution. Despite no differences in serial hematocrits, blood pressure, and measured plasma volume, kidney and nephron glomerular filtration rate (GFR) were reduced in CDA and returned to normal upon recovery 24 h later.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Alkalosis; Animals; Bicarbonates; Chlorides; Extracellular Space; Humans; Kidney; Models, Biological; Peritoneal Dialysis; Potassium; Sodium; Sodium Bicarbonate; Sodium Chloride; Water-Electrolyte Balance

This study compared the recommended dose of sodium citrate (SC, 500 mg/kg body mass) and sodium bicarbonate (SB, 300 mg/kg body mass) for blood alkalosis (blood [HCO3-]) and gastrointestinal symptoms (GIS; number and severity). Sixteen healthy individuals ingested the supplements in a randomized, crossover design. Gelatin capsules were ingested over 15 min alongside a carbohydrate-rich meal, after which participants remained seated for forearm venous blood sample collection and completion of GIS questionnaires every 30 min for 300 min. Time-course and session value (i.e., peak and time to peak) comparisons of SC and SB supplementation were performed using linear mixed models. Peak blood [HCO3-] was similar for SC (mean 34.2, 95% confidence intervals [33.4, 35.0] mmol/L) and SB (mean 33.6, 95% confidence intervals [32.8, 34.5] mmol/L, p = .308), as was delta blood [HCO3-] (SC = 7.9 mmol/L; SB = 7.3 mmol/L, p = .478). Blood [HCO3-] was ≥6 mmol/L above baseline from 180 to 240 min postingestion for SC, significantly later than for SB (120-180 min; p < .001). GIS were mostly minor, and peaked 80-90 min postingestion for SC, and 35-50 min postingestion for SB. There were no significant differences for the number or severity of GIS reported (p > .05 for all parameters). In summary, the recommended doses of SC and SB induce similar blood alkalosis and GIS, but with a different time course.

Topics: Alkalosis; Cross-Over Studies; Eating; Gastrointestinal Diseases; Humans; Sodium Bicarbonate; Sodium Citrate

The use of sodium bicarbonate (SB) as a preexercise ergogenic aid has been extensively studied in short-duration high-intensity exercise. Very few studies have considered the effects of SB ingestion before prolonged high-intensity exercise. The aim of the present study was to determine the effects of a 0.3 g·kg -1 body mass dose of SB ingested before the start of a 16.1-km cycling time trial in cyclists.. Ten trained male cyclists (age, 31.1 ± 9 yr; height, 1.84 ± 0.05 m; body mass, 82.8 ± 8.5 kg; and V̇O 2peak , 60.4 ± 3.1 mL·kg -1 ·min -1 ) completed this study. Participants ingested 0.3 g·kg -1 in gelatine (SB-G) and enteric capsules (SB-E) 1 wk apart to determine individualized time-to-peak alkalosis for each ingestion form. Using a randomized crossover design, participants then performed simulated 16.1-km time trials after ingestion of SB-G, SB-E, or a placebo.. There were significant differences in performance between the SB and placebo ingestion strategies ( f = 5.50, P = 0.014, p η2 = 0.38). Performance time was significantly improved by SB ingestion (mean improvement: 34.4 ± 42.6 s ( P = 0.031) and 40.4 ± 45.5 s ( P = 0.020) for SB-G and SB-E, respectively) compared with the placebo. Gastrointestinal symptoms were lower after SB-E compared with SB-G (36.3 ± 4.5 vs 5.6 ± 3.1 AU, P < 0.001, g = 7.09).. This study demonstrates that increased buffering capacity after acute preexercise SB ingestion can improve endurance cycling time-trial performances. The use of SB could be considered for use in 16.1-km cycling time trials, but further work is required to establish these effects after a preexercise meal.

Topics: Adult; Alkalosis; Bicycling; Cross-Over Studies; Dietary Supplements; Double-Blind Method; Eating; Humans; Male; Sodium Bicarbonate; Young Adult

Thomas, C, Delfour-Peyrethon, R, Dorel, S, and Hanon, C. Positive effects of pre-exercise metabolic alkalosis on perceived exertion and post-exercise squat jump performance in world-class cyclists. J Strength Cond Res 36(9): 2602-2609, 2022-This study aimed to determine the effects of pre-exercise alkalosis in world-class cyclists on their general (rate of perceived exertion [RPE]) and local (category-ratio scale [CR10]) perceived rates of exertion and acid-base status during 2 types of training sessions. Eight world-class cyclists ingested either sodium bicarbonate (BIC) or a placebo (PLA) in a double-blind and randomized order before performing 4 × 1,000 m constant-power sprints (CP) or 3 × 500 m all-out sprints (AO), with 20 minutes of recovery time between each session. For AO, the performance was assessed through the cycling sprint velocity and a squat jump test during recovery. During both tests, RPE, CR10, and acid-base status were measured. Sodium bicarbonate ingestion was effective in inducing pre-exercise alkalosis, compared with a PLA ( p < 0.05). During CP, performance and RPE were the same for BIC and PLA ( p > 0.05) with no time effect. The CR10 increased for the last sprint in PLA ( p < 0.05) but was attenuated in BIC (BIC: 6 vs. PLA: 8.2; p < 0.05), whereas there was no difference in acid-base status. During AO, RPE and CR10 increased with time, with no BIC effect, whereas blood lactate concentration was different ( p < 0.05). Sodium bicarbonate supplementation had no effect on overall repeated sprints ( p > 0.05). However, world-class athletes responded to BIC with higher squat jump performance than the PLA condition after AO ( p < 0.05). Our results suggest a positive influence of pre-exercise alkalosis in world-class cyclists on local perception of efforts after constant load sprints and an attenuation of muscle power output decline postsprint, as evidenced by improved squat jump performance after all-out cycling effort.

Topics: Alkalosis; Athletic Performance; Exercise Test; Humans; Lactic Acid; Physical Exertion; Polyesters; Sodium Bicarbonate

The present study investigated individualized sodium bicarbonate (NaHCO3-) supplementation in elite orienteers and its effects on alkalosis and performance in a simulated sprint orienteering competition. Twenty-one Danish male and female elite orienteers (age = 25.2 ± 3.6 years, height = 176.4 ± 10.9 cm, body mass = 66.6 ± 7.9 kg) were tested twice in order to identify individual time to peak blood bicarbonate (HCO3- peak) following supplementation of 0.3 g/kg body mass NaHCO3 with and without warm-up. The athletes also performed two 3.5 km time-trial runs (TT-runs) following individualized timing of NaHCO3 supplementation (SBS) or placebo (PLA) on separate days in a randomized, double-blind, cross-over design. The occurrence of individual peak HCO3- and pH ranged from 60 to 180 min. Mean HCO3- and pH in SBS were significantly higher compared with PLA 10 min before and following the TT-run (p < .01). SBS improved overall performance in the 3.5 km TT-run by 6 s compared with PLA (775.5 ± 16.2 s vs. 781.4 ± 16.1 s, respectively; p < .05). SBS improved performance in the last half of the TT-run compared with PLA (p < .01). In conclusion, supplementation with NaHCO3 followed by warm-up resulted in individualized alkalosis peaks ranging from 60 to 180 min. Individualized timing of SBS in elite orienteers induced significant alkalosis before and after a 3.5 km TT and improved overall performance time by 6 s, which occurred in the last half of the time trial. The present data show that the anaerobic buffer system is important for performance in these types of endurance events lasting 12-15 min.

Topics: Adult; Alkalosis; Athletic Performance; Cross-Over Studies; Dietary Supplements; Double-Blind Method; Female; Humans; Hydrogen-Ion Concentration; Male; Sodium Bicarbonate; Young Adult

This study determined the influence of a high- (HI) versus low-intensity (LI) cycling warm-up on blood acid-base responses and exercise capacity following ingestion of sodium bicarbonate (SB; 0.3 g/kg body mass) or a placebo (PLA; maltodextrin) 3 hr prior to warm-up. Twelve men (21 ± 2 years, 79.2 ± 3.6 kg body mass, and maximum power output [Wmax] 318 ± 36 W) completed a familiarization and four double-blind trials in a counterbalanced order: HI warm-up with SB, HI warm-up with PLA, LI warm-up with SB, and LI warm-up with PLA. LI warm-up was 15 min at 60% Wmax, while the HI warm-up (typical of elites) featured LI followed by 2 × 30 s (3-min break) at Wmax, finishing 30 min prior to a cycling capacity test at 110% Wmax. Blood bicarbonate and lactate were measured throughout. SB supplementation increased blood bicarbonate (+6.4 mmol/L; 95% confidence interval, CI [5.7, 7.1]) prior to greater reductions with HI warm-up (-3.8 mmol/L; 95% CI [-5.8, -1.8]). However, during the 30-min recovery, blood bicarbonate rebounded and increased in all conditions, with concentrations ∼5.3 mmol/L greater with SB supplementation (p < .001). Blood bicarbonate significantly declined during the cycling capacity test at 110%Wmax with greater reductions following SB supplementation (-2.4 mmol/L; 95% CI [-3.8, -0.90]). Aligned with these results, SB supplementation increased total work done during the cycling capacity test at 110% Wmax (+8.5 kJ; 95% CI [3.6, 13.4], ∼19% increase) with no significant main effect of warm-up intensity (+0.0 kJ; 95% CI [-5.0, 5.0]). Collectively, the results demonstrate that SB supplementation can improve HI cycling capacity irrespective of prior warm-up intensity, likely due to blood alkalosis.

Topics: Adult; Alkalosis; Bicycling; Dietary Supplements; Double-Blind Method; Humans; Male; Performance-Enhancing Substances; Sodium Bicarbonate

The aim of the present study was to test the effect of sodium bicarbonate (NaHCO. Double-blind cross-over study.. Twelve elite male BMX cyclists (age: 19.2±3.4 years; height: 174.2±5.3cm; body mass: 72.4±8.4kg) ingested either NaHCO3- (0.3g.kg. The main effect of condition (NaHCO. We present here the first field condition study to investigate the effect of bicarbonate ingestion over performance in BMX discipline. The results showed that NaHCO

Topics: Adolescent; Alkalosis; Athletic Performance; Bicycling; Cross-Over Studies; Double-Blind Method; Heart Rate; Humans; Hydrogen-Ion Concentration; Lactic Acid; Male; Sodium Bicarbonate; Young Adult

It is well established that ingestion of sodium bicarbonate (NaHCO. Twenty-one cyclists performed the following three double-blind trials: 1) ingestion of 0.3 g · kg. Lactate levels in the blood were significantly higher after exercise in 0.3 BC and 0.1 BC (15.12 ± 0.92 versus 10.3 ± 1.22 and 13.24 ± 0.87 versus 10.3 ± 1.22 mmol/L; P < 0.05) compared with control. Significant improvements in performance were only identified in 0.3 BC group (76.42 ± 2.14; P = 0.01).. The present study found that 0.3 g · kg

Topics: Alkalosis; Athletic Performance; Bicycling; Cross-Over Studies; Dose-Response Relationship, Drug; Double-Blind Method; Exercise Tolerance; Humans; Lactic Acid; Male; Sodium Bicarbonate; Young Adult

This study aimed to determine the effect of preexercise metabolic acidosis and alkalosis on power output (PO) and aerobic and anaerobic energy expenditure during a 4-km cycling time trial (TT).. Eleven recreationally trained cyclists (V˙O2peak 54.1 ± 9.3 mL·kg·min) performed a 4-km TT 100 min after ingesting in a double-blind matter 0.15 g·kg of body mass of ammonium chloride (NH4Cl, acidosis), 0.3 g·kg of sodium bicarbonate (NaHCO3, alkalosis), or 0.15 g·kg of CaCO3 (placebo). A preliminary study (n = 7) was conducted to establish the optimal doses to promote the desirable preexercise blood pH alterations without gastrointestinal distress. Data for PO, aerobic and anaerobic energy expenditure, and blood and respiratory parameters were averaged for each 1 km and compared between conditions using two-way repeated-measures ANOVA (condition and distance factors). Gastrointestinal discomfort was analyzed qualitatively.. Compared with placebo (pH 7.37 ± 0.02, [HCO3]: 27.5 ± 2.6 mmol·L), the NaHCO3 ingestion resulted in a preexercise blood alkalosis (pH +0.06 ± 0.04, [HCO3]: +4.4 ± 2.0 mmol·L, P < 0.05), whereas NH4Cl resulted in a blood acidosis (pH -0.05 ± 0.03, [HCO3]: -4.8 ± 2.1 mmol·L, P < 0.05). Anaerobic energy expenditure rate and PO were reduced throughout the trial in NH4Cl compared with placebo and NaHCO3, resulting in a lower total anaerobic work and impaired performance (P < 0.05). Plasma lactate, V˙CO2, and end-tidal CO2 partial pressure were lower and the V˙E/V˙CO2 higher throughout the trial in NH4Cl compared with placebo and NaHCO3 (P < 0.05). There was no difference between NaHCO3 and placebo for any of these variables (P > 0.05). Minimal gastrointestinal distress was noted in all conditions.. Preexercise acidosis, but not alkalosis, affects anaerobic metabolism and PO during a 4-km cycling TT.

Topics: Acidosis; Adult; Alkalosis; Aluminum Chloride; Aluminum Compounds; Athletic Performance; Bicycling; Chlorides; Double-Blind Method; Energy Metabolism; Gastrointestinal Diseases; Humans; Hydrogen-Ion Concentration; Lactic Acid; Male; Sodium Bicarbonate; Time Factors

This study investigated the effect of induced alkalosis on the curvature constant (W') of the power-duration relationship under normoxic and hypoxic conditions.. Eleven trained cyclists (mean ± SD) Age: 32 ± 7.2 years; body mass (bm): 77.0 ± 9.2 kg; VO. Pre-exercise alkalosis substantially increased W' and, therefore, may determine tolerance to exercise above CP under normoxic and hypoxic conditions. This may be due to NaHCO

Topics: Adult; Alkalosis; Anaerobic Threshold; Exercise; Exercise Tolerance; Humans; Hypoxia; Male; Oxygen Consumption; Sodium Bicarbonate

This study determined the effects of pre-exercise sodium bicarbonate ingestion (ALK) on changes in oxygen uptake (VO2) at the end of a supramaximal exercise test (SXT).. Eleven well-trained cyclists completed a 70-s all-out cycling effort, in double-blind trials, after oral ingestion of either 0.3 g kg(-1) of sodium bicarbonate (NaHCO3) or 0.2 g kg(-1) body mass of calcium carbonate (PLA). Blood samples were taken to assess changes in acid-base balance before the start of the supramaximal exercise, and 0, 5 and 8 min after the exercise; ventilatory parameters were also measured at rest and during the SXT.. At the end of the PLA trial, which induced mild acidosis (blood pH = 7.20), subjects presented a significant decrease in VO2 (P < 0.05), which was related to the amplitude of the decrease in minute ventilation (VE) during the SXT (r = 0.70, P < 0.01, n = 11). Pre-exercise metabolic alkalosis significantly prevented the exercise-induced decrease in VO2 in eleven well-trained participants (PLA:12.5 ± 2.1 % and ALK: 4.9 ± 0.9 %, P < 0.05) and the decrease in mean power output was significantly less pronounced in ALK (P < 0.05). Changes in the VO2 decrease between PLA and ALK trials were positively related to changes in the VE decrease (r = 0.74, P < 0.001), but not to changes in power output (P > 0.05).. Pre-exercise alkalosis counteracted the VO2 decrease related to mild acidosis, potentially as a result of changes in VE and in muscle acid-base status during the all-out supramaximal exercise.

Topics: Adult; Alkalosis; Double-Blind Method; Exercise; Exercise Test; Female; Humans; Hydrogen-Ion Concentration; Male; Oxygen Consumption; Physical Exertion; Sodium Bicarbonate; Time Factors; Young Adult

What is the central question of this study? Does metabolic alkalosis in humans, induced by sodium bicarbonate, affect rates of skeletal muscle fatigue differentially in muscle groups composed predominately of slow- and fast-twitch fibres? What is the main finding and its importance? Sodium bicarbonate exhibited no effect on the fatigue profile observed between triceps surae and brachii muscle groups during and after 2 min of tetanic stimulation. For the first time in exercising humans, we have profiled the effect of sodium bicarbonate on the voluntary and involuntary contractile characteristics of muscle groups representative of predominately slow- and fast-twitch fibres. The effect of metabolic alkalosis on fibre-specific maximal force production and rates of force development (RFD) has been investigated previously in animal models, with evidence suggesting an improved capacity to develop force rapidly in fast- compared with slow-twitch muscle. We have attempted to model in vivo the fatigue profile of voluntary and involuntary maximal force and RFD in the triceps surae and brachii after sodium bicarbonate (NaHCO

Topics: Alkalosis; Double-Blind Method; Electric Stimulation; Exercise; Humans; Muscle Fatigue; Muscle, Skeletal; Sodium Bicarbonate; Torque

Sodium bicarbonate intake has been shown to improve exercise tolerance, but the effects on high-intensity intermittent exercise are less clear. Thus, the aim of the present study was to determine the effect of sodium bicarbonate intake on Yo-Yo intermittent recovery test level 2 performance in trained young men.. Thirteen men aged 23 ± 1 year (height: 180 ± 2 cm, weight: 78 ± 3 kg; VO2max: 61.3 ± 3.3 mlO2 · kg(-1) · min(-1); means ± SEM) performed the Yo-Yo intermittent recovery test level 2 (Yo-Yo IR2) on two separate occasions in randomized order with (SBC) and without (CON) prior intake of sodium bicarbonate (0.4 g · kg(-1) body weight). Heart rate and rating of perceived exertion (RPE) were measured during the test and venous blood samples were taken frequently.. Yo-Yo IR2 performance was 14 % higher (P = 0.04) in SBC than in CON (735 ± 61 vs 646 ± 46 m, respectively). Blood pH and bicarbonate were similar between trials at baseline, but higher (P = 0.003) immediately prior to the Yo-Yo IR2 test in SBC than in CON (7.44 ± 0.01 vs 7.32 ± 0.01 and 33.7 ± 3.2 vs 27.3 ± 0.6 mmol · l(-1), respectively). Blood lactate was 0.9 ± 0.1 and 0.8 ± 0.1 mmol · l(-1) at baseline and increased to 11.3 ± 1.4 and 9.4 ± 0.8 mmol · l(-1) at exhaustion in SBC and CON, respectively, being higher (P = 0.03) in SBC. Additionally, peak blood lactate was higher (P = 0.02) in SBC than in CON (11.7 ± 1.2 vs 10.2 ± 0.7 mmol · l(-1)). Blood glucose, plasma K(+) and Na(+) were not different between trials. Peak heart rate reached at exhaustion was 197 ± 3 and 195 ± 3 bpm in SBC and CON, respectively, with no difference between conditions. RPE was 7% lower (P = 0.003) in SBC than in CON after 440 m, but similar at exhaustion (19.3 ± 0.2 and 19.5 ± 0.2).. In conclusion, high-intensity intermittent exercise performance is improved by prior intake of sodium bicarbonate in trained young men, with concomitant elevations in blood alkalosis and peak blood lactate levels, as well as lowered rating of perceived exertion.

Topics: Alkalosis; Blood Glucose; Body Weight; Cross-Over Studies; Fatigue; Heart Rate; Humans; Hydrogen-Ion Concentration; Lactic Acid; Male; Physical Endurance; Physical Exertion; Potassium; Single-Blind Method; Sodium; Sodium Bicarbonate; Young Adult

The purpose of this investigation was to assess the influence of sodium bicarbonate supplementation on maximal force production, rate of force development (RFD), and muscle recruitment during repeated bouts of high-intensity cycling. Ten male and female (n = 10) subjects completed two fixed-cadence, high-intensity cycling trials. Each trial consisted of a series of 30-s efforts at 120% peak power output (maximum graded test) that were interspersed with 30-s recovery periods until task failure. Prior to each trial, subjects consumed 0.3 g/kg sodium bicarbonate (ALK) or placebo (PLA). Maximal voluntary contractions were performed immediately after each 30-s effort. Maximal force (F max) was calculated as the greatest force recorded over a 25-ms period throughout the entire contraction duration while maximal RFD (RFD max) was calculated as the greatest 10-ms average slope throughout that same contraction. F max declined similarly in both the ALK and PLA conditions, with baseline values (ALK: 1,226 ± 393 N; PLA: 1,222 ± 369 N) declining nearly 295 ± 54 N [95% confidence interval (CI) = 84-508 N; P < 0.006]. RFD max also declined in both trials; however, a differential effect persisted between the ALK and PLA conditions. A main effect of condition was observed across the performance time period, with RFD max on average higher during ALK (ALK: 8,729 ± 1,169 N/s; PLA: 7,691 ± 1,526 N/s; mean difference between conditions 1,038 ± 451 N/s, 95% CI = 17-2,059 N/s; P < 0.048). These results demonstrate a differential effect of alkalosis on maximum force vs. maximum rate of force development during a whole body fatiguing task.

Topics: Adult; Alkalosis; Bicarbonates; Exercise; Fatigue; Female; Humans; Hydrogen-Ion Concentration; Isometric Contraction; Male; Muscle, Skeletal; Sodium Bicarbonate

The aim of this study was to observe the intracellular heat shock protein 72 (HSP72) and heme oxygenase-1 (HSP32) response to prolonged interval cycling following the ingestion of carbohydrates (CHO) and sodium bicarbonate (NaHCO(3)). Six recreationally active males (mean ± SD; age 23.2 ± 2.9 years, height 179.5 ± 5.5 cm, body mass 76.5 ± 6.8 kg, and peak power output 315 ± 36 W) volunteered to complete a 90 min interval cycling exercise on four occasions. The trials were completed in a random and blinded manner following ingestion of either: placebo and an artificial sweetener (P-P), NaHCO(3) and sweetener (B-P), placebo and CHO (P-CHO), and NaHCO(3) and CHO (B-CHO). Both HSP72 and HSP32 were significantly increased in monocytes and lymphocytes from 45 min post-exercise (p ≤ 0.039), with strong relationships between both cell types (HSP72, r = 0.83; HSP32, r = 0.89). Exogenous CHO had no influence on either HSP72 or HSP32, but the ingestion of NaHCO(3) significantly attenuated HSP32 in monocytes and lymphocytes (p ≤ 0.042). In conclusion, the intracellular stress protein response to 90 min interval exercise is closely related in monocytes and lymphocytes, and HSP32 appears to be attenuated with a pre-exercise alkalosis.

Topics: Adult; Alkalosis; Carbohydrate Metabolism; Eating; Exercise; Heme Oxygenase-1; HSP72 Heat-Shock Proteins; Humans; Lymphocytes; Male; Monocytes; Sodium Bicarbonate; Stress, Physiological; Young Adult

Although a considerable amount of literature exists on the ergogenic potential of ingesting sodium bicarbonate (NaHCO3) before short-term, high-intensity exercise, very little exists on optimal loading times before exercise. The purpose of this study was to determine the influence of NaHCO3 supplementation timing on repeated sprint ability (RSA). Eight men completed 3 (randomized and counterbalanced) trials of ten 10-second sprints separated by 50 seconds of active recovery (1:5 work-to-rest) on a nonmotorized treadmill. Before each trial, the subjects ingested 0.3 g·kg(-1) body weight of NaHCO3 at 60 (H1), 120 (H2), or 180 (H3) minutes before exercise. Additionally, the subjects were assessed for any side effects (gastrointestinal [GI] discomfort) from the NaHCO3 ingestion via a visual analog scale (VAS). Blood buffering was assessed using a 2-way analysis of variance (ANOVA) with repeated measures, whereas repeated sprint performance and GI discomfort were assessed via a 1-way ANOVA with repeated measures. Blood-buffering capacity was not different at preexercise times (HCO3(-) [millimoles per liter] H1: 30.2 ± 0.4, H2: 30.9 ± 0.6, H3: 31.2 ± 0.6; p > 0.74). Average speed, average power, and total distance covered progressively declined over the 10 sprints; however, there was no difference between conditions (p > 0.22). The incidence of GI discomfort was significantly higher (p < 0.05) from preingestion at all time points with the exception of 180 minutes, whereas severity was only different between 90 and 180 minutes. Ingestion times (between 60 and 180 minutes) did not influence the blood buffering or the ergogenic potential of NaHCO3 as assessed by RSA. However, VAS scores indicated that at 180 minutes postingestion, an individual is less prone to experiencing significant GI discomfort.

