phosphocreatine and Alkalosis

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

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

Metabolic alkalosis induced by sodium bicarbonate (NaHCO(3)) ingestion has been shown to enhance performance during brief high-intensity exercise. The mechanisms associated with this increase in performance may include increased muscle phosphocreatine (PCr) breakdown, muscle glycogen utilization, and plasma lactate (Lac(-)(pl)) accumulation. Together, these changes would imply a shift toward a greater contribution of anaerobic energy production, but this statement has been subject to debate. In the present study, subjects (n = 6) performed a progressive wrist flexion exercise to volitional fatigue (0.5 Hz, 14-21 min) in a control condition (Con) and after an oral dose of NaHCO(3) (Alk: 0.3 g/kg; 1.5 h before testing) to evaluate muscle metabolism over a complete range of exercise intensities. Phosphorus-31 magnetic resonance spectroscopy was used to continuously monitor intracellular pH, [PCr], [P(i)], and [ATP] (brackets denote concentration). Blood samples drawn from a deep arm vein were analyzed with a blood gas-electrolyte analyzer to measure plasma pH, Pco(2), and [Lac(-)](pl), and plasma [HCO(3)(-)] was calculated from pH and Pco(2). NaHCO(3) ingestion resulted in an increased (P < 0.05) plasma pH and [HCO(3)(-)] throughout rest and exercise. Time to fatigue and peak power output were increased (P < 0.05) by approximately 12% in Alk. During exercise, a delayed (P < 0.05) onset of intracellular acidosis (1.17 +/- 0.26 vs. 1.28 +/- 0.22 W, Con vs. Alk) and a delayed (P < 0.05) onset of rapid increases in the [P(i)]-to-[PCr] ratio (1.21 +/- 0.30 vs. 1.30 +/- 0.30 W) were observed in Alk. No differences in total [H(+)], [P(i)], or [Lac(-)](pl) accumulation were detected. In conclusion, NaHCO(3) ingestion was shown to increase plasma pH at rest, which resulted in a delayed onset of intracellular acidification during incremental exercise. Conversely, NaHCO(3) was not associated with increased [Lac(-)](pl) accumulation or PCr breakdown.

Topics: Adenosine Triphosphatases; Adult; Alkalosis; Bicarbonates; Carbon Dioxide; Exercise; Forearm; Humans; Lactates; Magnetic Resonance Spectroscopy; Male; Muscle Fatigue; Partial Pressure; Phosphocreatine

Resting and submaximal isometric exercise 31P magnetic resonance spectroscopy (MRS) was carried out on 7 endurance-trained males (26.0 +/- 3 yrs) and 7 sedentary males (27.0 +/- 4 yrs). Spectral analysis provided peak areas of phosphocreatine (PCr), inorganic phosphate (Pi), adenosine triphosphate (ATP), and the chemical shift of Pi relative to PCr. The ratio of PCr/Pi was moderately lower during rest (preexercise p = .13, postexercise p = .18), and significantly higher during exercise (p < .05) in the trained subjects. Intracellular pH patterns were the same for both groups; a transient alkalosis was observed at the onset of exercise with a return to resting levels after 2 min. Differences suggest improved ATP resynthesis rate in the trained subjects during exercise. Intracellular pH changes can be attributed to the utilization of hydrogen ions that accompany PCr hydrolysis during work. The findings are congruent with previous reports indicating a superior oxidative capacity in trained skeletal muscle.

Topics: Adenosine Triphosphate; Adult; Alkalosis; Energy Metabolism; Humans; Hydrogen-Ion Concentration; Hydrolysis; Isometric Contraction; Magnetic Resonance Spectroscopy; Male; Muscle, Skeletal; Oxidation-Reduction; Oxygen Consumption; Phosphates; Phosphocreatine; Phosphorus Isotopes; Physical Education and Training; Physical Endurance; Physical Exertion; Rest

Phosphorus magnetic resonance spectroscopic imaging has previously demonstrated localized metabolic abnormalities within the epileptogenic region in patients with temporal lobe epilepsy, including alkalosis, increased inorganic phosphate level, and decreased phosphomonoester levels. We studied 8 patients with frontal lobe epilepsy, finding interictal alkalosis in the epileptogenic region compared to the contralateral frontal lobe in all patients (7.10 +/- 0.05 vs 7.00 +/- 0.06, p < 0.001). Seven patients exhibited decreased phosphomonoester levels in the epileptogenic frontal lobe compared to the contralateral frontal lobe (16.0 +/- 6.0 vs 23.0 +/- 4.0, p < 0.01). In contrast to findings in temporal lobe epilepsy, inorganic phosphate level was not increased in the epileptogenic region. Based on values derived from normal control subjects, 5 patients had elevated pH in the seizure focus and 2 patients had decreased phosphomonoesters while none had abnormalities in the contralateral frontal lobe. These data suggest that magnetic resonance spectroscopy will be useful in the presurgical evaluation of patients with frontal lobe epilepsy.