Topics: Adult; Alkalosis; Analysis of Variance; Athletic Performance; Buffers; Colic; Diarrhea; Eructation; Exercise Test; Flatulence; Humans; Male; Nausea; Recovery of Function; Running; Sodium Bicarbonate; Vomiting; Young Adult

The aim of this study was to determine the effect and reliability of acute and chronic sodium bicarbonate ingestion for 2000-m rowing ergometer performance (watts) and blood bicarbonate concentration [HCO3-].. In a crossover study, 7 well-trained rowers performed paired 2000-m rowing ergometer trials under 3 double-blinded conditions: (1) 0.3 grams per kilogram of body mass (g/kg BM) acute bicarbonate; (2) 0.5 g/kg BM daily chronic bicarbonate for 3 d; and (3) calcium carbonate placebo, in semi-counterbalanced order. For 2000-m performance and [HCO3-], we examined differences in effects between conditions via pairwise comparisons, with differences interpreted in relation to the likelihood of exceeding smallest worthwhile change thresholds for each variable. We also calculated the within-subject variation (percent typical error).. There were only trivial differences in 2000-m performance between placebo (277 ± 60 W), acute bicarbonate (280 ± 65 W) and chronic bicarbonate (282 ± 65 W); however, [HCO3-] was substantially greater after acute bicarbonate, than with chronic loading and placebo. Typical error for 2000-m mean power was 2.1% (90% confidence interval 1.4 to 4.0%) for acute bicarbonate, 3.6% (2.5 to 7.0%) for chronic bicarbonate, and 1.6% (1.1 to 3.0%) for placebo. Postsupplementation [HCO3-] typical error was 7.3% (5.0 to 14.5%) for acute bicarbonate, 2.9% (2.0 to 5.7%) for chronic bicarbonate and 6.0% (1.4 to 11.9%) for placebo.. Performance in 2000-m rowing ergometer trials may not substantially improve after acute or chronic bicarbonate loading. However, performances will be reliable with both acute and chronic bicarbonate loading protocols.

Topics: Administration, Oral; Adolescent; Adult; Alkalosis; Athletic Performance; Buffers; Capsules; Cross-Over Studies; Dietary Supplements; Double-Blind Method; Female; Humans; Hydrogen-Ion Concentration; Male; Physical Endurance; Placebos; Reproducibility of Results; Sodium Bicarbonate; Time Factors; Treatment Outcome; Young Adult

Many studies have reported substantial performance gains in well-trained athletes after the acute ingestion of sodium bicarbonate (NaHCO3). However, acute NaHCO3 ingestion is not always practical. The aim of this study was to compare acute NaHCO3 loading with serial NaHCO3 loading (split doses over 3 days) in well-trained cyclists. Eight male cyclists (mean ± SD; age = 28 ± 8 years; VO2peak = 66.8 ± 8.4 ml·kg(-1)·min(-1)) completed 3 tests in a double-blind, randomized design over a 3-week timeframe: acute NaHCO3 loading (AL), serial NaHCO3 loading (SL), and a placebo loading condition (P). After each loading protocol, the cyclists completed a 4-minute performance test on a cycling ergometer. The VO2 was measured during each test, and blood samples were taken throughout the study to measure lactate, bicarbonate ion concentration ([HCO3(-)]), and pH levels. Both the AL and SL trials produced a significantly higher average power in the 4-minute test (mean ± SD; 3.3 ± 2.0 and 2.3 ± 2.5%; p < 0.001 and p = 0.01, respectively) when compared with the P trial, with no significant difference between AL and SL trials (p = 0.29). The AL trial produced a significantly greater postloading alkalosis as determined by blood [HCO3(-)] when compared with the SL and P trials. Both acute and serial NaHCO3 loading significantly improved 4-minute cycling performance when compared with that in a placebo trial. However, serial NaHCO3 loading may provide a convenient and practical alternative approach for athletes preparing for competition.

Topics: Adult; Alkalosis; Athletes; Athletic Performance; Bicycling; Double-Blind Method; Humans; Lactic Acid; Male; Oxygen Consumption; Sodium Bicarbonate; Young Adult

The aim of the present study was to examine the effect of sodium bicarbonate ingestion on consecutive "all out" sprint tests, analyzing the acid-base status and its influence on performance and perceived effort. Ten elite bicycle motocross (BMX) riders (20.7 ± 1.4 years, training experience 8-12 years) participated in this study which consisted of two trials. Each trial consisted of three consecutive Wingate tests (WTs) separated by 15 min recovery. Ninety minutes prior to exercise subjects ingested either NaHCO(3) (-) (0.3 g kg(-1) body weight) or placebo. Blood samples were collected for the assessment of blood acid-base status: bicarbonate concentration ([HCO(3) (-)]), pH, base excess (BE) and blood lactate concentration ([La(-)]). Performance variables of peak power (PP), mean power (MP), time to peak power and fatigue index were calculated for each sprint. Significant differences (p < 0.05) were observed in acid-base variables [pH before WT1: 7.47 ± 0.05 vs. 7.41 ± 0.03; [HCO(3) (-)] before WT1: 29.08 ± 2.27 vs. 22.85 ± 0.24 mmol L(-1) (bicarbonate vs. placebo conditions, respectively)], but there were not significant differences in performance variables between trials [PP WT1: 1,610 ± 373 vs. 1,599 ± 370 W; PP WT2: 1,548 ± 460 vs. 1,570 ± 428 W; PP WT3: 1,463 ± 361 vs. 1,519 ± 364 W. MP WT1: 809 ± 113 vs. 812 ± 108 W; MP WT2: 799 ± 135 vs. 799 ± 124 W; MP WT3: 762 ± 165 vs. 782 ± 118 W (bicarbonate vs. placebo conditions, respectively)]. Rating of perceived effort (RPE) was not influenced nor ratings of perceived readiness. Sodium bicarbonate ingestion modified significantly the blood acid-base balance, although the induced alkalosis did not improve the Wingate test performance, RPE and perceived readiness across three consecutive WTs in elite BMX cyclists.

Topics: Acid-Base Equilibrium; Adult; Alkalosis; Bicarbonates; Bicycling; Cross-Over Studies; Exercise; Exercise Test; Fatigue; Humans; Hydrogen-Ion Concentration; Lactic Acid; Physical Exertion; Sodium Bicarbonate; Young Adult

The heat shock protein 72 (HSP72) response following exercise is well documented, however, little is known on whether the expression may be mediated by the ingestion of ergogenic aids prior to performance. The purpose of this research was to investigate the effect of sodium bicarbonate (NaHCO(3)) ingestion on monocyte and lymphocyte expressed HSP72 and oxidative stress for 4-h post exercise. Seven active males (22.3 ± 2.9 years, 181.6 ± 4.5 cm, 78.1 ± 8.1 kg) performed a 4-min 'all-out' cycle test following a dose of 0.3 g kg(-1) body mass of NaHCO(3), or an equimolar placebo dose of sodium chloride. HSP72 was measured by flow cytometry and oxidative stress was determined via plasma thiobarbituric acid substances (TBARS) analysis. The NaHCO(3) ingestion significantly increased blood pH (p<0.001), bicarbonate (p<0.001) and base excess (p<0.001) pre-exercise. Despite this there was no evidence of a significantly improved exercise performance when compared with the placebo trials (p ≥ 0.26) (means ± SD; average power 292 ± 43 W vs. 291 ± 50 W; peak power 770 ± 218 W vs. 775 ± 211 W; work completed 71 ± 10 kJ vs. 68 ± 10 kJ). Monocyte expressed HSP72 was significantly lower under experimental conditions during the 4-h post-exercise (p=0.013), as was plasma TBARS (p<0.001). These findings suggest that pre-exercise alkalosis can attenuate the stress response to a single bout of anaerobic exercise.

Topics: Adult; Alkalosis; Athletic Performance; Exercise; Exercise Test; HSP72 Heat-Shock Proteins; Humans; Hydrogen-Ion Concentration; Lactic Acid; Lymphocytes; Male; Monocytes; Oxidative Stress; Sodium Bicarbonate; Thiobarbituric Acid Reactive Substances; Young Adult

The purpose of this investigation was to determine the effect of ingested caffeine, sodium bicarbonate, and their combination on 2,000-m rowing performance, as well as on induced alkalosis (blood and urine pH and blood bicarbonate concentration [HCO3-]), blood lactate concentration ([La-]), gastrointestinal symptoms, and rating of perceived exertion (RPE).. In a double-blind, crossover study, 8 well-trained rowers performed 2 baseline tests and 4 × 2,000-m rowing-ergometer tests after ingesting 6 mg/kg caffeine, 0.3 g/kg body mass (BM) sodium bicarbonate, both supplements combined, or a placebo. Capillary blood samples were collected at preingestion, pretest, and posttest time points. Pairwise comparisons were made between protocols, and differences were interpreted in relation to the likelihood of exceeding the smallest worthwhile-change thresholds for each variable. A likelihood of >75% was considered a substantial change.. Caffeine supplementation elicited a substantial improvement in 2,000-m mean power, with mean (± SD) values of 354 ± 67 W vs. placebo with 346 ± 61 W. Pretest [HCO3-] reached 29.2 ± 2.9 mmol/L with caffeine + bicarbonate and 29.1 ± 1.9 mmol/L with bicarbonate. There were substantial increases in pretest [HCO3-] and pH and posttest urine pH after bicarbonate and caffeine + bicarbonate supplementation compared with placebo, but unclear performance effects.. Rowers' performance in 2,000-m efforts can improve by ~2% with 6 mg/kg BM caffeine supplementation. When caffeine is combined with sodium bicarbonate, gastrointestinal symptoms may prevent performance enhancement, so further investigation of ingestion protocols that minimize side effects is required.

Topics: Alkalosis; Athletic Performance; Caffeine; Central Nervous System Stimulants; Cross-Over Studies; Dietary Supplements; Double-Blind Method; Female; Humans; Hydrogen-Ion Concentration; Male; Physical Exertion; Ships; Sodium Bicarbonate; Sports

We tested the hypotheses that sodium bicarbonate (NaHCO3) ingestion would result in no alteration in critical power (CP) but would improve performance in a 3-min all-out cycling test by increasing the total amount of work done above CP (W').. Eight habitually active subjects completed 3-min all-out sprints against fixed resistance in a blind randomized design after a dose of 0.3 g.kg body mass of NaHCO3 and 0.045 g.kg body mass of sodium chloride (placebo; PL trial). Blood acid-base status was assessed from arterialized fingertip blood samples before and after exercise. The CP was calculated as the mean power output during the final 30 s of the test, and the W' was estimated as the power-time integral >CP.. The NaHCO3 dose was effective in inducing preexercise alkalosis as indicated by changes in blood pH (PL = 7.40 +/- 0.02 vs NaHCO3 = 7.46 +/- 0.01, P < 0.001), [bicarbonate] (PL = 21.9 +/- 3.0 vs NaHCO3 = 29.0 +/- 3.8 mM, P < 0.05), and base excess (PL = -1.9 +/- 2.5 vs NaHCO3 = 5.0 +/- 3.0 mM, P < 0.05). There were no significant differences in the total work done (PL = 62.8 +/- 10.1 vs NaHCO3 = 62.7 +/- 10.1 kJ), the CP (PL = 248 +/- 50 vs NaHCO3 = 251 +/- 51 W), or the W' (PL = 18.2 +/- 6.4 vs NaHCO3 = 17.5 +/- 6.0 kJ) estimates between treatments.. Despite notably enhanced blood-buffering capacity, NaHCO3 ingestion had no effect on the W', the CP, or the overall performance during 3 min of all-out cycling. It is concluded that preexercise blood alkalosis had no influence on the power-duration relationship for all-out exercise.

Topics: Adult; Alkalosis; Bicycling; Humans; Male; Muscle Strength; Physical Exertion; Sodium Bicarbonate; Young Adult

The purpose of this study was to determine the effects of sodium bicarbonate (NaHCO3) ingestion on intermittent running and subsequent performance. Eight healthy men volunteered to take part in the study. One hour after the ingestion of either NaHCO(3) or placebo (sodium chloride; NaCl) participants undertook 20 x 24-second runs on a motorized treadmill at the velocity eliciting maximal oxygen uptake (100% v-VO(2)max). After sprint 20 participants performed a run to volitional exhaustion at 120% v-VO(2)max. Capillary blood samples for blood pH, bicarbonate ([HCO(3)]), and lactate ([Bla]) concentration were taken pre and postingestion, every fifth sprint and after the performance run. After ingestion of NaHCO(3), blood [HCO(3)] increased from resting values (p < 0.05), and the increase in pH approached significance. Blood [HCO(3)(-)] continually decreased throughout intermittent exercise (p < 0.05) and decreased further after performance in both trials (p < 0.05). [Bla] was similar in both trials throughout intermittent exercise but was greater at exhaustion for NaHCO(3) (main effect for trial; p < 0.05). There was no significant difference in performance of the group between trials (78 +/- 22 and 75 +/- 22 seconds for NaHCO(3) and NaCl, respectively). The intercept of the relationships between [Bla] and [HCO(3)(-)] and between [Bla] and pH was greater during NaHCO(3) (p < 0.05), whereas the relationship between pH and [HCO(3)(-)] was unchanged (p > 0.05). The results of this study suggest that the ingestion of NaHCO(3) before intermittent type exercise was sufficient to induce metabolic alkalosis but did not significantly affect performance. However, because significant individual variations in performance were observed, an individual approach to bicarbonate ingestion is recommended based on the intensity and duration of the required performance.

Topics: Alkalosis; Athletic Performance; Bicarbonates; Heart Rate; Humans; Hydrogen-Ion Concentration; Lactic Acid; Male; Oxygen Consumption; Running; Sodium Bicarbonate; Young Adult

This study investigated the effects of sodium bicarbonate (NaHCO3) ingestion on simulated water polo match performance. Twelve elite players from the Australian National Women's Water Polo Squad (age 23.7 +/- 3.0 yr, height 1.73 +/- 0.05 m, body mass 75.7 +/- 8.0 kg) participated in the study. In a randomized cross-over double-blind design, players ingested 0.3 g/kg of NaHCO3 or placebo 90 min before performing a 59-min match-simulation test (MST) that included 56 x 10-m maximal-sprint swims as the performance measure. Capillary blood samples were obtained preingestion, pre- and post-warm-up, and after each quarter of the MST. Preexercise ingestion of NaHCO3 was effective in enhancing extracellular pH from baseline levels of 7.41; +/- 0.01 (M; +/- 90% confidence limits) to 7.49; +/- 0.01 and bicarbonate levels from 24.4; +/- 0.3 to 28.5; +/- 0.5 mmol/L. The percentage difference in mean sprint times between trials showed no substantial effects of NaHCO3 (0.4; +/- 1.0, effect size = 0.09; +/- 0.23; p = .51). These findings are contrary to those of previous NaHCO3 studies on simulated team-sport performance, but this investigation is unique in that it examined highly trained athletes performing sport-specific tasks. In conclusion, water polo players should not expect substantial enhancement in intermittent-sprint performance from NaHCO3 supplementation.

Topics: Alkalosis; Athletic Performance; Cross-Over Studies; Double-Blind Method; Female; Humans; Hydrogen-Ion Concentration; Oxygen Consumption; Sodium Bicarbonate; Swimming; Task Performance and Analysis; Young Adult

Pre-exercise alkalosis and an active recovery improve the physiological state of recovery through slightly different mechanisms (e. g. directly increasing extracellular bicarbonate (HCO3 (-)) vs. increasing blood flow), and combining the two conditions may provide even greater influence on blood acid-base recovery from high-intensity exercise. Nine subjects completed four trials (Placebo Active ( PLAC A), sodium bicarbonate (NaHCO3) Active ( BICARB A), Placebo Passive ( PLAC P) and NaHCO3 Passive ( BICARB P)), each consisting of three, 30-s maximal efforts with a three min recovery between each effort. Pre-exercisealkalosis was evident in both NaHCO3 conditions, as pH and HCO3 (-) were significantly higher than both Placebo conditions (pH: 7.46 ± 0.04 vs. 7.39 ± 0.02; HCO3 (-): 28.8 ± 1.9 vs. 23.2 ± 1.4  mmol·L (-1); p<0.001). In terms of performance, significant interactions were observed for average speed (p<0.05), with higher speeds evident in the BICARB A condition (3.9 ± 0.3 vs. 3.7 ± 0.4  m·s (-1)). Total distance covered was different (p=0.05), with post hoc differences evident between the BICARB A and PLAC P conditions (368 ± 33 vs. 364 ± 35 m). These data suggest that successive 30-s high intensity performance may be improved when coupled with NaHCO3 supplementation.

Topics: Acid-Base Equilibrium; Alkalosis; Athletic Performance; Bicarbonates; Extracellular Space; Humans; Hydrogen-Ion Concentration; Male; Recovery of Function; Running; Single-Blind Method; Sodium Bicarbonate

The aim of this study was to determine if inducing metabolic alkalosis would alter neuromuscular control after 50 min of standardized submaximal cycling. Eight trained male cyclists (mean age 32 years, s = 7; [Vdot]O(2max) 62 ml . kg(-1) x min(-1), s = 8) ingested capsules containing either CaCO(3) (placebo) or NaHCO(3) (0.3 g x kg(-1) body mass) in eight doses over 2 h on two separate occasions, commencing 3 h before exercise. Participants performed three maximal isometric voluntary contractions (MVC) of the knee extensors while determining the central activation ratio by superimposing electrical stimulation both pre-ingestion and post-exercise, followed by a 50-s sustained maximal contraction in which force, EMG amplitude, and muscle fibre conduction velocity were assessed. Plasma pH, blood base excess, and plasma HCO(3) were higher (P < 0.01) during the NaHCO(3) trial. After cycling, muscle fibre conduction velocity was higher (P < 0.05) during the 50-s sustained maximal contraction with NaHCO(3) than with placebo (5.1 m x s(-1), s = 0.4 vs. 4.2 m x s(-1), s = 0.4) while the EMG amplitude remained the same. Force decline rate was less (P < 0.05) during alkalosis-sustained maximal contraction and no differences were shown in central activation ratio. These data indicate that induced metabolic alkalosis can increase muscle fibre conduction velocity following prolonged submaximal cycling.

Topics: Adult; Alkalosis; Bicycling; Calcium Carbonate; Electric Stimulation; Electromyography; Exercise; Humans; Hydrogen-Ion Concentration; Isometric Contraction; Knee; Male; Muscle Fatigue; Muscle Fibers, Skeletal; Muscle, Skeletal; Physical Endurance; Sodium Bicarbonate

The objective of this study was to examine the effect of sodium bicarbonate (NaHCO3-) ingestion on performance and perceptual responses in a laboratory-simulated bicycle motocross (BMX) qualification series. Nine elite BMX riders volunteered to participate in this study. After familiarization, subjects undertook two trials involving repeated sprints (3 x Wingate tests [WTs] separated by 30 minutes of recovery; WT1, WT2, WT3). Ninety minutes before each trial, subjects ingested either NaHCO3- or placebo in a counterbalanced, randomly assigned, double-blind manner. Each trial was separated by 4 days. Performance variables of peak power, mean power, time to peak power, and fatigue index were calculated for each sprint. Ratings of perceived exertion were obtained after each sprint, and ratings of perceived readiness were obtained before each sprint. No significant differences were observed in performance variables between successive sprints or between trials. For the NaHCO3- trial, peak blood lactate during recovery was greater after WT2 (p < 0.05) and tended to be greater after WT3 (p = 0.07), and ratings of perceived exertion were not influenced. However, improved ratings of perceived readiness were observed before WT2 and WT3 (p < 0.05). In conclusion, NaHCO3- ingestion had no effect on performance and RPE during a series of three WT simulating a BMX qualification series, possibly because of the short duration of each effort and the long recovery time used between the three WTs. On the contrary, NaHCO3- ingestion improved perceived readiness before each WT.

Topics: Acid-Base Equilibrium; Alkalosis; Analysis of Variance; Athletic Performance; Bicycling; Cross-Over Studies; Double-Blind Method; Humans; Lactates; Male; Sodium Bicarbonate; Young Adult

The aim of this study was to observe the influence of pre-exercise sodium bicarbonate (NaHCO3) ingestion and varying recovery modes on acid-base recovery from a single bout of supramaximal exercise. Nine male subjects completed four separate, randomized cycle ergometer exercise trials to volitional fatigue at 120% maximum power output, under the following conditions: 0.3 g.kg(-1) BW NaHCO3 ingestion with passive recovery (BICARB P), 0.3 g.kg (-1) BW NaHCO3 ingestion with active recovery (BICARB A), placebo ingestion with passive recovery (PLAC P) and placebo ingestion with active recovery (PLAC A). Capillary blood samples were obtained every minute for 15 min during recovery. Significant main effects for pH were observed for time (F = 42.1, p < 0.001), intervention (BICARB and PLAC) (F = 1117.3, p < 0.001) and recovery condition (F = 150.0, p < 0.001), as the BICARB condition reduced acid-base perturbation. Significant interaction effects were observed between conditions (BICARB and PLAC) for active and passive recovery modes (F = 29.1, p < 0.001) as the active recovery facilitated H+ removal better than the passive condition. Pre-exercise alkalosis attenuates blood acid-base perturbations from supramaximal exercise to exhaustion, regardless of whether the recovery mode is active or passive. These findings suggest that individuals may benefit from introducing a pre-exercise alkalotic condition while including passive recovery during high-intensity training protocols.

Topics: Acid-Base Equilibrium; Adult; Alkalosis; Bicycling; Carbon Dioxide; Double-Blind Method; Ergometry; Humans; Hydrogen-Ion Concentration; Lactic Acid; Male; Oxygen; Physical Exertion; Recovery of Function; Sodium Bicarbonate

The aim of the present study was to investigate whether preexercise sodium-bicarbonate ingestion improves judo-related performance. The study used 2 different protocols to evaluate performance: 3 bouts of a specific judo test (n = 9) and 4 bouts of the Wingate test for upper limbs (n = 14). In both protocols athletes ingested 0.3 g/kg of sodium bicarbonate or placebo 2 h before the tests. Blood samples were collected to determine lactate level, and levels of perceived exertion were measured throughout the trials. The study used a double-blind, counterbalanced, crossover design. Ingestion of sodium bicarbonate improved performance in Bouts 2 and 3 of Protocol 1 (P < 0.05), mean power in Bouts 3 and 4 of Protocol 2 (P < 0.05), and peak power in Bout 4 of Protocol 2 (P < 0.05). Ingestion of bicarbonate increased lactate concentration in Protocol 1 (P < 0.05) but not in Protocol 2. Ratings of perceived exertion did not differ between treatments. In conclusion, sodium bicarbonate improves judo-related performance and increases blood lactate concentration but has no effect on perceived exertion.

Topics: Acid-Base Equilibrium; Adult; Alkalosis; Cross-Over Studies; Double-Blind Method; Humans; Lactates; Martial Arts; Sodium Bicarbonate; Time Factors

The purpose of this study was to determine the effect of oral administration of sodium bicarbonate (NaHCO3) on surface electromyogram (SEMG) activity from the vastus lateralis (VL) during repeated cycling sprints (RCS). Subjects performed two RCS tests (ten 10-s sprints) interspersed with both 30-s and 360-s recovery periods 1 h after oral administration of either NaHCO3 (RCSAlk) or CaCO3 (RCSPla) in a random counterbalanced order. Recovery periods of 360 s were set before the 5th and 9th sprints. The rate of decrease in plasma HCO3- concentration during RCS was significantly greater in RCSAlk than in RCSPla, but the rates of decline in blood pH during the two RCS tests were similar. There was no difference between change in plasma lactate concentration in RCSAlk and that in RCSPla. Performance during RCSAlk was similar to that during RCSPla. There were no differences in oxygen uptake immediately before each cycling sprint (preVO2) and in SEMG activity between RCSAlk and RCSPla. In conclusion, oral administration of NaHCO3 did not affect SEMG activity from the VL. This suggests that the muscle recruitment strategy during RCS is not determined by only intramuscular pH.

Topics: Adult; Alkalosis; Bicycling; Blood Gas Analysis; Body Mass Index; Electromyography; Exercise Test; Humans; Hydrogen-Ion Concentration; Lactic Acid; Male; Muscle Fatigue; Muscle, Skeletal; Oxygen Consumption; Phosphocreatine; Sodium; Sodium Bicarbonate

Sodium bicarbonate (NaHCO3) ingestion may prevent exercise-induced perturbations in acid-base balance, thus resulting in performance enhancement. This study aimed to determine whether different levels of NaHCO3 intake influences acid-base balance and performance during high-intensity exercise after 5 d of supplementation.. Twenty-four men (22 +/- 1.7 yr) were randomly assigned to one of three groups (eight subjects per group): control (C, placebo), moderate NaHCO3 intake (MI, 0.3 g x kg(-1) x d(-1)), and high NaHCO3 intake (HI, 0.5 g x kg(-1) x d(-1)). Arterial pH, HCO3(-), PO2, PCO2, K+, Na, base excess (BE), lactate, and mean power (MP) were measured before and after a Wingate test pre- and postsupplementation.. HCO3(-) increased proportionately to the dosage level. No differences were detected in C. Supplementation increased MP (W x kg(-)) in MI (7.36 +/- 0.7 vs 6.73 +/- 1.0) and HI (7.72 +/- 0.9 vs 6.69 +/- 0.6), with HI being more effective than MI. NaHCO3 ingestion resulted postexercise in increased lactate (mmol x L(-1)) (12.3 +/- 1.8 vs 10.3 +/- 1.9 and 12.4 +/- 1.2 vs 10.4 +/- 1.5 in MI and HI, respectively), reduced exercise-induced drop of pH (7.305 +/- 0.04 vs 7.198 +/- 0.02 and 7.343 +/- 0.05 vs 7.2 +/- 0.01 in MI and HI, respectively) and HCO3(-) (mmol x L(-1)) (13.1 +/- 2.4 vs 17.5 +/- 2.8 and 13.2 +/- 2.7 vs 19.8 +/- 3.2 for HCO3 in MI and HI, respectively), and reduced K (3.875 +/- 0.2 vs 3.625 +/- 0.3 mmol x L(-1) in MI and HI, respectively).. NaHCO3 administration for 5 d may prevent acid-base balance disturbances and improve performance during anaerobic exercise in a dose-dependent manner.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Adult; Alkalosis; Dietary Supplements; Exercise; Humans; Male; Oxygen Consumption; Sodium Bicarbonate; Surveys and Questionnaires; Time Factors

The present study investigated the effect of preexercise metabolic alkalosis on the primary component of oxygen uptake (Vo(2)) kinetics, characterized by tau(1). Seven healthy physically active nonsmoking men, aged 22.4 +/- 1.8 (mean +/- SD) yr, maximum Vo(2) (Vo(2 max)) 50.4 +/- 4 ml.min(-1).kg(-1), performed two bouts of cycling, corresponding to 40 and 87% of Vo(2 max), lasting 6 min each, separated by a 20-min pause, once as a control study and a few days later at approximately 90 min after ingestion of 3 mmol/kg body wt of NaHCO(3). Blood samples for measurements of bicarbonate concentration and hydrogen ion concentration were taken from antecubital vein via catheter. Pulmonary Vo(2) was measured continuously breath by breath. The values of tau(1) were calculated by using six various approaches published in the literature. Preexercise level of bicarbonate concentration after ingestion of NaHCO(3) was significantly elevated (P < 0.01) compared with the control study (28.96 +/- 2.11 vs. 24.84 +/- 1.18 mmol/l; P < 0.01), and [H(+)] was significantly (P < 0.01) reduced (42.79 +/- 3.38 nmol/l vs. 46.44 +/- 3.51 nmol/l). This shift (P < 0.01) was also present during both bouts of exercise. During cycling at 40% of Vo(2 max), no significant effect of the preexercise alkalosis on the magnitude of tau(1) was found. However, during cycling at 87% of Vo(2 max), the tau(1) calculated by all six approaches was significantly (P < 0.05) reduced, compared with the control study. The tau(1) calculated as in Borrani et al. (Borrani F, Candau R, Millet GY, Perrey S, Fuchsloscher J, and Rouillon JD. J Appl Physiol 90: 2212-2220, 2001) was reduced on average by 7.9 +/- 2.6 s, which was significantly different from zero with both the Student's t-test (P = 0.011) and the Wilcoxon's signed-ranks test (P = 0.014).

Topics: Administration, Oral; Adult; Alkalosis; Computer Simulation; Dose-Response Relationship, Drug; Exercise Test; Humans; Kinetics; Male; Metabolic Clearance Rate; Models, Biological; Oxygen; Oxygen Consumption; Physical Endurance; Sodium Bicarbonate

Previous studies have shown that induced metabolic alkalosis, via sodium bicarbonate (NaHCO3) ingestion, can improve short-term, repeated-sprint ability. The purpose of this study was to assess the effects of NaHCO3 ingestion on a prolonged, intermittent-sprint test (IST).. Seven female team-sport athletes (mean +/- SD: age = 19 +/- 1 yr, VO2peak = 45.3 +/- 3.1 mL x kg(-1) x min(-1)) volunteered for the study, which had received ethics clearance. The athletes ingested two doses of either 0.2 g x kg(-1) of NaHCO3 or 0.138 g x kg(-1) of NaCl (placebo), in a double-blind, random, counterbalanced order, 90 and 20 min before performing the IST on a cycle ergometer (two 36-min "halves" of repeated approximately 2-min blocks: all-out 4-s sprint, 100 s of active recovery at 35% VO2peak, and 20 s of rest). Capillary blood samples were drawn from the ear lobe before ingestion, and before, during, and after each half of the IST. VO2 was also recorded at regular intervals throughout the IST.. Resting plasma bicarbonate concentration ([HCO3-]) averaged 22.6 +/- 0.9 mmol x L(-1), and at 90 min post-ingestion was 21.4 +/- 1.5 and 28.9 +/- 2.8 mmol x L-1 for the placebo and NaHCO3 conditions, respectively (P < 0.05). Plasma [HCO3-] during the NaHCO3 condition remained significantly higher throughout the IST compared with both placebo and pre-ingestion. There was a trend toward improved total work in the second (P = 0.08), but not first, half of the IST after the ingestion of NaHCO3. Furthermore, subjects completed significantly more work in 7 of 18 second-half, 4-s sprints after NaHCO3 ingestion.. The results of this study suggest that NaHCO3 ingestion can improve intermittent-sprint performance and may be a useful supplement for team-sport athletes.

Topics: Adult; Alkalosis; Bicarbonates; Double-Blind Method; Drug Administration Schedule; Ergometry; Female; Heart Rate; Humans; Hydrogen-Ion Concentration; Lactic Acid; Oxygen Consumption; Pulmonary Gas Exchange; Running; Sodium Bicarbonate

The purpose of this study was to measure the recovery kinetics of pH and lactate for the conditions of pre-exercise acidosis, alkalosis, and placebo states. Twelve trained male cyclists completed 3 exercise trials (110% workload at VO2max), ingesting either 0.3 g/kg of NH4Cl (ACD), 0.2 g/kg of Na+HCO3- and 0.2 g/kg of sodium citrate (ALK), or a placebo (calcium carbonate) (PLAC). Blood samples (heated dorsal hand vein) were drawn before, during, and after exercise. Exercise-induced acidosis was more severe in the ACD and PLAC trials (7.15 +/- 0.06, 7.21 +/- 0.07, 7.16 +/- 0.06, P < 0.05, for ACD, ALK, PLAC, respectively). Recovery kinetics for blood pH and lactate, as assessed by the monoexponential slope constant, were not different between trials (0.057 +/- 0.01, 0.050 +/- 0.01, 0.080 +/- 0.02, for ACD, ALK, PLAC, respectively). Complete recovery of blood pH from metabolic acidosis can take longer than 45 min. Such a recovery profile is nonlinear, with 50% recovery occurring in approximately 12 min. Complete recovery of blood lactate can take longer than 60 min, with 50% recovery occurring in approximately 30 min. Induced alkalosis decreases metabolic acidosis and improves pH recovery compared to acidodic and placebo conditions. Although blood pH and lactate are highly correlated during recovery from acidosis, they recover at significantly different rates.

Topics: Acid-Base Equilibrium; Acidosis; Adult; Alkalosis; Ammonium Chloride; Cross-Over Studies; Humans; Kinetics; Lactates; Male; Oxygen Consumption; Physical Exertion; Sodium Bicarbonate

During heavy-intensity exercise, the mechanisms responsible for the continued slow decline in phosphocreatine concentration ([PCr]) (PCr slow component) have not been established. In this study, we tested the hypothesis that a reduced intracellular acidosis would result in a greater oxidative flux and, consequently, a reduced magnitude of the PCr slow component. Subjects (n = 10) performed isotonic wrist flexion in a control trial and in an induced alkalosis (Alk) trial (0.3g/kg oral dose of NaHCO3, 90 min before testing). Wrist flexion, at a contraction rate of 0.5 Hz, was performed for 9 min at moderate- (75% of onset of acidosis; intracellular pH threshold) and heavy-intensity (125% intracellular pH threshold) exercise. 31P-magnetic resonance spectroscopy was used to measure intracellular [H+], [PCr], [Pi], and [ATP]. The initial recovery data were used to estimate the rate of ATP synthesis and oxidative flux at the end of heavy-intensity exercise. In repeated trials, venous blood sampling was used to measure plasma [H+], [HCO3-], and [Lac-]. Throughout rest and exercise, plasma [H+] was lower (P < 0.05) and [HCO3-] was elevated (P < 0.05) in Alk compared with control. During the final 3 min of heavy-intensity exercise, Alk caused a lower (P < 0.05) intracellular [H+] [246 (SD 117) vs. 291 nmol/l (SD 129)], a greater (P < 0.05) [PCr] [12.7 (SD 7.0) vs. 9.9 mmol/l (SD 6.0)], and a reduced accumulation of [ADP] [0.065 (SD 0.031) vs. 0.098 mmol/l (SD 0.059)]. Oxidative flux was similar (P > 0.05) in the conditions at the end of heavy-intensity exercise. In conclusion, our results are consistent with a reduced intracellular acidosis, causing a decrease in the magnitude of the PCr slow component. The decreased PCr slow component in Alk did not appear to be due to an elevated oxidative flux.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Adenosine Diphosphate; Adenosine Triphosphate; Adult; Alkalosis; Exercise; Forearm; Humans; Lactic Acid; Male; Muscle, Skeletal; Oxidative Phosphorylation; Phosphocreatine; Protons; Sodium Bicarbonate

The purpose of this study was to assess the effects of induced metabolic alkalosis, via sodium bicarbonate (NaHCO3) ingestion, on muscle metabolism and power output during repeated short-duration cycle sprints.. : Ten active females (mean +/- SD: age = 19 +/- 2 yr, VO2max = 41.0 +/- 8.8 mL x kg x min ) ingested either 0.3 g x kg NaHCO3 or 0.207 g x kg of NaCl (CON), in a double-blind, random, counterbalanced order, 90 min before performing a repeated-sprint ability (RSA) test (5 x 6-s all-out cycle sprints every 30 s).. Compared with CON, there was a significant increase in resting blood bicarbonate concentration [HCO3] (23.6 +/- 1.1 vs 30.0 +/- 3.0 mmol x L ) and pH (7.42 +/- 0.02 vs 7.50 +/- 0.04), but no significant difference in resting lactate concentration [La] (0.8 +/- 0.2 vs 0.8 +/- 0.3 mmol x L ) during the NaHCO3 trial. Muscle biopsies revealed no significant difference in resting muscle [La], pH, or buffer capacity (beta(in vitro)) between trials (P > 0.05). Compared with CON, the NaHCO3 trial resulted in a significant increase in total work (15.7 +/- 3.0 vs 16.5 +/- 3.1 kJ) and a significant improvement in work and power output in sprints 3, 4, and 5. Despite no significant difference in posttest muscle pH between conditions, the NaHCO3 trial resulted in significantly greater posttest muscle [La].. As NaHCO3 ingestion does not increase resting muscle pH or beta(in vitro), it is likely that the improved performance is a result of the greater extracellular buffer concentration increasing H efflux from the muscles into the blood. The significant increase in posttest muscle [La] in NaHCO3 suggests that an increased anaerobic energy contribution is one mechanism by which NaHCO3 ingestion improved RSA.

Topics: Adult; Alkalosis; Analysis of Variance; Bicycling; Exercise Test; Female; Humans; Hydrogen-Ion Concentration; Lactates; Muscle, Skeletal; Pulmonary Gas Exchange; Sodium Bicarbonate

We examined the effects of pre-exercise sodium bicarbonate (NaHCO3) ingestion on the slow component of oxygen uptake (VO2) kinetics in seven professional road cyclists during intense exercise. One hour after ingesting either a placebo or NaHCO3 (0.3 g x kg body mass(-1)), each cyclist (age, 25 +/- 2 years; VO2max, 74.7 +/- 5.9 ml x kg(-1) x min(-1); mean +/- s) performed two bouts of 6 min duration at an intensity of 90% VO2max interspersed by 8 min of active recovery. Gas exchange and blood data (pH, blood lactate concentration and [HCO3-]) were collected during the tests. In both bouts, the slow component of VO2 was defined as the difference between end-exercise VO2 and the VO2 at the end of the third minute. No significant difference was found in the slow component of VO2 between conditions in the first (NaHCO3, 210 +/- 69 ml; placebo, 239 +/- 105 ml) or second trial (NaHCO3, 123 +/- 88 ml; placebo, 197 +/- 101 ml). In conclusion, pre-exercise NaHCO3 ingestion did not significantly attenuate the VO2 slow component of professional road cyclists during high-intensity exercise.

Topics: Acid-Base Equilibrium; Adult; Alkalosis; Analysis of Variance; Bicycling; Exercise Test; Humans; Lactic Acid; Male; Oxygen Consumption; Physical Endurance; Physical Fitness; Pulmonary Gas Exchange; Sodium Bicarbonate

Administration of bicarbonate has been shown to cause metabolic alkalosis both in man and in horses and is, therefore, thought to increase the buffering capacity of the body and thereby delay the onset of fatigue. However, results regarding the influence of sodium bicarbonate loading on performance both in human athletes and in horses are conflicting. The aim of this study was, therefore, to investigate the metabolic response to a standardised treadmill exercise test to fatigue, in horses given bicarbonate (0.6 g/kg bwt), in comparison to horses given placebo (water). Five Standardbred trotters performed the test on 2 occasions. Venous blood samples were collected before and after administration of test substance, during exercise and during recovery. Muscle biopsy specimens were taken at rest, postexercise and at 15 min of recovery. The increases in pH and concentration of bicarbonate in the blood and the shift seen in base excess showed that the administration of sodium bicarbonate caused metabolic alkalosis. Exercise caused similar decreases in muscle ATP, CP and glycogen and similar increases in muscle IMP, lactate and plasma lactate and uric acid concentrations both in the placebo- and bicarbonate-treated group. The effect upon postexercise muscle and plasma metabolites was similar with both test treatments. Duration of exercise did not change after sodium bicarbonate intake. In conclusion, sodium bicarbonate caused metabolic alkalosis, but did not affect the metabolic response or duration of exercise.

Topics: Acid-Base Equilibrium; Alkalosis; Animals; Cross-Over Studies; Exercise Test; Female; Heart Rate; Horse Diseases; Horses; Hydrogen-Ion Concentration; Male; Muscle, Skeletal; Physical Conditioning, Animal; Physical Exertion; Sodium Bicarbonate

Acute metabolic alkalosis (NaHCO(3)), acidosis (NH(4)Cl), and placebo (NaCl) were induced in 15 healthy volunteers (12 females, median age 34 (range 24-56) years) in a double blind, placebo controlled study to evaluate the presence of the effects on airway calibre. Acid-base shifts were determined by capillary blood gas sampling. Measurements were performed at the maximal acid-base shift, 90 min after intervention. Airway resistance (R(aw)) and specific airway conductance (sG(aw)), were evaluated, as primary variables, pre and post intervention. Secondary variables, including bronchial responsiveness to histamine, maximal respiratory mouth pressures and grip strength, were evaluated post intervention. In alkalosis, base excess (BE) increased from -0.3 (-3.0-1.9) to 3.0 (1.0-4.8) mmol/l and pH increased from 7.41 (7.37-7.43) to 7.44 (7.39-7.47) (both P<0.01), accompanied by an increase in Pa(CO(2)): 4.7 (4.0-5.7) to 5.0 (4.7-6.1) kPa (P<0.05). R(aw) increased from 0.156 (0.134-0.263) to 0.169 (0.132-0.271) kPa s/L (P<0.05), sG(aw) decreased, but this was not statistically significantly. In acidosis, BE decreased from -0.2 (-2.0-2.2) to -3.5 (-6.3-1.1) mmol/l and pH decreased from 7.41 (7.39-7.45) to 7.36 (7.31-7.40) (both P<0.01), accompanied by a non-significant decrease in Pa(CO(2)). Changes in R(aw) and sG(aw) were contrary to those in alkalosis, but did not reach statistical significance. Acute metabolic acid-base shifts mildly influence the airway calibre in healthy human subjects.

Topics: Acidosis; Adult; Airway Resistance; Alkalosis; Ammonium Chloride; Blood Gas Analysis; Bronchoconstrictor Agents; Bronchodilator Agents; Double-Blind Method; Female; Forced Expiratory Volume; Hand Strength; Histamine; Humans; Hydrogen-Ion Concentration; Lung; Male; Middle Aged; Muscle, Skeletal; Pulmonary Ventilation; Random Allocation; Sodium Bicarbonate

Fifteen males were studied before, during, and in recovery from exhaustive resistance exercise 105 min after ingesting 0.3 g.kg-1 of either a placebo (white flour) or sodium bicarbonate (NaHCO3).. The exercise consisted of five maximal sets on a leg press machine, The load was adjusted to maintain the number of repetitions per set for each subject at approximately 12 repetitions. A significant (P < 0.05) increase in pH (7.40 to 7.47), oxygenated base excess (OxyBE) (-1.3 to 4.0 mEq.L-1), and bicarbonate concentration ([HCO3-]) (22.8 to 27.4 mM) was achieved before exercise with the ingestion of NaHCO3.. The exercise protocol produced significant changes in acid base status consistent with metabolic acidosis for both trials (pH sets 1-5: placebo, 7.4 to 7.26; NaHCO3, 7.47 to 7.33), (OxyBE sets 1-5: placebo, -1.3 to -12.3 mEq.L-1; NaHCO3, 4.0 to -6.9 mEq.L-1) and ([HCO3-] sets 1-5: placebo, 22.9 to 14.0 mM; NaHCO3, 27.4 to 17.6 mM). After every set; pH, OxyBE, and [HCO3-] were significantly higher in the NaHCO3 trial. Blood lactate concentration ([La-]) significantly increased throughout exercise for both trials ([La-] sets 1-5: placebo, 4.6 to 11.3 mM; NaHCO3, 4.8 to 13.4 mM). After sets 4 and 5, blood [La-] was significantly higher in the NaHCO3 trial. Bicarbonate ingestion did not improve performance (total repetitions: NaHCO3 = 59 +/- 3; placebo = 60 +/- 2).. This may be a result of a lower demand on the whole body metabolic system in comparison with that for other modes of exercise in which ergogenic effects have been found.

Topics: Adult; Alkalosis; Exercise; Humans; Leg; Male; Muscle Fatigue; Muscle, Skeletal; Physical Endurance; Sodium Bicarbonate; Weight Lifting

Seven healthy physically active nonsmoking men, aged 22.4 +/- (SD) 1.8 years performed two 6 min bouts of cycling at 40% VO2max (sub-lactate threshold/low power output exercise) and 87% VO2max (supra-lactate threshold/high power output exercise) at 70 rev.min-1, separated by 20 minutes rest, on two occasions: once as a control experiment (test C) and on a different day at approximately 1.5 h after ingestion of 250 mg (3 mmol).(kg body weight)-1 of NaHCO3 (test A). At the onset of low and high power output exercise performed after ingestion of NaHCO3, antecubital venous blood pH and HCO3- were significantly elevated (p < 0.05). Moreover, blood pH and HCO3-, tested at every minute of low and high power output exercise, was significantly higher (p < 0.05) in test A than in test C. No difference was found in plasma lactate concentration [La]pl during low power output exercise between A and C tests. In the terminal phase of the high power output exercise (87% VO2max) the level of [La]pl rose more rapidly in test A than in test C, reaching in the sixth minute of cycling 8.27 +/- 1.11 and 6.76 +/- 0.68 mmol.l-1 (p < 0.01) in test A and C, respectively. No significant differences were found in the rate of VO2 measured breath-by-breath between A and C tests, both during low and high power output exercise. The slow component of VO2 kinetics (expressed by difference between VO2 measured at the 6th minute of exercise minus the VO2 reached at the 3rd minute), occurring only during exercise corresponding to 87% VO2, was not significantly different in C and A tests (0.373 +/- 0.050 and 0.339 +/- 0.078 1 O2, respectively). The total VO2 consumed throughout the six minute cycling at power output of 40 and 87% VO2max performed in control conditions and after ingestion of NaHCO3 was not significantly different. We have demonstrated that significantly reduced exercise acidemia accompanied by a significantly elevated level of [La]pl accumulation, did not affect the slow component of the VO2 kinetics and the magnitude of oxygen uptake during exercise corresponding to 40 and 87% of VO2max.

Topics: Acid-Base Equilibrium; Adult; Alkalosis; Exercise; Exercise Test; Humans; Kinetics; Male; Oxygen Consumption; Pulmonary Gas Exchange; Sodium Bicarbonate

Sodium lactate inhibits ventilation when infused in healthy human subjects. This effect has been attributed to lactate-induced metabolic alkalosis. In order to further delineate the mechanisms responsible for this depression of ventilation, healthy humans were infused with sodium lactate with or without acetazolamide. Sodium lactate increased blood pH from 7.37 +/- 0.02 to 7.47 +/- 0.01 and induced a sustained urinary excretion of bicarbonate. PO2 of arterialized blood decreased by 10.3 +/- 2.1 mmHg, indicating an inhibition of ventilation. Acetazolamide decreased lactate-induced alkalinisation of blood (pH after lactate + acetazolamide 7.42 +/- 0.02), but did not prevent the drop in PO2. Acetazolamide alone tended to stimulate ventilation, as indicated by an increase in PO2. These results indicate that sodium lactate inhibits ventilation independently of changes in systemic blood pH. Alkalinization of the cerebrospinal fluid, or other central effects of lactate, is probably responsible for this ventilatory depression.