Topics: Adolescent; Adult; Alkalosis; Epilepsy, Frontal Lobe; Female; Functional Laterality; Humans; Magnetic Resonance Spectroscopy; Male; Organophosphates; Phosphates; Phosphocreatine

A study was performed to determine quantitatively the alterations in phosphorus metabolite concentrations and pH in regions of the human brain damaged by chronic stroke. Image-guided phosphorus-31 magnetic resonance spectroscopy was performed on the brains of eight healthy subjects and six patients with cerebral infarction of more than 3 months duration. Phosphorus metabolite concentrations in infarcted regions were reduced 8%-67%. Significant decreases occurred in phosphomonoester (PME), phosphodiester (PDE), and adenosine triphosphate (ATP) concentrations, while inorganic phosphate (Pi) and phosphocreatine (PCr) concentrations showed smaller, nonsignificant decreases. The PCr/ATP ratio was significantly increased, while the ATP/Pi ratio was somewhat lower. The phospholipid ratio PDE/PME was also significantly increased, while the ratios of phospholipid (PME, PDE) to phosphate (PCR, Pi) metabolites were significantly decreased. The pH of the infarcted region indicated significantly more alkalinity than in the normal brain. The results suggest that chronic stroke is associated with significant changes in brain metabolite concentrations and pH that are different from those reported for other brain diseases.

Topics: Adenosine Triphosphate; Adult; Aged; Alkalosis; Brain; Cerebral Infarction; Chronic Disease; Humans; Hydrogen-Ion Concentration; Magnetic Resonance Spectroscopy; Male; Phosphates; Phosphocreatine; Phospholipids; Phosphorus

The effect of pH of the reperfusion buffer on postischemic changes in tissue Ca and Na was examined in isolated Langendorff-perfused Sprague-Dawley rat hearts. Reperfusion began after 15-, 25-, or 60-min ischemia at 37 degrees C. After 60-min ischemia, reperfusion at pH 6.4 or 6.6 attenuated the reperfusion-induced Ca gain so long as the acidotic conditions were maintained (3.08 +/- 0.22, 1.37 +/- 0.41, and 16.96 +/- 1.18 mumol Ca gain/g dry wt for pH 6.4, 6.6, and 7.4, respectively after 15-min reperfusion). Conversely, reperfusion under alkalotic conditions (pH 7.9) after 60-min ischemia exacerbated the gain (27.45 +/- 4.75 and 8.92 +/- 1.53 mumol Ca gain/g dry wt during 5-min reperfusion at pH 7.9 and 7.4, respectively). Similar, but less pronounced Ca gains occurred during reperfusion after 15- or 25-min ischemia. Sodium content during reperfusion, but not during aerobic perfusion, was also found to be pH sensitive with acidosis causing a reduction and alkalosis an increase. These results could not be explained in terms of an effect of pH on recovery of high-energy phosphates, percentage "reflow" during reperfusion, or reperfusion-induced increases in tissue water or resting tension. The results are in agreement with the hypothesis that the "inhibitory" effect of acidosis on postischemic Ca overload could involve an effect of pH on the Na(+)-H+ exchanger and intracellular Ca storage.

Topics: Acidosis; Acidosis, Respiratory; Adenosine Triphosphate; Alkalosis; Alkalosis, Respiratory; Animals; Biomechanical Phenomena; Buffers; Coronary Disease; Female; Hydrogen-Ion Concentration; In Vitro Techniques; Mitochondria, Heart; Myocardial Reperfusion; Perfusion; Phosphocreatine; Rats; Rats, Inbred Strains; Time Factors

Topics: Acidosis; Adenosine Triphosphate; Alkalosis; Animals; Bicarbonates; Carbon Dioxide; Creatine Kinase; Female; Guinea Pigs; Heart; Heart Ventricles; Hydrogen-Ion Concentration; Male; Myocardium; Perfusion; Phosphates; Phosphocreatine; Tromethamine

Topics: Adenine Nucleotides; Adenosine Triphosphate; Alkalosis; Animals; Bicarbonates; Brain Chemistry; Carbon Dioxide; Hydrogen-Ion Concentration; Hyperventilation; Lactates; Male; NAD; Nitrous Oxide; Oxygen; Partial Pressure; Phosphocreatine; Pyruvates; Rats; Sodium Chloride

Topics: Acid-Base Equilibrium; Adenosine Triphosphate; Alkalosis; Animals; Bicarbonates; Carbon Dioxide; Carbon Isotopes; Glucose; Glycogen; Glycolysis; Hydrogen-Ion Concentration; In Vitro Techniques; Lactates; Male; Myocardium; Phosphocreatine; Phosphofructokinase-1; Rats

Topics: Acidosis; Adenosine Triphosphate; Alkalosis; Animals; Brain; Carbon Monoxide Poisoning; Glycolysis; Hemoglobins; Lactates; Mice; Phosphocreatine; Pyruvates; Sodium; Succinates