Topics: Acetazolamide; Acid-Base Equilibrium; Adult; Alkalosis; Blood Gas Analysis; Carbonic Anhydrase Inhibitors; Drug Combinations; Humans; Hydrogen-Ion Concentration; Infusions, Intravenous; Male; Reference Values; Respiration; Sodium Bicarbonate; Sodium Lactate

Previous studies have shown that sodium bicarbonate ingestion prior to exercise may improve performance during repeated (interval) bouts. To examine the practical implications of such findings, seven collegiate swimmers participated in simulated swim competitions of multiple events following sodium bicarbonate (B) ingestion, placebo (P) ingestion and control (C--no ingestion) treatments. Each swimmer reported to the laboratory 1 h prior to the simulated competitions (72 h apart) and was randomly assigned to one of the three experimental treatments. Competition consisted of one relay (100 yards; 91.4 m) and two individual (200 yards; 182.8 m) swimming events with 20 min rest between events. Analysis of variance (ANOVA) with repeated measures revealed no significant differences in performance times as a result of the three treatments (P greater than 0.05). The results suggest that sodium bicarbonate ingestion prior to swim competition consisting of significant rest intervals between events is not an ergogenic procedure.

Topics: Adult; Alkalosis; Analysis of Variance; Bicarbonates; Humans; Male; Physical Exertion; Sodium; Sodium Bicarbonate; Swimming; Time Factors

Four groups of male subjects participated in anaerobic testing on a Repco EX10 cycle ergometer to determine the effectiveness of sodium bicarbonate (0.3 g kg-1 body mass) as an ergogenic aid during exercise of 10, 30, 120 and 240 s duration. Blood was collected 90 min prior to ingestion of sodium bicarbonate (NaHCO3), after ingestion of NaHCO3 and immediately post-exercise from a heated (43-46 degrees C) fingertip and analysed immediately post-collection for pH, base excess, bicarbonate and lactate. The total work undertaken (kJ) and peak power achieved during the tests were also obtained via a Repco Work Monitor Unit. Blood bicarbonate levels were again increased above the control and placebo conditions (P < 0.001) and blood lactate levels were also increased following the bicarbonate trials. The pH levels fell significantly (P < 0.05) below the control and placebo conditions in all trials. The results indicate that NaHCO3 at this dosage has no ergogenic benefit for work of either 10 or 30 s duration, even though blood bicarbonate levels were significantly increased (P < 0.05) following ingestion of NaHCO3. For work periods of 120 and 240 s, performance was significantly increased (P < 0.05) above the control and placebo conditions following NaHCO3 ingestion.

Topics: Adult; Alkalosis; Anaerobic Threshold; Bicarbonates; Double-Blind Method; Exercise; Humans; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Male; Physical Endurance; Sodium; Sodium Bicarbonate

Seven healthy male subjects performed 10 maximal 6-s sprints, separated by 30-s recovery periods, on a non-motorized treadmill. On two occasions, separated by 3 days, the subjects ingested a solution of either sodium bicarbonate (NaHCO3; alkaline) or sodium chloride (NaCl; placebo), 2.5 h prior to exercise. The doses were 0.3 g kg-1 body mass for the alkaline treatment and 1.5 g total for the placebo, dissolved in 500 ml of water. The order of testing was randomly assigned. Pre-exercise blood pH was 7.43 +/- 0.02 and 7.38 +/- 0.01 for the alkaline and placebo trials respectively (P less than 0.01). Performance indices (i.e. mean and peak power outputs and mean and peak running speeds) were significantly reduced as a result of the cumulative effects of successive sprints, but not significantly affected by the treatments. However, the total work done (i.e. mean power output) in the alkaline condition was 2% higher than that achieved in the placebo condition. Post-exercise blood lactate concentrations were higher for the alkaline treatment than for the placebo condition (15.3 +/- 3.7 vs 13.6 +/- 3.0 mM respectively; P less than 0.01), but blood pH was similar in both conditions (alkaline: 7.15 +/- 0.13; placebo: 7.09 +/- 0.11). In both conditions, a relationship was found between post-exercise blood lactate and mean power output (alkaline: r = 0.82, P less than 0.01; placebo: r = 0.79, P less than 0.01). No significant differences were found in VE, VO2 and VCO2 between the two experimental conditions. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood, but has no effect on the power output during repeated bouts of brief maximal exercise.

Topics: Adult; Alkalosis; Bicarbonates; Exercise Test; Fatigue; Heart Rate; Humans; Hydrogen-Ion Concentration; Lactates; Male; Physical Exertion; Plasma Volume; Respiration; Running; Sodium; Sodium Bicarbonate; Sodium Chloride

In order to test the effect of artificially induced alkalosis and acidosis on the appearance of plasma lactate and work production, six well-trained oarsmen (age = 23.8 +/- 2.5 years; mass = 82.0 +/- 7.5 kg) were tested on three separate occasions after ingestion of 0.3 g.kg-1. NH4Cl (acidotic), NaHCO3 (alkalotic) or a placebo (control). Blood was taken from a forearm vein immediately prior to exercise for determination of pH and bicarbonate. One hour following the ingestion period, subjects rowed on a stationary ergometer at a pre-determined sub-maximal rate for 4 min, then underwent an immediate transition to a maximal effort for 2 min. Blood samples from an indwelling catheter placed in the cephalic vein were taken at rest and every 30 s during the 6 min exercise period as well as at 1, 3, 6, 9, 12, 15, 18, 21, 25 and 30 min during the passive recovery period. Pre-exercise blood values demonstrated significant differences (p less than 0.01) in pH and bicarbonate in all three conditions. Work outputs were unchanged in the submaximal test and in the maximal test (p greater than 0.05), although a trend toward decreased production was evident in the acidotic condition. Analysis of exercise blood samples using ANOVA with repeated measures revealed that the linear increase in plasma lactate concentration during control was significantly greater than acidosis (p less than 0.01). Although plasma lactate values during alkalosis were consistently elevated above control there was no significant difference in the linear trend (p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acid-Base Equilibrium; Acidosis; Adult; Alkalosis; Ammonium Chloride; Bicarbonates; Economics; Humans; Hydrogen-Ion Concentration; Lactates; Male; Physical Exertion; Sodium; Sodium Bicarbonate

Six trained male athletes who competed regularly in 400 metre races, were studied under control, alkalotic (NaHCO3) and placebo (CaCO3) conditions to study the effect of induced metabolic alkalosis on 400 m racing time. Pre and post exercise blood samples in the three conditions were analysed for pH, bicarbonate and base excess. Following ingestion of NaHCO3, pre-exercise pH, bicarbonate and base excess levels were significantly higher than either control or placebo conditions. In the alkalotic condition the subjects ran significantly (p less than 0.005) faster (1.52 s) than either the control of placebo conditions. The post-exercise pH, bicarbonate and base excess levels were all lower in the alkalotic condition than in the others. The results suggest that NaH-CO3 can be used as an effective ergogenic aid and support the speculation that the increased extracellular buffering afforded by NaHCO3 ingestion facilitated efflux of H+ from the working tissues, thus decreasing intracellular pH and hence offsetting fatigue.

Topics: Adult; Alkalosis; Bicarbonates; Humans; Hydrogen-Ion Concentration; Male; Running; Sodium; Sodium Bicarbonate

It is uncertain whether, in humans, potassium depletion can cause or sustain metabolic alkalosis of clinically important degree in the absence of coexisting known alkalosis-producing conditions. Previously we found, in normal humans ingesting abundant NaCl, that dietary K+ depletion alone can induce and sustain a small decrease in blood acidity and increase in plasma bicarbonate concentration; we hypothesized that more severe alkalosis was prevented by mitigating mechanisms initiated by renal retention of dietary NaCl that was induced by K+ depletion. To ascertain the acid-base response to dietary K+ depletion under conditions in which the availability of NaCl for retention is greatly limited, in the present study of six normal men we restricted dietary K+ as in the previous study except that intake of NaCl was maintained low (2 to 7 mEq/day, Low NaCl Group) instead of high (126 mEq/day, High NaCl Group). Plasma acid-base composition and renal net-acid excretion (NAE) did not differ significantly between groups during the control period. In the steady state of K+ depletion (days 11 to 15 of K+ restriction), neither plasma K+ concentration (2.9 +/- 0.9 mEq/liter vs. 3.0 +/- 0.1 mEq/liter) nor cumulative K+ deficit (399 +/- 59 mEq vs. 466 +/- 48 mEq) differed significantly between groups. During K+ restriction, persisting metabolic alkalosis developed in both groups, which was more severe in the Low NaCl Group: increment in [HCO3-]p, 7.5 +/- 1.0 mEq/liter versus 2.0 +/- 0.3 mEq/liter, P less than 0.001; decrement in [H+]p, 5.5 +/- 0.6 nEq/liter versus 2.9 +/- 0.4 nEq/liter, P less than 0.003. A significantly more severe alkalosis in the Low NaCl Group was evident at all degrees of K+ deficiency achieved during the course of the 15 days of K+ restriction, and the severity of alkalosis in the Low NaCl Group correlated with the degree of K+ deficiency. During the generation of alkalosis (days 1 to 7 of K+ restriction), NAE increased in the Low NaCl Group whereas it decreased in the High NaCl Group. During the maintenance of alkalosis (days 11 to 15), NAE stabilized in both groups after it returned to values approximating the control values. In both groups, urine Cl- excretion decreased during K+ restriction even though Cl- intake had not been changed, with the result that body Cl- content increased negligibly in the Low NaCl Group (28 +/- 6 mEq) and substantially in the High NaCl Group (355 +/- 64 mEq).(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Adult; Aldosterone; Alkalosis; Bicarbonates; Creatinine; Diet, Sodium-Restricted; Humans; Hydrogen-Ion Concentration; Male; Potassium; Potassium Deficiency; Sodium; Sodium Bicarbonate; Time Factors

Severe metabolic alkalosis is rarely seen in end stage renal disease (ESRD) patients on long-term hemodialysis. This can be life threatening and mortality is exponentially increased when the pH exceeds 7.60. Persistent vomiting, ingestion of alkali for dyspepsia and pica behavior are all potential causes of such severe metabolic alkalosis. The prevalence of pica is increased in chronic kidney disease and ESRD patients, with ice being the most commonly ingested substance. It can cause a myriad of complications including death, but the diagnosis may be elusive unless the pica behavior is witnessed firsthand by others since patients do not typically disclose their behavior. We present the case of a hemodialysis patient with severe alkalemia, hypernatremia, and excessive interdialytic weight gains resulting in recurrent hospitalizations for fluid overload due to baking soda pica behavior.

Topics: Alkalosis; Humans; Kidney Failure, Chronic; Pica; Renal Dialysis; Sodium Bicarbonate

Sodium bicarbonate, in the form of baking soda, is widely used as a home remedy, and as an additive for personal and household cleaning products. Its toxicity has previously been reported following oral ingestion in the setting of dyspepsia. However, its use as a non-ingested agent, like a toothpaste additive, has not been reported as a potential cause of toxicity.. We are reporting a case of an 80-year-old woman who presented with chronic metabolic alkalosis and hypokalemia secondary to exogenous alkali exposure from baking soda as a toothpaste additive, which might have represented an underreported ingestion of the substance.. Considering that one teaspoon of baking soda provides approximately 59 m-equivalents (mEq) of bicarbonate, specific questioning on its general use should be pursued in similar cases of chloride resistant metabolic alkalosis.

Topics: Aged, 80 and over; Alkalosis; Chlorides; Female; Humans; Hypokalemia; Renal Insufficiency, Chronic; Sodium Bicarbonate; Toothpastes

This study evaluated the ingestion of sodium bicarbonate (NaHCO

Topics: Acid-Base Equilibrium; Adult; Alkalosis; Bicarbonates; Bicycling; Double-Blind Method; Eating; Exercise Test; Fatigue; Heart Rate; Humans; Hydrogen-Ion Concentration; Male; Oxygen Consumption; Sodium Bicarbonate; Young Adult

Baking soda (sodium bicarbonate) is a common household item that has gained popularity as an alternative cancer treatment. Some have speculated that alkali therapy neutralizes the extracellular acidity of tumor cells that promotes metastases. Internet blogs have touted alkali as a safe and natural alternative to chemotherapy that targets cancer cells without systemic effects. Sodium bicarbonate overdose is uncommon, with few reports of toxic effects in humans. The case described here is the first reported case of severe metabolic alkalosis related to topical use of sodium bicarbonate as a treatment for cancer. This case highlights how a seemingly benign and readily available product can have potentially lethal consequences.

Topics: Administration, Topical; Aged; Alkalies; Alkalosis; Female; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Hypokalemia; Neoplasms; Sodium Bicarbonate; Treatment Outcome

The aim of this study was to investigate if a pre-exercise alkalosis-mediated attenuation of HSP72 had any effect on the response of the same stress protein after a subsequent exercise. Seven physically active males [25.0 ± 6.5 years, 182.1 ± 6.0 cm, 74.0 ± 8.3 kg, peak aerobic power (PPO) 316 ± 46 W] performed a repeated sprint exercise (EXB1) following a dose of 0.3 g kg(-1) body mass of sodium bicarbonate (BICARB), or a placebo of 0.045 g kg(-1) body mass of sodium chloride (PLAC). Participants then completed a 90-min intermittent cycling protocol (EXB2). Monocyte expressed HSP72 was significantly attenuated after EXB1 in BICARB compared to PLAC, however, there was no difference in the HSP72 response to the subsequent EXB2 between conditions. Furthermore there was no difference between conditions for measures of oxidative stress (protein carbonyl and HSP32). These findings confirm the sensitivity of the HSP72 response to exercise-induced changes in acid-base status in vivo, but suggest that the attenuated response has little effect upon subsequent stress in the same day.

Topics: Adult; Alkalosis; Exercise; HSP72 Heat-Shock Proteins; Humans; Male; Oxidative Stress; Sodium Bicarbonate; Sodium Chloride

Topics: Alkalosis; Apnea; Female; Gastrointestinal Agents; Humans; Infant; Recurrence; Sodium Bicarbonate

The purpose of this study was to investigate the effects of sodium bicarbonate (NaHCO3) ingestion and acute hypoxic exposure on repeated bouts of high-intensity cycling to task failure. Twelve subjects completed 4 separate intermittent cycling bouts cycling bouts to task failure (120% peak power output for 30-second interspersed with 30-second active recovery) under the following conditions: normoxia (FIO2% at 20.93%) alkalosis (NA), normoxia placebo (NP), hypoxia (FIO2% at 14.7%) alkalosis (HA), and hypoxia placebo (HP). For the NA and HA trials, the buffer solution (0.3 g·kg of NaHCO3) was dispensed into gelatin capsules and consumed over 90 minutes with 1 L of water. Whole-blood acid-base findings demonstrated metabolic alkalosis in both NA and HA before exercise (HCO3: 32.8 ± 1.8 mmol·L). Time to task failure was significantly impaired in the hypoxic conditions (NA: 199.1 ± 62.3 seconds, NP: 183.8 ± 45.0 seconds, HA: 127.8 ± 27.9 seconds, HP: 133.3 ± 28.7 seconds; p < 0.001; η = 0.7). There was no difference between the HA and HP conditions (p = 0.41); however the 2 normoxic conditions approached significance with the NA condition on average resulting in approximately 15-second improvement in time to task failure (p = 0.09). These findings suggest that an acute decline in FIO2% consistent with hypoxic exposure is more inhibiting than metabolic acidosis during intermittent high-intensity cycling to task failure. In application, the use of hypoxia and NaHCO3 concurrently to improve performance under these conditions does not seem warranted.

Topics: Adult; Alkalosis; Buffers; Exercise; Exercise Test; Exercise Tolerance; Female; Humans; Hypoxia; Male; Physical Conditioning, Human; Sodium Bicarbonate; Time Factors; Young Adult

This case report describes a 66-year-old man, previously healthy besides mild hypertension. He ingested a self-made folk remedy consisting of baking soda and water against acid reflux in dosages that resulted in severe metabolic alkalosis (pH 7.8). Diagnosing and treating MA is easy and cheap, but if the condition is not treated, consequences can be severe. The challenge is to uncover patients' use of non prescription medications and folk remedies in the diagnostic process. Having this information it is possible to prevent MA in both high- and low-risk patients.

Topics: Aged; Alkalosis; Gastroesophageal Reflux; Humans; Male; Medicine, Traditional; Self Medication; Sodium Bicarbonate

Topics: Alkalosis; Antacids; Diagnosis, Differential; Drug Overdose; Gastritis; Gastrointestinal Agents; Heartburn; Humans; Male; Medicine, Traditional; Middle Aged; Self Medication; Severity of Illness Index; Sodium Bicarbonate; Tachycardia, Ventricular; Treatment Outcome

Pseudomyxoma peritonei causes marked accumulation of jelly-like ascites in the peritoneal cavity. Removal of much mucinous ascites by irrigating the cavity appears to be an effective treatment. We describe a patient who underwent the irrigation with sodium bicarbonate solution and developed critical alkalemia. A 68-year-old woman with normal renal function was operated on for recurrent pseudomyxoma peritonei. Fol- lowing the excision of primary lesion, her intraperitoneal cavity was irrigated with 10 1 of 7% sodium bicarbonate in about 45 minutes. Thirty minutes after irrigation, blood gas analysis revealed severe metabolic alkalosis (pH 7.714, BE 25.6 mmol x l-1 ) with electrolyte disorder (Na 157.8 mmol x l-1 K 2.31mmol x l-1, Ca 0.73 mmol x l-1). Hypotension (<60 mmHg) and sinus tachycardia (>130 beats x min -1) supervened 75 minutes later. Transferring to the ICU, she was given KC1 solution intravenously based on serial blood analysis while on mechanical ventilation. The next day acid-base disturbance returned spontaneously to normal (pH 7.45, BE 8.0mmol x l-1), leading to endotracheal extubation. Electrolyte imbalance was gradually resolved on 2nd POD and she was discharged from the ICU. Intraperitoneal irrigation with sodium bicarbonate requires special perioperative considerations for lifethreatening alkalemia, especially in a patient with renal impairment.

Topics: Acid-Base Imbalance; Aged; Alkalosis; Anesthesia, Epidural; Anesthesia, General; Female; Humans; Peritoneal Lavage; Peritoneal Neoplasms; Pseudomyxoma Peritonei; Recurrence; Severity of Illness Index; Sodium Bicarbonate; Surgical Procedures, Operative

Topics: Adult; Alkalosis; Humans; Male; Sodium Bicarbonate; Ulcer

The purpose of this study was to investigate the effects of pre-exercise alkalosis on the physiological stress response to high-intensity exercise. Seven physically active males (age 22 ± 3 years, height 1.82 ± 0.06 m, mass 81.3 ± 8.4 kg and peak power output 300 ± 22 W) performed a repeated sprint cycle exercise following a dose of 0.3 g kg(-1) body mass of sodium bicarbonate (NaHCO(3)) (BICARB), or a placebo of 0.045 g kg(-1) body mass of sodium chloride (PLAC). Monocyte-expressed heat shock protein 72 (HSP72) and plasma thiobarbituric acid reactive substances (TBARS) were significantly attenuated in BICARB compared to PLAC (p = 0.04 and p = 0.039, respectively), however total anti-oxidant capacity, the ratio of oxidised to total glutathione, cortisol, interleukin 6 and interleukin 8 were not significantly induced by the exercise. In conclusion, monocyte-expressed HSP72 is significantly increased following high-intensity anaerobic exercise, and its attenuation following such exercise with the ingestion of NaHCO(3) is unlikely to be due to a decreased oxidative stress.

Topics: Administration, Oral; Alkalosis; Anaerobic Threshold; HSP72 Heat-Shock Proteins; Humans; Male; Oxidative Stress; Performance-Enhancing Substances; Physical Exertion; Running; Sodium Bicarbonate; Treatment Outcome; Young Adult

Underlying causes of metabolic alkalosis may be evident from history, evaluation of effective circulatory volume, and measurement of urine chloride concentration. However, identification of causes may be difficult for certain conditions associated with clandestine behaviors, such as surreptitious vomiting, use of drugs or herbal supplements with mineralocorticoid activity, abuse of laxatives or diuretics, and long-term use of alkalis. In these circumstances, clinicians often are bewildered by unexplained metabolic alkalosis from an incomplete history or persistent deception by the patient, leading to misdiagnosis and poor outcome. We present a case of severe metabolic alkalosis and hypokalemia with a borderline urine chloride concentration in an alcoholic patient treated with a thiazide. The cause of the patient's metabolic alkalosis eventually was linked to surreptitious ingestion of baking soda. This case highlights the necessity of a high index of suspicion for the diverse clandestine behaviors that can cause metabolic alkalosis and the usefulness of urine pH and anion gap in its differential diagnosis.

Topics: Acid-Base Equilibrium; Aged; Alcoholism; Alkalosis; Chlorides; Comorbidity; Eating; Humans; Hydrogen-Ion Concentration; Hypokalemia; Male; Sodium Bicarbonate; Thiazides; Urine

A 68-year-old man presented to the Emergency Department with a severe metabolic alkalosis after ingesting large quantities of baking soda to treat his dyspepsia. His underlying pulmonary disease and a progressively worsening mental status necessitated intubation for respiratory failure. Laboratory studies revealed a hyponatremic, hypochloremic, hypokalemic metabolic alkalosis. The patient was successfully treated after cessation of the oral bicarbonate, initiation of intravenous hydration, and correction of electrolyte abnormalities.

Topics: Aged; Alkalosis; Dyspepsia; Emergency Service, Hospital; Humans; Male; Respiratory Insufficiency; Self Medication; Sodium Bicarbonate

It is well known that acid/base disturbances modulate proton/bicarbonate transport in the cortical collecting duct. To study the adaptation further we measured the effect of three days of acidosis followed by the rapid recovery from this acidosis on the number and type of intercalated cells in the rabbit cortical collecting duct. Immunofluorescence was used to determine the expression of apical pendrin in β-intercalated cells and the basolateral anion exchanger (AE1) in α-intercalated cells. Acidosis resulted in decreased bicarbonate and increased proton secretion, which correlated with reduced pendrin expression and the number of pendrin-positive cells, as well as decreased pendrin mRNA and protein abundance in this nephron segment. There was a concomitant increase of basolateral AE1 and α-cell number. Intercalated cell proliferation did not seem to play a role in the adaptation to acidosis. Alkali loading for 6-20 h after acidosis doubled the bicarbonate secretory flux and reduced proton secretion. Pendrin and AE1 expression patterns returned to control levels, demonstrating that adaptive changes by intercalated cells are rapidly reversible. Thus, regulation of intercalated cell anion exchanger expression and distribution plays a key role in adaptation of the cortical collecting duct to perturbations of acid/base.

Topics: Acid-Base Equilibrium; Acidosis; Adaptation, Physiological; Alkalosis; Animals; Anion Exchange Protein 1, Erythrocyte; Anion Transport Proteins; Disease Models, Animal; Female; Kidney Tubules, Collecting; Membrane Transport Proteins; Proton-Translocating ATPases; Rabbits; Sodium Bicarbonate

Intracellular acidosis during early reperfusion after coronary artery occlusion was recently linked to cardioprotection resulting from myocardial ischemic postconditioning. We tested the hypotheses that transient alkalosis during early reperfusion abolishes helium preconditioning and that the mitochondrial permeability transition pore inhibitor cyclosporin A (CsA) restores the cardioprotective effects of helium during alkalosis in vivo.. Rabbits (n = 36) instrumented for hemodynamics measurement were subjected to a 30-min left anterior descending coronary artery occlusion and 3-h reperfusion. The rabbits received 0.9% saline (control) or three cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture before left anterior descending coronary artery occlusion in the absence or presence of transient alkalosis (pH = 7.5) produced by administration of IV sodium bicarbonate (10 mEq) 2 min before reperfusion. Other rabbits preconditioned with helium received CsA (5 mg/kg) in the presence of alkalosis or CsA alone.. Helium reduced myocardial infarct size (25% +/- 4% of left ventricular area at risk; P < 0.05) compared with control (44% +/- 6%). Alkalosis during early reperfusion did not alter infarct size alone (46% +/- 2%), but this intervention abolished helium-induced cardioprotection (45% +/- 3%). CsA restored reductions in infarct size produced by helium preconditioning in the presence of alkalosis (28% +/- 6%; P < 0.05 versus control) but did not affect myocardial necrosis alone (43% +/- 6%).. The results demonstrate that transient alkalosis during early reperfusion abolishes helium preconditioning in rabbits. CsA restored helium-induced cardioprotection during alkalosis, suggesting that helium preconditioning inhibits mitochondrial permeability transition pore formation by maintaining intracellular acidosis during early reperfusion.

Topics: Acidosis; Administration, Inhalation; Alkalosis; Animals; Cyclosporine; Disease Models, Animal; Drug Administration Schedule; Helium; Hemodynamics; Male; Mitochondrial Membrane Transport Proteins; Mitochondrial Permeability Transition Pore; Myocardial Infarction; Myocardial Reperfusion Injury; Myocardium; Necrosis; Rabbits; Sodium Bicarbonate

Intravenous sodium bicarbonate (SB) administration during cardiopulmonary arrest (CPA) is intended to counteract lactic acidosis due to hypoxia, poor perfusion, and anaerobic metabolism. Despite a lack of documented efficacy and a level III recommendation from the American Heart Association, SB is widely used during resuscitation events. SB has both theoretical and measurable adverse effects. Excess or poorly timed administration during a CPA may elevate a patient's pH, inducing alkalemia. Despite decades of controversy surrounding use of this drug, the prevalence of SB-induced alkalemia has not been previously documented.. To estimate the prevalence of SB-induced alkalemia in inpatients after CPA and to investigate the pattern of SB administration.. Medical records were retrospectively reviewed with attention to SB administration and arterial blood gas (ABG) data. After application of inclusion and exclusion criteria to 264 CPA patients, the study group comprised 88 patients. When measured, if PCO(2) and pH were above normal limits after SB administration, we concluded that SB contributed to the alkalemia.. Twenty-seven (31%) patients received SB without any ABG data, and 70 (79%) patients received at least one empiric SB dose. Of the 61 patients with ABG data, alkalemia occurred in 10, a prevalence of 16%. Administration of SB increased pH in only 9 (15%) other CPA patients and had no effect in the 42 (69%) remaining patients.. Administration of SB during CPA was causally linked with inducing alkalemia in 16% of patients. Early collection of ABG samples may assist in optimizing pH during CPA and thus reduce unwarranted empiric use of SB.

Topics: Adult; Aged; Aged, 80 and over; Alkalosis; Blood Gas Analysis; Carbon Dioxide; Cardiopulmonary Resuscitation; Drug Administration Schedule; Female; Heart Arrest; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Prevalence; Retrospective Studies; Sodium Bicarbonate

Pseudomyxoma peritonei (PMP) is a rare disease, presenting with large amounts of mucinous ascites, and treatment with intraperitoneal irrigation with mucolytic agents has been tried. We report a patient with PMP who underwent intraperitoneal irrigation with sodium bicarbonate and exhibited marked alkalosis. The patient was a 78-year-old woman who had mucinous ascites, and an appendiceal and an ovarian tumor. Bilateral salpingo-oophorectomy and appendectomy were performed, and she then underwent intraperitoneal irrigation with sodium bicarbonate (7%, 1000 ml). Shortly after the irrigation, blood gas analysis showed critical alkalosis (pH, 7.66; base excess [BE], 24 mEq x l(-1); HCO3 (-), 50 mEq x l(-1)) with electrolyte imbalance (Na+, 153 mEq x l(-1); K+, 2.8 mEq x l(-1); Ca2+, 0.98 mEq x l(-1), Cl(-1), 99 mEq x l(-1)). The alkalosis and electrolyte imbalance were ameliorated with the administration of potassium chloride and calcium chloride intravenously, and the patient was extubated after the 2-h surgical procedure. The patient was discharged home after 15 days without problems. Sodium bicarbonate may be an effective mucolytic agent for PMP. However, during irrigation with sodium bicarbonate, careful evaluation of the acid-base balance and serum electrolytes, and prompt treatment of alkalosis or electrolyte imbalance, should this occur, are of great importance.

Topics: Aged; Alkalosis; Appendiceal Neoplasms; Blood Gas Analysis; Electrolytes; Female; Humans; Ovarian Neoplasms; Peritoneal Lavage; Peritoneal Neoplasms; Pseudomyxoma Peritonei; Sodium Bicarbonate

We investigated the involvement of carbonic anhydrase (CA) in mediating V-H(+)-ATPase translocation into the basolateral membrane in gills of alkalotic Squalus acanthias. Immunolabeling revealed that CA is localized in the same cells as V-H(+)-ATPase. Blood plasma from dogfish injected with acetazolamide [30 mg/kg at time (t) = 0 and 6 h] and infused with NaHCO(3) for 12 h (1,000 microeq.kg(-1).h(-1)) had significantly higher plasma HCO(3)(-) concentration than fish that were infused with NaHCO(3) alone (28.72 +/- 0.41 vs. 6.57 +/- 2.47 mmol/l, n = 3), whereas blood pH was similar in both treatments (8.03 +/- 0.11 vs. 8.04 +/- 0.11 pH units at t = 12 h). CA inhibition impaired V-H(+)-ATPase translocation into the basolateral membrane, as estimated from immunolabeled gill sections and Western blotting on gill cell membranes (0.24 +/- 0.08 vs. 1.00 +/- 0.28 arbitrary units, n = 3; P < 0.05). We investigated V-H(+)-ATPase translocation during a postfeeding alkalosis ("alkaline tide"). Gill samples were taken 24-26 h after dogfish were fed to satiety in a natural-like feeding regime. Immunolabeled gill sections revealed that V-H(+)-ATPase translocated to the basolateral membrane in the postfed fish. Confirming this result, V-H(+)-ATPase abundance was twofold higher in gill cell membranes of the postfed fish than in fasted fish (n = 4-5; P < 0.05). These results indicate that 1) intracellular H(+) or HCO(3)(-) produced by CA (and not blood pH or HCO(3)(-)) is likely the stimulus that triggers the V-H(+)-ATPase translocation into the basolateral membrane in alkalotic fish and 2) V-H(+)-ATPase translocation is important for enhanced HCO(3)(-) secretion during a naturally occurring postfeeding alkalosis.

Topics: Alkalosis; Animals; Carbonic Anhydrases; Dogfish; Feeding Behavior; Gills; Hydrogen-Ion Concentration; Postprandial Period; Protein Transport; Sodium Bicarbonate; Time Factors; Vacuolar Proton-Translocating ATPases

Uncommon metabolic abnormalities in the emergency department could be a result of drug overdose due to uncommon agents.. A 35-year-old male presented to the emergency department with a Glasgow Coma Scale (GCS) of 3/15 and a normal pulse rate and blood pressure. Subsequent questioning after recovery revealed he had ingested 2 L of Gaviscon over the preceding 48 hours. He had normal haematology, liver, and renal function during admission. The electrocardiogram showed T wave inversion in the inferior leads on admission. Arterial blood gas on air was: pH 7.54, HCO3 50 mmol/L (50 meq/L), Chloride 66 mmol/L, anion gap was 19, pO2 11 kPa (82.5 mmHg), and pCO2 8 kPa (60 mmHg). Serum sodium was 127 mmol/L and serum potassium was 1.6 mmol/L. His GCS improved within one hour of admission with supportive care, and his serum potassium and bicarbonate improved within 24 hours. He subsequently made a full recovery. Discussion. Bicarbonate ingestion in the form of Gaviscon(R) and vomiting made this patient alkalotic, and simple supportive care provided effective management with a complete recovery.. This case illustrates how a severe metabolic alkalosis can result from a significant ingestion of Gaviscon, and that such presentations can give rise to diagnostic dilemma.

Topics: Adult; Alginates; Alkalosis; Aluminum Hydroxide; Antacids; Drug Combinations; Humans; Hypokalemia; Male; Severity of Illness Index; Silicic Acid; Sodium Bicarbonate; Treatment Outcome

This study investigated the effects of high-intensity training, with or without induced metabolic alkalosis, on lactate transporter (MCT1 and MCT4) and sodium bicarbonate cotransporter (NBC) content in rat skeletal muscles. Male Wistar rats performed high-intensity training on a treadmill 5 times/wk for 5 wk, receiving either sodium bicarbonate (ALK-T) or a placebo (PLA-T) prior to each training session, and were compared with a group of control rats (CON). MCT1, MCT4, and NBC content was measured by Western blotting in soleus and extensor digitorum longus (EDL) skeletal muscles. Citrate synthase (CS) and phosphofructokinase (PFK) activities and muscle buffer capacity (betam) were also evaluated. Following training, CS and PFK activities were significantly higher in the soleus only (P < 0.05), whereas betam was significantly higher in both soleus and EDL (P < 0.05). MCT1 (PLA-T: 30%; ALK-T: 23%) and NBC contents (PLA-T: 85%; ALK-T: 60%) increased significantly only in the soleus following training (P < 0.01). MCT4 content in the soleus was significantly greater in ALK-T (115%) but not PLA-T compared with CON. There was no significant change in protein content in the EDL. Finally, NBC content was related only to MCT1 content in soleus (r = 0.50, P < 0.01). In conclusion, these results suggest that MCT1, MCT4, and NBC undergo fiber-specific adaptive changes in response to high-intensity training and that induced alkalosis has a positive effect on training-induced changes in MCT4 content. The correlation between MCT1 and NBC expression suggests that lactate transport may be facilitated by NBC in oxidative skeletal muscle, which may in turn favor better muscle pH regulation.

Topics: Alkalosis; Animals; Chronic Disease; Citrate (si)-Synthase; Lactic Acid; Male; Monocarboxylic Acid Transporters; Muscle Proteins; Muscle, Skeletal; Phosphofructokinase-1; Physical Conditioning, Animal; Physical Exertion; Rats; Rats, Wistar; Sodium Bicarbonate; Sodium-Bicarbonate Symporters; Symporters

We report a case of baking soda pica in a woman at 31 weeks of pregnancy causing severe hypokalemic metabolic alkalosis and rhabdomyolysis.. A multigravida at 31 weeks of gestation presented with weakness and muscle pain. She was found to have severe hypokalemic metabolic alkalosis and rhabdomyolysis, with elevation in serum transaminases and hypertension. We initially thought the patient had an atypical presentation of preeclampsia until it was realized that she was ingesting 1 full box of baking soda (454 g sodium bicarbonate) per day. Symptoms and abnormal laboratory findings resolved with discontinuation of the patient's pica practices.. Pica is a common but often overlooked practice that can potentially lead to life-threatening disorders. A thorough evaluation of a patient's dietary intake is extremely important, especially in the setting of atypical presentations of disease in pregnancy.

Topics: Adult; Alkalosis; Female; Humans; Hypokalemia; Pica; Pregnancy; Pregnancy Complications; Rhabdomyolysis; Sodium Bicarbonate

Topics: Adult; Alkalosis; Aspirin; Citrates; Drug Combinations; Female; Humans; Iron Deficiencies; Kidney Failure, Chronic; Pica; Renal Dialysis; Seizures; Sodium Bicarbonate

We describe a case of medication induced metabolic alkalosis in a maintenance dialysis patient who developed severe hypotension while undergoing a lactate hemofiltration procedure. A 73-year-old man with ESRD due to renovascular disease was used to ingesting up to 30 grams per day of a non-prescription medication (Effervescent granulare 250 grams, CRASTAN, Pisa Italy) consisting of sodium bicarbonate, citric acid, glucose and lemon flavor. For technical problem lactate hemofiltration was performed and thirty minutes after dialysis was started a severe symptomatic hypotension occurred (blood pressure 65/35 mmHg). Lactate hemofiltration was suspended and one-hour later standard bicarbonate dialysis was performed without any clinical problem. The different mechanisms in acidosis buffering occurring in lactate and bicarbonate hemofiltration were discussed.

Topics: Aged; Alkalosis; Hemodiafiltration; Humans; Hypotension; Kidney Failure, Chronic; Male; Severity of Illness Index; Sodium Bicarbonate

Endothelial and local metabolic mechanisms contribute in concert to the regulation of blood flow. In vivo extracellular alkalosis induces a vasoconstriction, hyperosmolarity a vasodilatation. The interaction between local metabolic and endothelial mechanisms is poorly understood. Therefore we investigated in endothelial-derived EA.hy926 cells the secretion of endothelial modulators of vascular tone under hypertonic stress with and without alkalosis: hyperosmolality was generated by either the addition of NaHCO subset 3 (25, 50, 100 mM, pH up to > 8) or mannitol (50, 100, 200 mM) to the cell culture media. The cells were studied using automated cell counting, measurement of the activity of the lactate dehydrogenase (LDH) and a bromo-deoxyuridine (BrdU) cell proliferation assay. Endothelin and cGMP, a surrogate marker for nitric oxide (NO), were measured with specific ELISAs. EA.hy 926 cells formed stable monolayers in vitro. The secretion of endothelin, but not of cGMP was inversely correlated with the osmolality of the incubation media: the endothelin concentration in the supernatants decreased in both mannitol- and NaHCO subset 3 -treated cells in a concentration-dependent manner (152.4 +/- 6.2 pg/ml (control) to 24.4 +/- 2.4 pg/ml (200 mM mannitol), res. to 18.2 +/- 2.7 pg/ml (100 mM NaHCO subset 3). Neither hypertonic bicarbonate nor mannitol solutions decreased the monolayer cell density or cell viability during the 6 hour incubation period. In conclusion, EA.hy926 cells are quite resistant against a 6-hour hypertonic/alkaline stress. Hypertonicity decreases the secretion of endothelin and has no effect on cGMP. At each level of hypertonicity the endothelin concentration was similar in the NaHCO subset 3 and mannitol media arguing against a direct role of endothelin in alkalosis-induced vasoconstriction in vivo. The decreased secretion of endothelin during hypertonicity could contribute to the hyperosmolal vasodilation seen in vivo.

Topics: Alkalosis; Cell Line; Cell Survival; Cyclic GMP; Dose-Response Relationship, Drug; Endothelial Cells; Endothelins; Humans; Hypertonic Solutions; Mannitol; Osmotic Pressure; Sodium Bicarbonate

The Cl(-)/HCO(3)(-) exchanger AE2 is believed to be involved in transcellular bicarbonate reabsorption that occurs in the thick ascending limb of Henle's loop (TAL). The purpose of this study was to test whether chronic changes in acid-base status and sodium intake regulate AE2 polypeptide abundance in the TAL of the rat. Rats were subjected to 6 d of loading with NaCl, NH(4)Cl, NaHCO(3), KCl, or KHCO(3). AE2 protein abundance was estimated by semiquantitative immunoblotting in renal membrane fractions isolated from the cortex and the outer medulla of treated and control rats. In the renal cortex, AE2 abundance was markedly increased in response to oral loading with NH(4)Cl or with NaCl. In contrast, AE2 abundance was unchanged in response to loading with KCl or with NaHCO(3) and was decreased by loading with KHCO(3). The response of AE2 in the outer medulla differed from that in the cortex in that HCO(3)(-) loading increased AE2 abundance when administered with Na(+) but had no effect when administered with K(+). Immunohistochemistry revealed that NaCl loading increased AE2 abundance in the basolateral membrane of both the cortical and the medullary TAL. In contrast, NH(4)Cl loading increased AE2 abundance only in the cortical TAL but not in the medullary TAL. These results suggest that regulation of the basolateral Cl(-)/HCO(3)(-) exchanger AE2 plays an important role in the adaptation of bicarbonate absorption in the TAL during chronic acid-base disturbances and high sodium intake. The present study also emphasizes the contribution of cortical TAL adaptation in the renal regulation of acid-base status.

Topics: Acid-Base Equilibrium; Acidosis; Administration, Oral; Alkalosis; Ammonium Chloride; Animals; Anion Transport Proteins; Antiporters; Bicarbonates; Down-Regulation; Immunohistochemistry; Kidney Cortex; Kidney Medulla; Loop of Henle; Male; Potassium Chloride; Potassium Compounds; Rats; Rats, Sprague-Dawley; SLC4A Proteins; Sodium; Sodium Bicarbonate; Sodium Chloride

The anion exchanger pendrin is present in the apical plasma membrane of type B and non-A-non-B intercalated cells of the cortical collecting duct (CCD) and connecting tubule and is involved in HCO(3)(-) secretion. In this study, we investigated whether the abundance and subcellular localization of pendrin are regulated in response to experimental metabolic acidosis and alkalosis with maintained water and sodium intake. NH(4)Cl loading (0.033 mmol NH(4)Cl/g body wt for 7 days) dramatically reduced pendrin abundance to 22 +/- 4% of control values (n = 6, P < 0.005). Immunoperoxidase labeling for pendrin showed reduced intensity in NH(4)Cl-loaded animals compared with control animals. Moreover, double-label laser confocal microscopy revealed a reduction in the fraction of cells in the CCD exhibiting pendrin labeling to 65% of the control value (n = 6, P < 0.005). Conversely, NaHCO(3) loading (0.033 mmol NaHCO(3)/g body wt for 7 days) induced a significant increase in pendrin expression to 153 +/- 11% of control values (n = 6, P < 0.01) with no change in the fraction of cells expressing pendrin. Immunoelectron microscopy revealed no major changes in the subcellular distribution, with abundant labeling in both the apical plasma membrane and the intracellular vesicles in all conditions. These results indicate that changes in pendrin protein expression play a key role in the well-established regulation of HCO(3)(-) secretion in the CCD in response to chronic changes in acid-base balance and suggest that regulation of pendrin expression may be clinically important in the correction of acid-base disturbances.

Topics: Acidosis; Alkalosis; Ammonium Chloride; Animals; Carrier Proteins; Cell Membrane; Hydrogen-Ion Concentration; Immunohistochemistry; Kidney; Kidney Tubules, Collecting; Male; Membrane Transport Proteins; Microscopy, Immunoelectron; Osmolar Concentration; Potassium; Rats; Rats, Wistar; Sodium; Sodium Bicarbonate; Sulfate Transporters; Urine

Topics: Aged; Alkalosis; Anti-Ulcer Agents; Humans; Male; Sodium Bicarbonate

Increasing blood bicarbonate content has long been cited as a potential mechanism to improve contractile function. We investigated whether sodium bicarbonate-induced metabolic alkalosis could positively affect force development during the rest-to-work transition in ischaemic skeletal muscle. Secondly, assuming it could, we investigated whether bicarbonate could augment acetyl group availability through the same equilibrium reaction as sodium acetate pre-treatment and whether this underpins, at least in part, its ergogenic effect. Multiple biopsy samples were obtained from the canine gracilis muscle during 5 min of electrically evoked ischaemic contraction, which enabled the determination of the time course of acetyl group accumulation, substrate utilisation, pyruvate dehydrogenase complex activation and tension development in animals treated with saline (control; n = 6) or sodium bicarbonate (n = 5). Treatment with bicarbonate elevated acetylcarnitine content above the control level at rest (P < 0.05), but at no time point during subsequent contraction. The pyruvate dehydrogenase complex was activated following 40 s of contraction in both groups, with no differences existing between treatments at any time point. The requirement for ATP re-synthesis from non-oxygen-dependent routes was no different between groups at any time point during contraction. No difference in peak twitch force production existed between groups. However, at 3 min of stimulation, tension development was better maintained in the bicarbonate group (P < 0.05), being approximately 20% greater than control following 5 min of contraction (P < 0.05). The results demonstrate, for the first time, that bicarbonate can augment acetyl group availability prior to contraction, independent of pyruvate dehydrogenase complex activation, but cannot influence the requirement for non-oxidative ATP re-synthesis during subsequent contraction. It would appear, therefore, that the bicarbonate-induced improvement in muscle tension development was probably mediated through the metabolic alkalosis and not via the increased availability of acetyl groups within the cell.

Topics: Acetylcarnitine; Alkalosis; Animals; Carnitine; Dogs; Electric Stimulation; Female; Infusions, Intravenous; Ischemia; Isometric Contraction; Muscle, Skeletal; Pyruvate Dehydrogenase Complex; Reference Values; Reproducibility of Results; Rest; Sensitivity and Specificity; Sodium Bicarbonate; Stress, Mechanical

In this investigation we studied the effect of manipulating the acid-base balance through sodium bicarbonate (NaHCO(3)) ingestion on ratings of perceived exertion for the overall body (RPE-O) and on differentiated ratings for the leg and chest (RPE-L, RPE-C) during exercise recovery. Six women of college age underwent 3 experimental conditions in which NaHCO(3) was ingested in either a single (bolus) or periodic (distributed throughout the exercise) dosage, with calcium carbonate serving as a placebo control. Each subject pedaled a cycle ergometer at 90% Vo(2)peak for three 5-minute exercise sessions, each separated by 10 minutes of recovery. Repeated-measures analysis of variance with Tukey post hoc analysis was performed for acid-base and perceptual variables. Results indicate that a gradient of acid-base balance was established such that pH and bicarbonate concentration were significantly greater (p < 0.05) for the single condition in comparison with periodic and placebo conditions, and the periodic condition was significantly greater (p < 0.05) than placebo. The average percentage of recovery for RPE-L and RPE-C was 8% greater (p < 0.05) for the single condition than for the periodic and placebo conditions, at the first and second minutes of recovery. During the first minute of recovery, the average percentage of recovery for RPE-O was 10% greater (p < 0.05) for the single condition than for the placebo condition. During the second minute of recovery, the percentage of recovery for RPE-O for the single condition was significantly greater than those for both the periodic and placebo conditions by an average of 9%. These results strengthen the relationship between the acid-base balance and the subjective perception of exertion. In addition, this study provides preliminary data in support of RPE as an adjunct measure to quantify the extent of recovery from exercise.

Topics: Adult; Alkalosis; Analysis of Variance; Anthropometry; beta-Galactosidase; Blood Chemical Analysis; Body Mass Index; Case-Control Studies; Exercise Test; Female; Heart Rate; Humans; Oxygen Consumption; Perception; Physical Exertion; Probability; Recovery of Function; Reference Values; Sensitivity and Specificity; Sodium Bicarbonate; Time Factors

Pendrin belongs to a superfamily of Cl-/anion exchangers and is expressed in the inner ear, the thyroid gland, and the kidney. In humans, mutations in pendrin cause Pendred syndrome characterized by sensorineural deafness and goiter. Recently pendrin has been localized to the apical side of non-type A intercalated cells of the cortical collecting duct, and reduced bicarbonate secretion was demonstrated in a pendrin knockout mouse model. To investigate a possible role of pendrin in modulating acid-base transport in the cortical collecting duct, we examined the regulation of expression of pendrin by acid-base status in mouse kidney.. Mice were treated orally either with an acid or bicarbonate load (0.28 mol/L NH4Cl or NaHCO3) or received a K+-deficient diet for one week. Immunohistochemistry and Western blotting was performed.. Acid-loading caused a reduction in pendrin protein expression levels within one day and decreased expression to 23% of control levels after one week. Concomitantly, pendrin protein was shifted from the apical membrane to the cytosol, and the relative abundance of pendrin positive cells declined. Similarly, in chronic K+-depletion, known to elicit a metabolic alkalosis, pendrin protein levels decreased and pendrin expression was shifted to an intracellular pool with the relative number of pendrin positive cells reduced. In contrast, following oral bicarbonate loading pendrin was found exclusively in the apical membrane and the relative number of pendrin positive cells increased.. These results are in agreement with a potential role of pendrin in bicarbonate secretion and regulation of acid-base transport in the cortical collecting duct.

Topics: Acid-Base Equilibrium; Alkalosis; Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Carrier Proteins; Cell Polarity; Cytosol; Kidney Cortex; Kidney Tubules, Collecting; Male; Membrane Transport Proteins; Mice; Mice, Inbred C57BL; Potassium, Dietary; Sodium Bicarbonate; Sulfate Transporters

To determine whether induced metabolic alkalosis affects sweat composition, 10 males cycled for 90 min at 62.5 +/- 1.3% peak oxygen uptake, on two separate occasions. Subjects ingested either empty capsules (placebo) or capsules containing NaHCO3- (0.3 g kg-1 body mass; six equal doses) over a 2-h period, which commenced 3 h prior to exercise. Arterialized-venous blood samples were drawn prior to and after 15, 30, 60 and 90 min of exercise. Sweat was aspirated at the end of exercise from a patch located on the right scapula region. NaHCO3- ingestion elevated blood pH, [HCO3-] and serum [Na+], whereas serum [Cl-] and [K+] were reduced, both at rest and during exercise (P < 0.05). Sweat pH was greater in the NaHCO3- trial (6.24 +/- 0.18 vs. 6.38 +/- 0.18; P < 0.05), whereas sweat [Na+] (49.5 +/- 4.8 vs. 50.2 +/- 4.3 mEq L-1), [Cl-] (37.5 +/- 5.1 vs. 39.3 +/- 4.2 mEq L-1) and [K+] (4.66 +/- 0.19 vs. 4.64 +/- 0.34 mEq L-1) did not differ between trials (P > 0.05). Sweat [HCO3-] (2.49 +/- 0.58 vs. 3.73 +/- 1.10 mEq L-1) and [lactate] (8.92 +/- 0.79 vs. 10.51 +/- 0.32 mmol L-1) tended to be greater after NaHCO3- ingestion, although significance was not reached (P=0.07 and P=0.08, respectively). These data indicate that induced metabolic alkalosis can modify sweat composition, although it is unclear whether the secretory coil, reabsorptive duct, or both are responsible for this alteration.

Topics: Adult; Alkalosis; Bicarbonates; Chlorides; Exercise Test; Humans; Hydrogen-Ion Concentration; Lactates; Male; Potassium; Sodium; Sodium Bicarbonate; Sweat

Sodium bicarbonate (NaHCO3) ingestion has been shown to increase both muscle glycogenolysis and glycolysis during brief submaximal exercise. These changes may be detrimental to performance during more prolonged, exhaustive exercise. This study examined the effect of NaHCO3 ingestion on muscle metabolism and performance during intense endurance exercise of approximately 60 min in seven endurance-trained men.. Subjects ingested 0.3 g.kg-1 body mass of either NaHCO3 or CaCO3 (CON) 2 h before performing 30 min of cycling exercise at 77 +/- 1% .VO(2peak) followed by completion of 469 +/- 21 kJ as quickly as possible (approximately 30 min, approximately 80% .VO(2peak)).. Immediately before, and throughout exercise, arterialized-venous plasma HCO3- concentrations were higher (P < 0.05) whereas plasma and muscle H+ concentrations were lower (P < 0.05) in NaHCO3 compared with CON. Blood lactate concentrations were higher (P < 0.05) during exercise in NaHCO3, but there was no difference between trials in muscle glycogen utilization or muscle lactate content during exercise. Reductions in PCr and ATP and increases in muscle Cr during exercise were also unaffected by NaHCO3 ingestion. Accordingly, exercise performance time was not different between treatments.. NaHCO3 ingestion resulted in a small muscle alkalosis but had no effect on muscle metabolism or intense endurance exercise performance in well-trained men.

Topics: Administration, Oral; Adult; Alkalosis; Bicarbonates; Bicycling; Glycogen; Humans; Hydrogen-Ion Concentration; Lactic Acid; Male; Muscle, Skeletal; Physical Endurance; Physical Fitness; Sodium Bicarbonate; Time Factors

In the proximal tubule, the apical Na(+)/H(+) exchanger identified as NHE3 mediates most NaCl and NaHCO(3) absorption. The purpose of this study was to analyze the long-term regulation of NHE3 during alkalosis induced by dietary NaHCO(3) loading and changes in NaCl intake. Sprague-Dawley rats exposed to a low-NaCl, high-NaCl, or NaHCO(3) diet for 6 days were studied. Renal cortical apical membrane vesicles (AMV) were prepared from treated and normal rats. Na(+)/H(+) exchange was assayed as the initial rate of (22)Na(+) uptake in the presence of an outward H(+) gradient. (22)Na(+) uptake measured in the presence of high-dose 5-(N-ethyl-N-isopropyl) amiloride was not different among models. Changes in NaCl intake did not affect NHE3 activity, whereas NaHCO(3) loading inhibited (22)Na(+) uptake by 30%. AMV NHE3 protein abundance assessed by Western blot analysis was unaffected during changes in NaCl intake. During NaHCO(3) loading, NHE3 protein abundance was decreased by 65%. We conclude that proximal NHE3 adapts to chronic metabolic acid-base disorders but not to changes in dietary NaCl intake.

Topics: Acid-Base Imbalance; Adaptation, Physiological; Alkalosis; alpha-Glucosidases; Animals; Biological Transport; Blotting, Western; Cell Membrane; gamma-Glutamyltransferase; Hydrogen-Ion Concentration; Kidney Cortex; Kinetics; Male; Natriuresis; Rats; Rats, Sprague-Dawley; Sodium; Sodium Bicarbonate; Sodium Chloride, Dietary; Sodium Radioisotopes; Sodium-Hydrogen Exchanger 3; Sodium-Hydrogen Exchangers

A maintenance hemodialysis patient developed metabolic alkalosis in the absence of vomiting or nasogastric suction. The cause of the metabolic alkalosis was ingestion of an exogenous alkali in the form of Bromoseltzer. The metabolic alkalosis improved with hemodialysis using a low-bicarbonate bath.

Topics: Alkalosis; Antacids; Bicarbonates; Humans; Male; Middle Aged; Renal Dialysis; Sodium Bicarbonate

The purpose of the study was to examine the roles of active pyruvate dehydrogenase (PDH(a)), glycogen phosphorylase (Phos), and their regulators in lactate (Lac(-)) metabolism during incremental exercise after ingestion of 0.3 g/kg of either NaHCO(3) [metabolic alkalosis (ALK)] or CaCO(3) [control (CON)]. Subjects (n = 8) were studied at rest, rest postingestion, and during constant rate cycling at three stages (15 min each): 30, 60, 75% of maximal O(2) uptake (VO(2 max)). Radial artery and femoral venous blood samples, leg blood flow, and biopsies of the vastus lateralis were obtained during each power output. ALK resulted in significantly (P < 0.05) higher intramuscular Lac(-) concentration ([Lac(-)]; ALK 72.8 vs. CON 65.2 mmol/kg dry wt), arterial whole blood [Lac(-)] (ALK 8.7 vs. CON 7.0 mmol/l), and leg Lac(-) efflux (ALK 10.0 vs. CON 4.2 mmol/min) at 75% VO(2 max). The increased intramuscular [Lac(-)] resulted from increased pyruvate production due to stimulation of glycogenolysis at the level of Phos a and phosphofructokinase due to allosteric regulation mediated by increased free ADP (ADP(f)), free AMP (AMP(f)), and free P(i) concentrations. PDH(a) increased with ALK at 60% VO(2 max) but was similar to CON at 75% VO(2 max). The increased PDH(a) may have resulted from alterations in the acetyl-CoA, ADP(f), pyruvate, NADH, and H(+) concentrations leading to a lower relative activity of PDH kinase, whereas the similar values at 75% VO(2 max) may have reflected maximal activation. The results demonstrate that imposed metabolic alkalosis in skeletal muscle results in acceleration of glycogenolysis at the level of Phos relative to maximal PDH activation, resulting in a mismatch between the rates of pyruvate production and oxidation resulting in an increase in Lac(-) production.

Topics: Adenine Nucleotides; Adult; Alkalosis; Biopsy; Exercise; Femoral Vein; Glucose; Glycogen; Humans; Hydrogen-Ion Concentration; Lactic Acid; Leg; Male; Muscle, Skeletal; Oxygen Consumption; Phosphorylases; Pyruvate Dehydrogenase Complex; Pyruvic Acid; Radial Artery; Sodium Bicarbonate

Topics: Adult; Alkalosis; Calcium; Humans; Male; Myoclonus; Paresthesia; Peripheral Nervous System Diseases; Sodium Bicarbonate

The present studies examined the effects of chronic NaCl administration and metabolic alkalosis on NHE-3, an apical Na+/H+ exchanger of the rat medullary thick ascending limb of Henle (MTAL). NaCl administration had no effect on NHE-3 mRNA abundance as assessed by competitive RT-PCR, as well as on NHE-3 transport activity estimated from the Na+-dependent cell pH recovery of Na+-depleted acidified MTAL cells, in the presence of 50 microM Hoe-694, which specifically blocks NHE-1 and NHE-2. Two models of metabolic alkalosis were studied, one associated with high sodium intake, i.e., NaHCO3 administration, and one not associated with high sodium intake, i.e., chloride depletion alkalosis (CDA). In both cases, the treatment induced a significant metabolic alkalosis that was associated with a decrease in NHE-3 transport activity (-27% and -25%, respectively). Negative linear relationships were observed between NHE-3 activity and plasma pH or bicarbonate concentration. NHE-3 mRNA abundance and NHE-3 protein abundance, assessed by Western blot analysis, also decreased by 35 and 25%, respectively, during NaHCO3-induced alkalosis, and by 47 and 33%, respectively, during CDA. These studies demonstrate that high sodium intake has per se no effect on MTAL NHE-3. In contrast, chronic metabolic alkalosis, regardless of whether it is associated with high sodium intake or not, leads to an appropriate adaptation of NHE-3 activity, which involves a decrease in NHE-3 protein and mRNA abundance.

Topics: Adaptation, Physiological; Alkalosis; Animals; Blood; Chlorides; Chronic Disease; Diet; Hydrogen-Ion Concentration; In Vitro Techniques; Loop of Henle; Male; Rats; Rats, Sprague-Dawley; RNA, Messenger; Sodium; Sodium Bicarbonate; Sodium-Hydrogen Exchanger 3; Sodium-Hydrogen Exchangers; Time Factors

Topics: Alkalosis; Circadian Rhythm; Humans; Hypertension; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Sleep Apnea Syndromes; Sodium Bicarbonate; Substance-Related Disorders

By enzyme-linked in situ hybridization (ISH), direct evidence is provided that acid-secreting intercalated cells (type A IC) of both the cortical and medullary collecting ducts of the rat kidney selectively express the mRNA of the kidney splice variant of anion exchanger 1 (kAE1) and no detectable levels of the erythrocyte AE1 (eAE1) mRNA. Using single-cell quantification by microphotometry of ISH enzyme reaction, medullary type A IC were found to contain twofold higher kAE1 mRNA levels compared with cortical type A IC. These differences correspond to the higher intensity of immunostaining in medullary versus cortical type A IC. Chronic changes of acid-base status induced by addition of NH(4)Cl (acidosis) or NaHCO3 (alkalosis) to the drinking water resulted in up to 35% changes of kAE1 mRNA levels in both cortical and medullary type A IC. These experiments provide direct evidence at the cellular level of kAE1 expression in type A IC and show moderate capacity of type A IC to respond to changes of acid-base status by modulation of kAE1 mRNA levels.

Topics: Acidosis; Alkalosis; Alternative Splicing; Ammonium Chloride; Animals; Antiporters; Chloride-Bicarbonate Antiporters; Chlorides; Erythrocytes; Gene Expression Regulation; Genetic Variation; In Situ Hybridization; Kidney; Kidney Cortex; Kidney Medulla; Kidney Tubules, Collecting; Male; Rats; Rats, Wistar; RNA, Messenger; Sodium Bicarbonate; Transcription, Genetic

Using antibodies against the 31-kD and 70-kD subunits of vacuolar type H+-ATPase (V-ATPase) and light microscopic immunocytochemistry, we have demonstrated the presence of this V-ATPase in rat submandibular gland. We have also investigated the adaptive changes of this transporter during acid-base disturbances such as acute and chronic metabolic acidosis or alkalosis. Our results show intracellularly distributed V-ATPase in striated, granular, and main excretory duct cells in controls, but no V-ATPase immunoreaction in acinar cells. Both acute and chronic metabolic acidosis caused a shift in V-ATPase away from diffuse distribution towards apical localization in striated and granular duct cells, suggesting that a V-ATPase could be involved in the regulation of acid-base homeostasis. In contrast, during acidosis the main excretory duct cells showed no changes in the V-ATPase distribution compared to controls. With acute and chronic metabolic alkalosis, no changes in the V-ATPase distribution occurred. (J Histochem Cytochem 46:91-100, 1998)

Topics: Acid-Base Imbalance; Acidosis; Adaptation, Physiological; Alkalosis; Ammonium Chloride; Animals; Blotting, Western; Immunohistochemistry; Male; Proton-Translocating ATPases; Rats; Rats, Wistar; Salivary Ducts; Sodium Bicarbonate; Submandibular Gland; Vacuolar Proton-Translocating ATPases

Topics: Alkalosis; Female; Humans; Kidney Failure, Chronic; Middle Aged; Pica; Renal Dialysis; Sodium Bicarbonate

To describe changes in blood constituents of horses after oral and i.v. administration of sodium bicarbonate (NaHCO3), and to determine whether the changes are dose dependent.. 6 adult Standardbred mares.. 3 oral doses (1,500, 1,000, and 250 mg/kg of body weight) or 1 intravenous dose (250 mg/kg, 5% solution) of NaHCO3 in 3 L of water, or water (3 L orally), were given to the mares; then changes in blood constituents were measured. Access to food and water was denied during the experiment. Blood samples were collected immediately before treatment and at hourly intervals for 12 hours after treatment, and were analyzed for blood gas tensions; serum osmolality; serum sodium, potassium, chloride, and creatinine concentrations; PCV; and total solids concentration in plasma.. All NaHCO3 treatments induced significant (P < 0.05) metabolic alkalosis, hypernatremia, hypokalemia, and hyperosmolality for at least 8 hours. In mares given the 1,500- and 1,000-mg doses of NaHCO3 orally, hypercapnia persisted for at least 12 hours, whereas hypercapnia lasted 2 hours in mares given the 250-mg dose orally or i.v. (P < 0.05). A tendency for reduction in PCV, proteins in plasma concentration, and serum concentration of chloride was observed 1 hour after i.v. administered doses of NaHCO3.. Oral or i.v. administration of NaHCO3 (> or = 250 mg/kg) to resting horses without ad libitum access to water induces significant and persistent acid-base and electrolyte changes.

Topics: Acid-Base Equilibrium; Administration, Oral; Alkalosis; Animals; Blood Gas Analysis; Blood Proteins; Chlorides; Creatinine; Dose-Response Relationship, Drug; Female; Horses; Hydrogen-Ion Concentration; Hyperkalemia; Hypernatremia; Injections, Intravenous; Osmolar Concentration; Potassium; Sodium; Sodium Bicarbonate; Time Factors

As acid-base status has an effect on bone formation and remodelling, chronic metabolic alkalosis was induced in 3-week-old rats for 6 and 7 weeks with 0.25 mol/1 of NaHCO3 in their drinking water to determine whether it has any effect on dentinogenesis in the molars. One group of rats was fed a high-sucrose diet and the other two a standard diet. The control groups had the same diets but drank distilled water. All the rats were injected with tetracycline to mark the onset of dentine apposition. The alkalotic effect of the NaHCO3 drinking water was confirmed by blood gas analysis at the end of the experiment. After death, tetracycline-marked dentine apposition was measured from sagittally sectioned mandibular molars. Chronic metabolic alkalosis did not affect dentine apposition in the groups with the high-sucrose diet, nor in the groups with the standard diet at 6 weeks, but reduced it significantly in first and second molars in 7 weeks at rats on the standard diet. A high-sucrose diet alone caused a greater reduction in the amount of dentine. The general growth of the rats was not affected in any of the groups.

Topics: Alkalosis; Analysis of Variance; Animals; Carbon Dioxide; Dentinogenesis; Dietary Sucrose; Female; Hydrogen-Ion Concentration; Male; Oxygen; Partial Pressure; Rats; Rats, Wistar; Sodium Bicarbonate

We induced metabolic alkalosis and acidosis in 10 healthy volunteers in order to analyse in vivo relation between pH and ionized calcium (cCa2+). In the alkalinization test, 2.7 mol/kg NaHCO3 was injected. In the acidification test, volunteers took 4 mmol/kg NH4Cl. Blood pH and cCa2+ (mmol/l) mean values (SD) baseline, after alkalinization and acidification tests, were: 7.363 (0.018), 7.456 (0.031), 7.244 (0.031), 1.27 (0.03), 1.14 (0.03) and 1.38 (0.04). Mean slope of regression log cCa2+/pH was -0.39 (SD 0.11). Such a slope differs after in vivo or in vitro changes, due to the in vivo rapid restoration of equilibrium between the plasmatic and interstitial compartments following changes in water and electrolyte concentrations. The type of acid-base alteration-respiratory or metabolic-influences pH changes, and consequently the regression slope. The in vivo slope for log cCa2+/pH in normal subjects (-0.21) is much the same as in acute respiratory alterations (-0.17), whereas it differs in acute metabolic alterations (present study). Bicarbonates play different roles: the same changes in pH cause greater changes in cCa2+ after acute metabolic rather than respiratory alterations. Ca2+ homeostasis is maintained in acute respiratory acid-base imbalance, despite wide shifts in pH, whereas in acute metabolic alterations even small pH changes have striking repercussions on cCa2+. The experimental angular coefficient for in vivo acute metabolic acid-base alterations differs from the theoretical one calculated by Thode's differential equation (-0.25).

Topics: Acid-Base Equilibrium; Acidosis; Adult; Alkalosis; Ammonium Chloride; Calcium; Female; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Sodium Bicarbonate

The case is described of a 29-year-old man with renal failure and recurrent hyperparathyroidism who 3 weeks postparathyroidectomy developed hypocalcemic tetany because he was taking one-half the prescribed dose of calcitriol. He interpreted his symptoms as those of potassium intoxication and self-administered almost 1,500 mEq sodium bicarbonate. The increase in plasma sodium and osmolarity led to increased fluid intake, and at presentation he had an ionized calcium of 0.50 mmol/L, K 5.3 mmol/L, Na 148 mmol/L, total CO2 52.6 mmol/L, pO2 51.2 mm Hg, and pH of 7.61. He had gained 7 kg in weight. All abnormalities were corrected by dialysis, using initially a calcium-free dialyzate with extra calcium infused. The case illustrates the effect of alkalosis in reducing the amount of calcium that exists in ionized form, and it is suggested that complexing of calcium as calcium bicarbonate together with the pH change contributed to the decrease in ionized calcium. It is also an example of the hazards of treating patients who devise their own therapeutic regimens.

Topics: Adult; Alkalosis; Calcitriol; Calcium; Humans; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Male; Parathyroidectomy; Postoperative Complications; Renal Dialysis; Self Medication; Sodium Bicarbonate; Tetany

In a previous paper, we showed that an inhibition of amino acid transport across the liver plasma membrane is responsible for the decrease in urea synthesis in acute metabolic acidosis. We have now studied the mechanism responsible for the decline in urea synthesis in chronic acidosis. Chronic metabolic acidosis and alkalosis were induced by feeding three groups of rats HCl, NH4Cl, and NaHCO3 (8 mmol/day) for 7 days. Amino acids and NH4+ were measured in portal vein, hepatic vein, and aortic plasma, and arteriovenous differences were calculated. The rates of urinary urea and NH4+ excretion were also determined. Hepatic amino acid consumption was lower in both HCl and NH4Cl acidosis compared with NaHCO3-fed rats. Glutamine release was not different in the three conditions. Because intrahepatic concentrations of amino acids and intracellular protein degradation were similar under these conditions, it can be concluded that at low blood pH amino acid catabolism may be inhibited and might explain the observed decrease in urea excretion in HCl, but not NH4Cl, acidosis; urea excretion was comparable in the NH4Cl and NaHCO3 groups presumably because the increased NH4+ load in the former group was processed, uninhibited, to urea. Amino acids not used by the liver in acidosis could account for the 25-fold increase in NH4+ excretion in HCl and NH4Cl compared with alkalosis (P < 0.05). These findings indicate that urea synthesis is decreased in chronic HCl acidosis. They show that urea synthesis is controlled in chronic, as in acute, acidosis by amino acid uptake by the liver and/or intrahepatic degradation and that the ornithine cycle per se has only minor control of acid-base homeostasis.

Topics: Acidosis; Alkalosis; Amino Acids; Ammonium Chloride; Animals; Chronic Disease; Female; Hepatic Veins; Hydrochloric Acid; Liver; Portal Vein; Quaternary Ammonium Compounds; Rats; Rats, Wistar; Sodium Bicarbonate; Urea

A patient with a history of cerebrovascular disease, hypertension, and previous gastrectomy developed metabolic alkalosis and myoclonus. His medications included the anti-hypertensive agents nicardipine hydrochloride, delapril, prazosin; dihydroergotoxin and ticlopidine for cerebral infarction; estazolam for insomnia; azuren-L-glutamine compound and S-M powder. In addition, he had taken 12 grams per day of Ohta's Isan antacid, which contained 625 mg sodium bicarbonate per 1.3 g of antacid powder over a 6-month period. This antacid is commonly used in Japan. This is the first report of a case of metabolic alkalosis and myoclonus secondary to ingestion of a commercially available antacid in Japan.

Topics: Aged; Alkalosis; Antacids; Cardiovascular Agents; Cerebral Infarction; Dyspepsia; Gastrectomy; Humans; Hypertension; Hypnotics and Sedatives; Hypokalemia; Male; Myoclonus; Sleep Initiation and Maintenance Disorders; Sodium Bicarbonate

Hypertonic sodium salts are used to treat sodium channel-blocking drug cardiotoxicity. The relative roles of alkalinization and increased sodium concentration ([Na+]o) for various drugs are incompletely known.. The effects of four class I drugs on action potential characteristics of canine Purkinje fibers at equieffective concentrations (disopyramide 30 mumol/L, mexiletine 80 mumol/L, flecainide 7 mumol/L, imipramine 5 mumol/L) were studied in the presence of normal Tyrode solution and one altered solution (increased [Na+]o, increased bicarbonate concentration, or both) in each experiment. Combined increases in sodium and bicarbonate concentration significantly reduced the depressant effects of flecainide, imipramine, and mexiletine on phase 0 upstroke (Vmax) but did not alter the effects of disopyramide. The effects of sodium bicarbonate were entirely due to alkalinization in the case of imipramine, but both alkalinization and increased [Na+]o contributed to the interaction with flecainide and mexiletine. The reversal of Vmax depression by increased [Na+]o and pH was due in part to hyperpolarization. In addition, alkalosis directly reversed the hyperpolarizing shift in Vmax inactivation caused by flecainide and imipramine without altering the shift caused by disopyramide and mexiletine.. Increases in sodium bicarbonate concentration reverse the effects of class I antiarrhythmic drugs to a varying extent, with drug-specific contributions of the sodium and bicarbonate moiety. The molecular basis for this drug specificity remains to be elucidated, but it has important potential implications for the use of hypertonic sodium salts to treat cardiotoxicity caused by sodium channel-blocking drugs.

Topics: Alkalosis; Animals; Anti-Arrhythmia Agents; Antidepressive Agents, Tricyclic; Dogs; Electrophysiology; Female; Hydrogen-Ion Concentration; Male; Sodium; Sodium Bicarbonate; Sodium Channel Blockers; Sodium Channels

Topics: Alkalosis; Blood Gas Analysis; Electrolytes; Female; Humans; Hypoventilation; Middle Aged; Sodium Bicarbonate; Time Factors

To investigate the effect of acute induced metabolic alkalosis on the haematological, biochemical and metabolic responses to sprint exercise, six greyhound dogs with previously placed carotid arterial catheters were raced four times over a distance of 400 metres. Each dog was raced twice after receiving oral sodium bicarbonate solution (NaHCO3) (400 mg kg-1) or lactated Ringer's solution (LRS). Before, and for intervals of up to one hour after, the exercise arterial blood samples were collected for the measurement of blood gases, packed cell volume, total protein, serum biochemistry and plasma lactate. The time to complete the 400 metre sprint ranged from 32.7 seconds to 36.9 seconds. There was no significant difference in racing times between the dogs treated with NaHCO3 and LRS, and there was no significant difference between the plasma lactate measurements after the treatments with NaHCO3 or LRS. Serum chloride concentrations were significantly lower after NaHCO3 than after LRS, and there was a trend towards a lower serum potassium concentration after NaHCO3 treatment. Plasma lactate concentrations showed a similar increase and time course of disappearance after both LRS and NaHCO3 treatments. There were significant changes in all the parameters measured after the exercise, but there were large variations between individual dogs and between races when the dogs were receiving the same treatment.

Topics: Acid-Base Equilibrium; Administration, Oral; Alkalosis; Animals; Blood Proteins; Carbon Dioxide; Dogs; Electrolytes; Hydrogen-Ion Concentration; Lactates; Oxygen; Partial Pressure; Physical Conditioning, Animal; Physical Exertion; Sodium Bicarbonate; Time Factors

The authors examined 40 patients with malignant tumors of various histogenesis, sites and extent, as well as 5 patients with benign tumors and other non-tumorous diseases. They also studied their electroencephalography and peripheral blood lymphocytic and erythrocytic ultrastructure in metabolic alkalosis temporarily induced by intravenous sodium hydrogen carbonate. In cancer patients without late metastases, alkalosis caused a transient normalization of previously altered electroencephalography, erythrocyte disaggregation and substantially reduced the count of killer cells in small and middle lymphocytes. These findings suggest that patients with malignant neoplasms have a generalized intracellular acidosis which can be temporarily abolished by plasma alkalinization.

Topics: Adult; Alkalosis; Ampulla of Vater; Common Bile Duct Neoplasms; Electroencephalography; Erythrocyte Aggregation; Erythrocytes; Female; Humans; Killer Cells, Natural; Liver Neoplasms; Lymphocyte Subsets; Lymphocytes; Male; Middle Aged; Neoplasms; Sodium Bicarbonate; Stomach Neoplasms

To examine further the role of the liver in acid-base homeostasis, we studied hepatic amino acid uptake and urea synthesis in rats in vivo during acute acidosis and alkalosis, induced by infusion of 1.8 mmol of HCl or NaHCO3 over 3 h. Amino acids and NH4+ were measured in portal vein, hepatic vein, and aortic plasma, and arteriovenous differences of amino acids and urinary urea and NH4+ excretion were measured. In acidosis, urinary urea excretion was reduced 36% (P < 0.01), whereas urinary NH4+ excretion increased ninefold (P < 0.01), but the sum of urea and NH4+ excretion was unchanged. Total hepatic amino acid uptake, as determined from arteriovenous differences, was decreased by 63% (P < 0.01) in acidosis, with the major effect being noted with alanine and glycine. Only glutamine was released in both acidosis and alkalosis but was not significantly different in the two conditions. Since intracellular concentrations of readily transportable amino acids were not different at low pH despite accelerated protein degradation, these results indicate that hepatic amino acid transport was inhibited markedly and sufficiently to explain the observed decrease in urea synthesis. Total hepatic vein amino acid content was greater in acidosis than alkalosis (P < 0.01). Directly or indirectly, by conversion to glutamine elsewhere, these increased amino acids were degraded in kidney and accounted for the ninefold increase in urinary NH4+ excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acid-Base Equilibrium; Acidosis; Alkalosis; Amino Acids; Animals; Aorta; Biological Transport; Female; Hepatic Veins; Hydrochloric Acid; Hydrogen-Ion Concentration; Liver; Portal Vein; Quaternary Ammonium Compounds; Rats; Rats, Wistar; Sodium Bicarbonate; Urea

Sodium bicarbonate is an extremely well-known agent that historically has been used for a variety of medical conditions. Despite the widespread use of oral bicarbonate, little documented toxicity has occurred, and the emergency medicine literature contains no reports of toxicity caused by the ingestion of baking soda. Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The case of a patient with three hospital admissions in 4 months, all the result of excessive oral intake of bicarbonate for symptomatic relief of dyspepsia is reported. Evaluation and treatment of patients with acute bicarbonate ingestion is discussed.

Topics: Acute Disease; Alkalosis; Humans; Hypokalemia; Male; Middle Aged; Poisoning; Sodium Bicarbonate

Experiments on white rats found that both chronic acidosis and chronic alkalosis cause fasting hyperglycemia and decreases glucose tolerance. In hypophysectomized animals, alkalosis causes similar effects and acidosis leads to hypoglycemia. Acute acidosis stimulates insulin and corticotropin secretions acute alkalosis reduces blood insulin and corticotropin levels and increases glucagon concentration. Chronic acidosis and alkalosis decrease insulin secretion and stimulates corticotropin secretion. Glucagon levels remain increased in chronic alkalosis. It has been concluded that primary cause of diabetogenic action of chronic acidosis is glucocorticoid hyperfunction and exhausting stimulation of B cells with glucose. Alkalosis causes a direct inhibitory action on B cells and activates A cells of Langerhans' islets.

Topics: Acid-Base Imbalance; Acidosis; Alkalosis; Ammonium Chloride; Animals; Blood Glucose; Chronic Disease; Diabetes Mellitus, Experimental; Hypophysectomy; Male; Rats; Sodium Bicarbonate

Furosemide produces fetal wavy ribs when administered to pregnant rats during late gestation. The compound is also known to produce metabolic alkalosis in laboratory animals and man. In order to evaluate the effect of furosemide on maternal blood pH, Crj:CD(SD) female rats received an oral administration of 150 or 200 mg/kg of furosemide by gavage on day 16 of gestation and were bled at 4 hr post-dose. Compared to an average pH of 7.39 in control females, there was a significant elevation in blood pH in these furosemide-treated females (average pH of 7.44 to 7.48). When 2% sodium bicarbonate was provided in the drinking water for females treated with 150 mg/kg of furosemide, there was a further rise in maternal blood pH (7.52) compared to females treated with furosemide alone. Associated with this elevation in maternal blood pH was a marked increase in the incidence of fetal wavy ribs (87.6% compared to 27.6%). When females treated with 200 mg/kg of furosemide were provided with 0.5% ammonium chloride, furosemide-induced maternal alkalosis was corrected (pH decreased to 7.35) and there was a reduction in the incidence of fetal wavy ribs (7.0% compared to 37.2%). In addition, maternal blood pH among individual females was positively correlated with the incidence of fetal wavy ribs (r = 0.714). These results suggest that maternal metabolic alkalosis is involved in the pathogenesis of furosemide-induced wavy ribs.

Topics: Alkalosis; Ammonium Chloride; Animals; Body Weight; Drug Interactions; Female; Furosemide; Male; Pregnancy; Rats; Rats, Sprague-Dawley; Ribs; Sodium Bicarbonate; Teratogens

We evaluated the effects of acid-base changes in pregnant and lactating dams on intercalated cell morphology and populations in newborn and 2-wk-old rats. Collecting ducts were studied with transmission electron microscopy with intercalated cells identified by the presence of 10-nm studs in the cytoplasmic face of apical membranes (A-type intercalated cells) or basolateral membranes (B-type intercalated cells). In newborn and 2-wk-old pups from dams with metabolic alkalosis, there was a significantly larger percentage of B-type intercalated cells and a smaller percentage of A-type intercalated cells. Acid loading with NH4Cl, however, did not produce an increase in the percentage of A-type intercalated cells, but reduced the percentage of B-type intercalated cells. We conclude that maternal metabolic alkalosis is associated with an increase in the percentage of B-type intercalated cells, suggesting that the initial differentiation of intercalated cells is responsive to maternal acid-base disturbances.

Topics: Acid-Base Imbalance; Alkalosis; Ammonium Chloride; Animals; Animals, Newborn; Bicarbonates; Cell Count; Female; Kidney Tubules, Collecting; Lactation; Microscopy, Electron; Pregnancy; Pregnancy Complications; Rats; Rats, Sprague-Dawley; Sodium; Sodium Bicarbonate

We have presented the case of a 34 year old male patient who was admitted with severe metabolic alkalosis (MA). Peak serum HCO3 was 96 mg/dl and compensatory PCO2 was 95 which, to our knowledge, has never been reported before in a patient with MA. MA was probably generated by consumption of high amount of NaHCO3 and renal impairment and maintained by impaired renal function due to volume depletion hypokalemia and hyochloremia. The patient was successfully treated with IV administration of saline and KCL.

Topics: Adult; Alkalosis; Bicarbonates; Fluid Therapy; Humans; Male; Renal Insufficiency; Self Medication; Sodium; Sodium Bicarbonate

The effect of bicarbonate ingestion on total excess volume of CO2 output (CO2 excess), due to bicarbonate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g.kg-1 body mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arterialized venous blood pH (P < 0.05) and bicarbonate concentration ([HCO3-]b; P < 0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO3-]b, 29.4 (SD 1.5) mmol.l-1] than in the control [pH, 7.39 (SD 0.03); [HCO3-]b, 25.5 (SD 1.0) mmol.l-1]. The blood lactate concentrations ([la-]b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la-]b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol.l-1, P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol.l-1, P < 0.05] were found in AMA compared with the control. The CO2 excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml; P < 0.05]. The CO2 excess per body mass was found to be significantly correlated with both the increase of [la-]b from rest to 3 min after exercise (delta[la-]b; r = 0.926, P < 0.001) and with the decrease of [HCO3-]b from rest to 3 min after exercise (delta [HCO3-]b; r = 0.872, P < 0.001), indicating that CO2 excess per body mass increased linearly with both delta [la-]b and delta [HCO3-]b.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Alkalosis; Bicarbonates; Buffers; Carbon Dioxide; Exercise; Humans; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Male; Pulmonary Gas Exchange; Respiration; Sodium; Sodium Bicarbonate

An N-ethylmaleimide (NEM)-sensitive adenosinetriphosphatase (ATPase) displaying the kinetic and pharmacological properties of an electrogenic proton pump has been described in the different segments of rat nephron, where it mediates part of the active tubular proton secretion. This study was therefore designed to evaluate whether changes in urinary acidification observed during metabolic acidosis or alkalosis were associated with alterations of the activity of tubular NEM-sensitive ATPase, and if so, to localize the nephron segments responsible for these changes. Within 1 wk after the onset of ammonium chloride treatment, rats developed a metabolic acidosis, and NEM-sensitive ATPase activity was markedly increased in the medullary thick ascending limb of Henle's loop and outer medullary collecting tubule, and slightly increased in the cortical collecting tubule. Conversely, treatment with sodium bicarbonate induced a metabolic alkalosis that was accompanied by decreased NEM-sensitive ATPase activity in medullary thick ascending limb and outer medullary collecting tubule. NEM-sensitive ATPase activity was not altered in any other nephron segment tested in alkalotic and acidotic rats, i.e., the proximal tubule and the cortical thick ascending limb of Henle's loop. Changes qualitatively similar were observed as soon as 3 h after the onset of NaHCO3 or NH4Cl-loading. In the medullary collecting tubule, alterations of NEM-sensitive ATPase activity are in part due to hyperaldosteronism observed in both acidotic and alkalotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acid-Base Equilibrium; Acidosis; Adenosine Triphosphatases; Aldosterone; Alkalosis; Ammonium Chloride; Animals; Bicarbonates; Ethylmaleimide; In Vitro Techniques; Male; Nephrons; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Time Factors

There is considerable debate regarding the ergogenic effects of sodium bicarbonate (NaHCO3) on racing performance in horses. Anecdotal evidence suggests that NaHCO3 improves performance by increasing the buffering capacity of the blood and delaying the onset of hydrogen ion-induced fatigue. In a cross-over study, 16 Thoroughbred racehorses were given an aqueous solution of NaHCO3 (0.4 g/kg in 1 litre H2O) or a control treatment (1 litre H2O) before a 1600-m race. Treatments were administered 3 h before the race, which was the time to peak buffering capacity (2.5-3.0 h) determined in a separate study. Before the race, there was a significant increase in venous HCO3- and pH in the NaHCO3-treated horses. After the race, there was a significant increase in venous blood pH and lactate in the NaHCO3-treated horses. Collectively, the data suggest an improved buffering capacity of the blood after NaHCO3 treatment. However, there was no change in race times or venous partial pressure of carbon dioxide. Therefore, the administration of NaHCO3 provided no ergogenic benefit to horses competing in a 1,600-m race.

Topics: Acid-Base Equilibrium; Alkalosis; Animals; Bicarbonates; Breeding; Buffers; Carbon Dioxide; Doping in Sports; Female; Horse Diseases; Horses; Humidity; Hydrogen-Ion Concentration; Lactates; Male; Physical Exertion; Sodium; Sodium Bicarbonate; Temperature; Time Factors; Wind

We have sought to define urinary acid-base excretion in the marine teleost using the long-horned sculpin, Myoxocephalus octodecimspinosus. Urine flow (1.7 ml.h-1.kg-1) is relatively high, and glomerular filtration rate is very low (2.9 ml.h-1.kg-1). The urine-to-plasma ratio of inulin is 2. Renal clearance of p-aminohippurate is very high (108 ml.h-1.kg-1); phosphate and divalent cations are also secreted. In this framework we found urinary pH to average 6.6, but infusion of acid or alkali elicited a pH range of 6.1-7.8. Untreated fish may also have alkaline urine; so it is not surprising that precipitates of calcium or magnesium phosphate are sometimes found in bladder. These are of fine sandy quality and never cause blockage. Infusion of buffer (imidazole) increased the concentration of titratable acid 11-fold and output 2.5-fold. Carbonic anhydrase inhibitors had no effect on any urinary component, and histochemical studies revealed that cytoplasm and membranes did not yield the specific cobalt stain for the enzyme. An alkaline load (NaHCO3) is rapidly dissipated by gill excretion, mediated in part by carbonic anhydrase. An acid load (HCl) is rapidly dissipated by gill excretion, not dependent on carbonic anhydrase, and some renal excretion. Comparison and contrast of the low rates of HCO3- reabsorption in the marine teleost (and elasmobranch) with those of mammals suggest strongly that renal carbonic anhydrase evolved in connection with these high reabsorptive rates beginning in freshwater fish and continuing through amphibia and birds.

Topics: Acid-Base Equilibrium; Acidosis; Acids; Alkalosis; Animals; Benzolamide; Bicarbonates; Carbonic Anhydrase Inhibitors; Electrolytes; Female; Fishes; Hydrochloric Acid; Imidazoles; Kidney; Male; Methazolamide; Sodium; Sodium Bicarbonate

The influence of molecular charge on the tubular reabsorption of proteins was studied in conscious rats injected intravenously with beta 2-microglobulins of different isoelectric points (pI). Native human beta 2-microglobulin (pI 5.8), two anionized (pI 4.85 and 5.55) and three cationized derivatives (pI 7.2, 8.35 and 8.7) were used. The six forms of beta 2-microglobulin had a molecular radius between 15.7 and 15.9 A. The renal uptake was estimated by measuring the amount excreted in urine with a sensitive immunoassay. The ability of rat kidney to reabsorb beta 2-microglobulin was clearly related to the net charge of the protein. Increasing the pI of the protein significantly reduced the urinary excretion, whereas lowering it had the opposite effect. Anionization was particularly effective in reducing the beta 2-microglobulin uptake, since a decrease of the pI of one unit enhanced the urinary output by two orders of magnitude. This charge-dependency persisted when the tubular reabsorption of proteins was partly inhibited by lysozyme. By contrast, it was practically abolished by lysine, probably because the inhibitory effect of this amino acid on protein tubular reabsorption is not competitive. The administration of ammonium chloride in rats produced an immediate and transient elevation of rat beta 2-microglobulinuria. This phenomenon, which was partly inhibited by the subsequent administration of sodium bicarbonate, presumably results from a competition between the NH4+ ion and beta 2-microglobulin for tubular binding sites. These data support the hypothesis that proteins bind to the luminal membrane of tubular cells mainly via positively charged amino groups.

Topics: Acidosis; Alkalosis; Ammonium Chloride; Animals; beta 2-Microglobulin; Bicarbonates; Electrochemistry; Electrophoresis, Agar Gel; Female; Humans; Isoelectric Point; Kidney; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.

Topics: Acidosis; Alkalosis; Animals; Bicarbonates; Carbonates; Cardiac Output; Dogs; Drug Combinations; Hemodynamics; Hydrochloric Acid; Hypercapnia; Lung; Oleic Acid; Oleic Acids; Pulmonary Edema; Pulmonary Gas Exchange; Pulmonary Wedge Pressure; Sodium Bicarbonate

Studies were performed on previously nephrectomized dogs to examine roles of hormonal factors in plasma potassium alterations in acute alkalosis. Respiratory and metabolic alkalosis were induced by hyperventilation and intravenous NaHCO3 or tris(hydroxymethyl)aminomethane (Tris) infusion, respectively. Respiratory and NaHCO3-induced alkalosis provoked decreases in plasma potassium from the control value of 5.12 +/- 0.68 (SE) to 4.21 +/- 0.55 meq/l (P less than 0.01) and from 4.65 +/- 0.26 to 3.91 +/- 0.16 meq/l (P less than 0.01) within 180 min, respectively. In contrast, Tris-induced alkalosis elicited an increase in plasma potassium from the control value of 4.56 +/- 0.30 to 5.31 +/- 0.30 meq/l (P less than 0.01). Hypokalemia in respiratory alkalosis was associated with a decrease in the plasma norepinephrine concentration from the control level of 377 +/- 104 to 155 +/- 41 pg/ml (P less than 0.05) but not with changes in plasma levels of epinephrine, insulin, glucagon, cortisol, and aldosterone. However, this hypokalemia was not affected by phentolamine. Also, somatostatin did not modify the hypokalemic response. NaHCO3-induced hypokalemia was associated with a decline in the plasma aldosterone and norepinephrine concentrations. The decline in plasma norepinephrine in NaHCO3-induced alkalosis followed the decrease in plasma potassium. In Tris-induced alkalosis, plasma insulin increased but norepinephrine decreased. The findings do not suggest fundamental roles of the hormonal factors in the plasma potassium alterations in bilaterally nephrectomized dogs with acute alkalosis.

Topics: Acid-Base Equilibrium; Acute Disease; Alkalosis; Alkalosis, Respiratory; Animals; Bicarbonates; Dogs; Female; Hormones; Hydrogen-Ion Concentration; Male; Nephrectomy; Norepinephrine; Potassium; Saline Solution, Hypertonic; Sodium; Sodium Bicarbonate

The effect of metabolic alkalosis was studied in 10 healthy volunteers. In each person urea synthesis was determined in two periods of 2 h as urinary excretion corrected for accumulation in body water and for intestinal hydrolysis. Infusion of bicarbonate (115 mmol/h) increased pH of the venous blood by 0.10 units. In four subjects fasting urea synthesis was 24 mmol N/h at normal pH and unaffected by alkalosis (mean difference +/- SED was 1.04 +/- 4.1). In six subjects alanine was infused so as to increase blood alanine concentration from 0.4 to 2.5 mmol/l and urea synthesis to 107 mmol N/h. Alkalosis did not change urea synthesis (mean difference +/- SED was 1.5 +/- 7.4 mmol N/h). The results favour the view that urea synthesis mainly serves to eliminate nitrogen, but do not support the hypothesis that urea synthesis is an important immediate and direct regulatory process in acute acid-base disturbances.

Topics: Adult; Alanine; Alkalosis; Ammonia; Bicarbonates; Blood; Female; Humans; Hydrogen-Ion Concentration; Male; Nitrogen; Sodium; Sodium Bicarbonate; Urea

Inhibition of angiotensin II activity reduces reabsorption of both bicarbonate and chloride predominantly in the S1 subsegment of the proximal convoluted tubule (PCT). Because the S2 PCT is intrinsically better able to compensate for the increased delivery of bicarbonate compared with chloride under normal conditions, we reasoned that angiotensin II inhibition might selectively raise the amount of sodium chloride emerging from the PCT. Free-flow micropuncture techniques were used in normal and alkalotic Munich-Wistar rats that were euvolemic or plasma volume depleted. In the normal volume-depleted animals, saralasin caused a small rise in single-nephron glomerular filtration rate (29.5 +/- 0.6 to 31.5 +/- 0.6 nl/min, P less than 0.025) and fall in bicarbonate and chloride reabsorption in the 1st mm (S1) PCT (387 +/- 22 to 348 +/- 23 peq.mm-1.min-1, P less than 0.05, and 341 +/- 27 to 217 +/- 57 peq.mm-1.min-1, P less than 0.05, respectively). Reabsorptive compensation by the S2 PCT maintained the end-PCT delivery of bicarbonate unchanged (76 +/- 4 to 78 +/- 3 peq.mm-1.min-1, NS), but end-PCT chloride delivery increased significantly (2,014 +/- 41 to 2,248 +/- 29 peq.mm-1.min-1, P less than 0.01). Early distal convoluted tubule (DCT) and urinary bicarbonate excretion were unchanged, but DCT chloride delivery increased associated with a chloruresis. When metabolic alkalosis was present, however, S2 compensation for increased bicarbonate delivery was attenuated so that end-PCT, DCT, and urinary bicarbonate as well as chloride delivery rates increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Alkalosis; Angiotensin II; Animals; Bicarbonates; Biological Transport; Hydrogen-Ion Concentration; Kidney Glomerulus; Kidney Tubules; Male; Rats; Rats, Inbred Strains; Saralasin; Sodium; Sodium Bicarbonate; Sodium Chloride; Water-Electrolyte Balance

To determine the effects of acute metabolic acidosis and alkalosis on leucine metabolism in vivo, mongrel dogs were infused with [1-14C]leucine for 8 h, along with NaCl, HCI, or NaHCO3 over the last 4 h. Arterial pH did not change from the basal value during NaCl infusion but decreased (P less than .01) and increased (P less than .01) during HCl and NaHCO3 infusions, respectively. Total leucine carbon entry did not change from the basal value during saline infusion but increased (P less than .01) with acidosis and decreased (P less than .05) with alkalosis. Compared with saline controls, acidosis increased (P less than .01) leucine oxidation. During alkalosis decreased (P less than .01) leucine oxidation. During acidosis, total plasma essential and nonessential amino acid concentrations increased (P less than .05), whereas during alkalosis, total plasma essential and nonessential amino acid concentrations decreased (P less than .05). These studies suggest that acute alterations in arterial pH may affect the regulation of protein metabolism in vivo and must be considered in the interpretation of results from experiments in which alterations of acid-base homeostasis may have occurred.

Topics: 3-Hydroxybutyric Acid; Acetoacetates; Acidosis; Alkalosis; Amino Acids; Animals; Bicarbonates; Blood Gas Analysis; Blood Glucose; Consciousness; Dogs; Fatty Acids, Nonesterified; Glucagon; Hydrochloric Acid; Hydrogen-Ion Concentration; Hydroxybutyrates; Infusions, Intra-Arterial; Insulin; Keto Acids; Leucine; Oxidation-Reduction; Pyruvates; Sodium; Sodium Bicarbonate; Sodium Chloride

The mechanism by which extracellular alkalosis inhibits hypoxic pulmonary vasoconstriction is unknown. We investigated whether the inhibition was due to intrapulmonary production of a vasodilator prostaglandin such as prostacyclin (PGI2). Hypoxic vasoconstriction in isolated salt-solution-perfused rat lungs was blunted by both hypocapnic and NaHCO3-induced alkalosis (perfusate pH increased from 7.3 to 7.7). The NaHCO3-induced alkalosis was accompanied by a significant increase in the perfusate level of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), an hydrolysis product of PGI2. Meclofenamate, an inhibitor of cyclooxygenase, counteracted both the blunting of hypoxic vasoconstriction and the increased level of 6-keto-PGF1 alpha. In intact anesthetized dogs, hypocapnic alkalosis (blood pH increased from 7.4 to 7.5) blunted hypoxic pulmonary vasoconstriction before but not after administration of meclofenamate. In separate cultures of bovine pulmonary artery endothelial and smooth muscle cells stimulated by bradykinin, the incubation medium levels of 6-keto-PGF1 alpha were increased by both hypocapnic and NaHCO3-induced alkalosis (medium pH increased from 7.4 to 7.7). These results suggest that inhibition of hypoxic pulmonary vasoconstriction by alkalosis is mediated at least partly by PGI2.

Topics: 6-Ketoprostaglandin F1 alpha; Alkalosis; Animals; Bicarbonates; Bradykinin; Carbon Dioxide; Cells, Cultured; Dogs; Endothelium, Vascular; Epoprostenol; Hypoxia; Male; Muscle, Smooth, Vascular; Oxygen; Pulmonary Artery; Rats; Sodium; Sodium Bicarbonate; Vasoconstriction

Metabolic alkalosis has previously been shown to have an antimagnesiuric influence. To further clarify this phenomenon, short-term clearance studies were performed on intact anesthetized rats subjected to 0.9% saline infusion, 0.15 M NaHCO3 infusion or acute respiratory alkalosis. The experimental protocols resulted in a similar degree of natriuresis in each of the three groups. The increase in plasma pH value was similar both in animals treated with NaHCO3 and animals with respiratory alkalosis. Filtered loads of Mg did not differ in the three experimental groups. However, only acute metabolic alkalosis was associated with a reduction in the absolute rate of Mg excretion (saline: 0.49 +/- 0.05 mu Eq/min; 0.15 M NaHCO3: 0.29 +/- 0.04 mu Eq/min; acute respiratory alkalosis: 0.48 +/- 0.03 mu Eq/min) and fractional Mg excretion (saline: 40.3 +/- 5.3%; 0.15 NaHCO3: 18.7 +/- 1.4%; acute respiratory alkalosis: 37.2 +/- 6.9%). A similar decrease in urinary Mg excretion in animals treated with bicarbonate infusion was observed following removal of the parathyroid gland. Moreover, for any given rate of urinary Na excretion, Mg excretion was lower in bicarbonate-treated animals than in rats infused with saline solution. Intact animals treated with increasing doses of NaHCO3 revealed a statistically significant inverse correlation between the Mg to Na clearance ratio and urinary and plasma bicarbonate concentration. In contrast, such a correlation was not observed during respiratory alkalosis. The findings suggest that bicarbonate ion directly stimulates tubular magnesium reabsorption independent of the presence or absence of parathyroid hormone.

Topics: Alkalosis; Alkalosis, Respiratory; Animals; Bicarbonates; Carbon Dioxide; Magnesium; Male; Natriuresis; Parathyroid Glands; Parathyroid Hormone; Rats; Sodium; Sodium Bicarbonate; Thyroidectomy

The frog skin has been shown to excrete various electrolytes, the rates can be altered by varying metabolic conditions. The present study was performed to determine if metabolic alkalosis results in histological changes in the skin that are characteristic of this state. Rana pipiens were loaded with NaHCO3 and skin biopsies obtained (I). These biopsies were compared with biopsies from either control, unloaded frogs (II), or from NaCl loaded (III) frogs. In blind studies of microscopic sections, 13 of 15 biopsies of a mixture of I and II were correctly diagnosed, and similarly, 18 of 20 of I and III were correctly diagnosed (P = 0.0037, and 0.0002, respectively). The changes due to NaHCO3 treatment included; (1) an abundance of large euchromatin cells on or near the surface; (2) changes in the basal cell layer with elongation and rotation of the nuclei; (3) lighter cells in the spinosal layer; and, (4) sometimes the skin became thicker. We conclude that metabolic alkalosis results in characteristic histological changes in the skin, and that this is probably related to the ability of the skin to excrete bicarbonate.

Topics: Alkalosis; Animals; Bicarbonates; Female; Male; Mitochondria; Rana pipiens; Skin; Sodium; Sodium Bicarbonate

Metabolic alkalosis was induced in 10 clinically normal horses by administration of furosemide (1 mg/kg of body weight, IM) followed 4.5 hours later by sodium bicarbonate (NaHCO3; 500 g in 8 L water) via nasogastric tube. Furosemide diuresis resulted in a mean weight loss of 21.1 kg, which was associated with small, but significant, increases in venous blood pH, bicarbonate, and plasma protein concentrations (P less than 0.001), while plasma potassium, chloride, and calcium concentrations declined significantly (P less than 0.001). Oral administration of the hypertonic NaHCO3 solution resulted in clinical evidence of hypovolemia, which was accompanied by a marked increase (P less than 0.001) in plasma protein concentration. Seven of the 10 horses developed signs of neuromuscular excitability, as evidenced by muscle fasciculations, and 5 of the horses developed diaphragmatic flutter. Hypernatremia was transiently induced, but it resolved as the horses were allowed access to water. The alkalosis induced by furosemide and NaHCO3 was profound and persisted for a 24-hour period and was associated with marked hypochloremia and hypokalemia. Partial replacement of the electrolyte deficits and correction of the metabolic alkalosis was attempted, using 1,000 mEq of NaCl or KCl given as an isotonic solution via nasogastric tube. In the KCl-treated group, there was a prompt and significant decline in venous blood pH and bicarbonate concentration (P less than 0.001) accompanied by a significant increase in plasma potassium concentration (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Alkalosis; Animals; Bicarbonates; Electrolytes; Furosemide; Horse Diseases; Horses; Hydrogen-Ion Concentration; Male; Osmolar Concentration; Potassium; Potassium Chloride; Sodium; Sodium Bicarbonate; Sodium Chloride

Determination of the appropriateness of the compensatory response is essential in evaluation of any acid-base disturbance. Adequate compensation supports the presence of a single acid-base event. Inadequate compensation may indicate that a second primary acid-base event is present or, in some circumstances, that time has been inadequate for maximal physiologic compensation. When acid-base disturbances are mixed, treatment of one disorder may unmask the full pH-altering potential of the second disorder. Close monitoring of patients at risk for the development of acid-base disorders permits detection of problems at a time when intervention may prevent serious complications. Relatively inexpensive and easy-to-use chemical analytic systems to assist early diagnosis are now present in many office-based laboratories.

Topics: Acid-Base Imbalance; Acidosis; Alkalosis; Alkalosis, Respiratory; Bicarbonates; Diabetic Ketoacidosis; Humans; Potassium Chloride; Primary Health Care; Risk Factors; Sodium; Sodium Bicarbonate; Sodium Chloride

A case of severe metabolic alkalosis (MA) resulting from ingestion of baking soda (sodium bicarbonate) is presented. On admission to the emergency department, the patient was alert and stable with an initial examination that was remarkable only for carpopedal spasm. Shortly thereafter, the patient had a sudden, unexpected cardiopulmonary arrest. Following resuscitation, without administration of sodium bicarbonate, the arterial blood gas revealed a pH of 7.73, pO2 of 51 mm Hg, and pCO2 of 52 mm Hg. After admission to the intensive care unit, the patient's MA was corrected using IV 0.25 N hydrochloric acid. The patient remained comatose as a result of severe anoxic encephalopathy and died two weeks after admission. We believe this is the first reported case of severe MA resulting in sudden cardiopulmonary arrest in a previously ambulatory patient.

Topics: Acute Disease; Alkalosis; Bicarbonates; Emergencies; Heart Arrest; Humans; Male; Middle Aged; Sodium; Sodium Bicarbonate

Upon sulfate administration, UpH falls more in alkalotic rats than in controls. Alkalosis can lead to a reduction in UNH3 V at highly acidic urine. The significance of this process is doubtful at UpH ranging from about 6 to 7. At lower UpH less NH3 would be excreted, thereby less H+ would be trapped in urine and some acid would be conserved.

Topics: Alkalosis; Ammonia; Animals; Bicarbonates; Hydrogen-Ion Concentration; Kidney; Male; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Urine

1. The basis for the existence of a lower concentration of salicylate in the foetal than in the maternal blood was investigated in rats on day 20 of gestation. 2. Bolus injections of sodium salicylate were made into the mother and of [14C]-salicylic acid into its foetuses and serial maternal and foetal blood samples were collected. When derived on the basis of serum salicylic acid uncorrected for differences in ionization in the maternal and foetal blood, the placental clearance was 2.2 fold greater from the foetal to maternal side than that from the maternal to foetal side. 3. The greater foetal placental clearance relative to the maternal placental clearance was not due to any active placental transfer, since there was no evidence of saturation of this process and it was not affected by pretreatment with probenecid. Moreover, salicylic acid was not concentrated by placental slices in vitro and its placental uptake was not affected by dinitrophenol or by cooling. 4. Maternal blood pH was 0.19 units higher than the foetal blood pH. Administration of ammonium chloride or of sodium bicarbonate into the mother increased the foetal to maternal ratio of salicylic acid from 0.6 to approximately 1. 5. It is concluded that a foetal to maternal serum salicylate concentration-ratio of less than 1 simply reflects lower ionization in the foetus than in the mother, because foetal blood pH is lower than the maternal blood pH.

Topics: Acidosis; Alkalosis; Ammonium Chloride; Animals; Bicarbonates; Blood Gas Analysis; Female; Hydrogen-Ion Concentration; In Vitro Techniques; Maternal-Fetal Exchange; Placenta; Pregnancy; Probenecid; Rats; Rats, Inbred Strains; Salicylates; Sodium; Sodium Bicarbonate

When used appropriately, baking soda (sodium bicarbonate, USP) is a nontoxic, readily available, multipurpose product found in many households. We report an infant who presented with hypernatremia and metabolic alkalosis due to the addition of baking soda to her water. This case represents the possible dangerous use of a common household product in infants owing to the lack of proper warning labels.

Topics: Alkalosis; Bicarbonates; Female; Fluid Therapy; Hospitalization; Humans; Hypernatremia; Infant; Sodium; Sodium Bicarbonate

Non-pretrained, randomized adult rats were tested in a panic-inducing model of passive avoidance. Intravenous treatment with alkalinizing agents (sodium lactate 0.5 M, 0.5 ml/100 g b.wt., or NaHCO3, 0.5 mEq/100 g b.wt.), but not with a hypocalcemic dose of EDTA (75 mg/kg) 3 min before testing, significantly increased panic behavior. These data may support the hypothesis that panic attacks are due to alkalosis and not to lactate-induced hypocalcemia.

Topics: Alkalosis; Animals; Behavior, Animal; Bicarbonates; Fear; Female; Hypocalcemia; Lactates; Lactic Acid; Panic; Random Allocation; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate

Topics: Adult; Alkalosis; Arm; Bicarbonates; Blood Pressure; Exercise Test; Humans; Leg; Male; Physical Exertion; Random Allocation; Sodium; Sodium Bicarbonate; Work Capacity Evaluation

Sodium bicarbonate abuse is unusual, and rarely reported. A patient was extensively investigated at several hospitals for a recurrent hypokalaemic metabolic alkalosis; it transpired that she had been abusing sodium bicarbonate for 8 years and had gained hospital admission at will by taking large amounts. She also showed features of the Munchausen syndrome.

Topics: Adult; Alkalosis; Bicarbonates; Female; Humans; Hypokalemia; Munchausen Syndrome; Sodium; Sodium Bicarbonate; Substance-Related Disorders

Studies were performed to assess the role of changes in the excretion of citrate, a metabolic precursor of bicarbonate, in acid-base balance in diuretic-induced metabolic alkalosis. Rats on a low-chloride diet with sodium sulfate added were studied during a base-line period, 3 days of furosemide administration, and 4 days post-furosemide. During the period of furosemide administration, net acid excretion and plasma bicarbonate concentration increased. In the post-furosemide period, net acid excretion remained higher than base line but plasma bicarbonate concentration did not increase further. Citrate excretion was significantly higher in the post-furosemide period than in base line. Studies substituting sodium neutral phosphate or sodium bicarbonate for dietary sodium sulfate demonstrated greater increases in net acid excretion post-furosemide and, again, no increase in plasma bicarbonate concentration during this period. Citrate excretion was greater than in the sulfate group. The increment in citrate excretion was proportional to the base "load," defined with respect to changes in net acid excretion and/or dietary bicarbonate. Thus, in these studies alterations of base excretion in the form of citrate play an important role in acid-base balance during diuretic-induced metabolic alkalosis.

Topics: Acid-Base Equilibrium; Aldosterone; Alkalosis; Animals; Bicarbonates; Chlorides; Citrates; Citric Acid; Diet; Diuretics; Furosemide; Male; Potassium; Potassium Compounds; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Sulfates

The renal handling of bicarbonate during acute metabolic alkalosis was examined in Munich-Wistar rats using micropuncture techniques. Group I received an acute bicarbonate load, and fractional delivery of total CO2 (tCO2) (FDtCO2) to the superficial late distal tubule (LD) was significantly lower than to the base of the papillary collecting duct (B) (18.4 +/- 1.7 vs. 22.9 +/- 1.5%; P less than 0.01), indicating net addition of bicarbonate between LD and B. When acutely bicarbonate-loaded rats had their deep nephrons destroyed with bromoethylamine hydrobromide (BEA) (group II), net addition of tCO2 between LD and B was abolished and net reabsorption uncovered (FDtCO2 LD: 28.0 +/- 3.6 vs. B: 17.5 +/- 2.5%; P less than 0.01). The infusion of amiloride (2.5 mg/kg body wt) to alkalotic rats treated with BEA (group III) completely inhibited distal bicarbonate reabsorption but did not reestablish addition (FDtCO2 LD: 27.6 +/- 1.6 vs. B: 26.1 +/- 3.7%; P = NS). The values obtained for sham-operated animals (group IV) were the same for group I. The patterns that were observed between LD and B were reproduced for the four groups of animals when FDtCO2 LD was compared with the fractional excretion of bicarbonate in the urine of the intact contralateral kidney. These studies suggest that juxtamedullary nephrons contribute a higher load of bicarbonate than superficial nephrons to the final urine during acute metabolic alkalosis in the rat.

Topics: Alkalosis; Amiloride; Animals; Bicarbonates; Carbon Dioxide; Ethylamines; Female; Glomerular Filtration Rate; Kidney Concentrating Ability; Male; Nephrons; Rats; Sodium; Sodium Bicarbonate

Topics: Alkalosis; Aluminum Hydroxide; Antacids; Bicarbonates; Brain Diseases; Calcium; Constipation; Diarrhea; Drug Interactions; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Kidney Calculi; Magnesium Hydroxide; Osteomalacia; Phosphates; Sodium; Sodium Bicarbonate; Urine; Water-Electrolyte Imbalance

Dietary acid or alkali loading was given to rats by providing 150 mM NH4Cl or 150 mM NaHCO3 in place of drinking water for 6 days; control animals received 150 mM NaCl. After 6 days, the citrate clearance was 0.04 +/- 0.01 ml/min (mean +/- SE) in the acid-loaded group, 0.9 +/- 0.1 ml/min in the control group, and 2.5 +/- 0.2 ml/min in the alkali-loaded group. At the end of the experiment, the rats were killed, and the Na+ gradient-dependent (Nao+ greater than Nai+) citrate uptake (pmol/mg protein) was measured in brush border membrane (BBM) vesicles prepared from each group. At 0.3 min, the [14C]citrate uptake was 198 +/- 8 pmol/mg protein (mean +/- SE) in the acid-loaded group, 94 +/- 16 pmol/mg protein in the control group, and 94 +/- 13 pmol/mg protein in the alkali-loaded group. The rate of Na+-independent (NaCl in medium replaced by KCl) [14C]-citrate uptake by BBM vesicles was the same for acid-loaded, control, and alkali-loaded animals. Thus, the increased capacity of the proximal tubular BBM to transport citrate from the tubular lumen into the cell interior may be an important factor that contributes to decreased urinary citrate in the presence of metabolic acidosis induced by chronic dietary acid loading.

Topics: Acid-Base Equilibrium; Acidosis; Alkalosis; Ammonium Chloride; Animals; Bicarbonates; Biological Transport, Active; Carbon Radioisotopes; Citrates; Citric Acid; Diet; Kidney; Kidney Tubules, Proximal; Male; Microvilli; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Alkalosis; Amino Acids; Animals; Bicarbonates; Cats; Drug Combinations; Drug Evaluation, Preclinical; Infusions, Parenteral; Sodium; Sodium Bicarbonate; Sorbitol; Time Factors

Topics: Acid-Base Equilibrium; Adult; Alkalosis; Bicarbonates; Dental Prophylaxis; Humans; Hydrogen-Ion Concentration; Male; Sodium; Sodium Bicarbonate

Early-lactation Holstein cows fed a corn silage-based diet low in chloride and supplemented with sodium bicarbonate were observed for clinical, metabolic, and production alterations over the course of 8 to 11 weeks. In 3 of the more severely affected cows, metabolic derangements included a rapidly developing primary hypochloremic, secondary hypokalemic and hyponatremic metabolic alkalosis, and hemoconcentration. Clinical signs included severe hypophagia, weight loss, muscle weakness, hypogalactia, dehydration, constipation, cardiopulmonary depression, and a depraved appetite. It was concluded that the rapid progression of these derangements, apart from any anatomic abnormalities or infectious causes, emphasizes the need for rapid assessment and therapeutic intervention in primary imbalance associated with body chloride depletion and metabolic alkalosis.

Topics: Alkalosis; Animals; Bicarbonates; Carbon Dioxide; Cattle; Cattle Diseases; Chlorides; Diet; Electrolytes; Female; Lactation; Pregnancy; Sodium Bicarbonate; Water-Electrolyte Imbalance

Topics: Alkalosis; Animals; Bicarbonates; Cattle; Cattle Diseases; Electrocardiography; Female; Heart; Respiration; Respiratory Function Tests; Sodium Bicarbonate

The effects of hyperlactatemia on cerebral glucose metabolism of normoglycemic 20-day-old rats were studied in animals breathing air or 20% CO2:21% O2:59% N2. Sodium lactate or sodium bicarbonate were given intraperitoneally, together with a mixture of [3H]deoxyglucose and [2-14C]glucose. Animals were sacrificed in a freeze-blowing apparatus at intervals of 2-15 min after injection. Blood lactate levels in the lactate-injected rats were 4-6 mM. Hyperlactatemia caused a gradual decline in the brain rate of glucose utilization in air-breathing animals to 50-70% of control rates. Results with both tracers were similar. Concentrations of Krebs cycle intermediates and glutamate did not decrease. These findings indicate that lactate can partially replace glucose as an oxidative fuel for developing rat brain. Hypercapnia depressed the rate of glucose utilization by developing brain and rates were 30-40% lower still in lactate-injected hypercapnic rats. Decreases in levels of Krebs cycle intermediates and glutamate were similar in both groups. Thus, lactate and CO2 are additive in their depressant effects on brain glucose utilization. The observation that lactate did not prevent the decreases in Krebs cycle intermediates and glutamate caused by hypercapnic acidosis suggests an inhibition of flux through pyruvate dehydrogenase during hypercapnia. The data from this study, coupled with data on lactate transport across the blood-brain barrier, indicate that the direction of movement of lactate and its rate of utilization by developing brain are functions of its concentration on blood relative to brain. Physiological and pathological conditions which elevate blood lactate levels above those in brain will, then, have a sparing effect upon brain glucose utilization.

Topics: Alkalosis; Animals; Bicarbonates; Blood Glucose; Brain; Glucose; Hypercapnia; Lactates; Lactic Acid; Rats; Rats, Inbred Strains; Sodium Bicarbonate

Sodium bicarbonate has been recommended for the treatment of arrhythmias induced by tricyclic antidepressants. It is unclear, however, whether this therapy is effective only in the presence of acidosis. A case is presented in which there was an immediate response to sodium bicarbonate in three episodes of ventricular tachycardia despite the presence of alkalosis on two of the three occasions. Given the poor response to conventional therapy of arrhythmias induced by tricyclic antidepressants the use of sodium bicarbonate may be reasonable even in the presence of alkalosis. However, in the presence of pre-existing respiratory or metabolic alkalosis, such therapy is not without risk, and it is suggested that it be reserved for life-threatening situations when the arrhythmia has failed to respond to hyperventilation or antiarrhythmics or both.

Topics: Adult; Alkalosis; Alkalosis, Respiratory; Arrhythmias, Cardiac; Bicarbonates; Electrocardiography; Female; Humans; Hydrogen-Ion Concentration; Imipramine; Sodium Bicarbonate

Topics: Adult; Alkalosis; Bicarbonates; Diabetes Complications; Humans; Male; Seizures; Self Medication; Sodium Bicarbonate; Vomiting

Topics: Adult; Alkalosis; Bicarbonates; Candy; Female; Glycyrrhiza; Humans; Plants, Medicinal; Sodium Bicarbonate

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.

Topics: Action Potentials; Alkalosis; Animals; Bicarbonates; Carbon Dioxide; Carotid Sinus; Cats; Chemoreceptor Cells; Female; Hypercapnia; Hypoxia; Oxygen; Partial Pressure; Sodium Bicarbonate

Topics: Administration, Topical; Alkalosis; Bicarbonates; Diaper Rash; Gastroenteritis; Humans; Hypernatremia; Infant; Male; Sodium Bicarbonate

Since the few data available concerning the effect of acid/base disturbances on renal amino acid reabsorption were conflicting, and there were sound theoretical reasons for an effect, we have studied the clearance of endogenous amino acids in the rat in vivo under control conditions and after induction of either metabolic acidosis or alkalosis by administration of NH4Cl or NaHCO3, respectively. The effectiveness of treatment was assessed by examination of plasma and urinary levels of HCO3, Cl, Na and K. It was found that the renal clearance of amino acids, measured during acidosis or alkalosis, did not differ from those found under control conditions, the majority of values being less than 1% of the glomerular filtration rate. Thus, the amino acid reabsorptive mechanism appears unaffected by changes in the pH of the glomerular filtrate and/or by changes in tubular hydrogen ion secretion which would accompany such disturbances. These data are thus in agreement with findings during acidosis in man and in both acidosis and alkalosis in the dog. The findings are contrary to earlier reports from in vitro studies in the rat, and suggest the presence of severe functional impairment in the isolated perfused kidneys used in these earlier studies where very large changes in amino acid clearance were obtained.

Topics: Acid-Base Imbalance; Acidosis; Alkalosis; Amino Acids; Ammonium Chloride; Animals; Bicarbonates; Electrolytes; Kidney; Male; Rats; Rats, Inbred Strains; Sodium Bicarbonate

In anaesthetized dogs, a mixed acid-base disturbance was induced by adding a pronounced metabolic alkaline to an established respiratory acidosis or alkalosis. Cerebral blood flow (CBF) was measured by the radioisotope washout method. In the hypocapnic dogs, the addition of metabolic alkalosis did not significantly change cerebral blood flow. In the hypercapnic dogs, the intravenous infusion of alkali led to a substantial reduction of cerebral blood flow, parallelled by a reduction of cerebrovenous oxygen tension. Acid-base analysis of cerebrospinal fluid (CSF) indicated an increased bicarbonate concentration. Hypercapnia is suggested to facilitate the passage of bicarbonate over the blood-brain barrier, leading to cerebral vasoconstriction by means of increased extravascular pH.

Topics: Acidosis, Respiratory; Alkalosis; Alkalosis, Respiratory; Animals; Bicarbonates; Carbon Dioxide; Cerebrovascular Circulation; Dogs; Homeostasis; Infusions, Parenteral; Oxygen; Sodium Bicarbonate

Topics: Acetates; Acidosis; Alkalosis; Animals; Bicarbonates; Dog Diseases; Dogs; Injections, Intravenous; Lactates; Sodium Bicarbonate

Topics: Alkalosis; Humans; Hypokalemia; Ketone Bodies; Nausea; Paralysis; Potassium; Sodium Bicarbonate; Vomiting

Topics: Alkalosis; Humans; Potassium; Sodium Bicarbonate

Topics: Alkalosis; Bicarbonates; Kidney; Peptic Ulcer; Pharmaceutical Preparations; Sodium Bicarbonate