sodium-bicarbonate and Hypertrophy

The aim of the present study was to examine the effects of sodium bicarbonate (NaHCO(3)) administration on lower-body, hypertrophy-type resistance exercise (HRE). Using a double-blind randomized counterbalanced design, 12 resistance-trained male participants (mean ± SD; age = 20.3 ± 2 years, mass = 88.3 ± 13.2 kg, height = 1.80 ± 0.07 m) ingested 0.3 g kg(-1) of NaHCO(3) or placebo 60 min before initiation of an HRE regimen. The protocol employed multiple exercises: squat, leg press, and knee extension, utilizing four sets each, with 10-12 repetition-maximum loads and short rest periods between sets. Exercise performance was determined by total repetitions generated during each exercise, total accumulated repetitions, and a performance test involving a fifth set of knee extensions to failure. Arterialized capillary blood was collected via fingertip puncture at four time points and analyzed for pH, [HCO(3)(-)], base excess (BE), and lactate [Lac(-)]. NaHCO(3) supplementation induced a significant alkaline state (pH: NaHCO(3): 7.49 ± 0.02, placebo: 7.42 ± 0.02, P < 0.05; [HCO(3)(-)]: NaHCO(3): 31.50 ± 2.59, placebo: 25.38 ± 1.78 mEq L(-1), P < 0.05; BE: NaHCO(3): 7.92 ± 2.57, placebo: 1.08 ± 2.11 mEq L(-1), P < 0.05). NaHCO(3) administration resulted in significantly more total repetitions than placebo (NaHCO(3): 139.8 ± 13.2, placebo: 134.4 ± 13.5), as well as significantly greater blood [Lac(-)] after the exercise protocol (NaHCO(3): 17.92 ± 2.08, placebo: 15.55 ± 2.50 mM, P < 0.05). These findings demonstrate ergogenic efficacy for NaHCO(3) during HRE and warrant further investigation into chronic training applications.

Topics: Adolescent; Adult; Athletic Performance; Dietary Supplements; Double-Blind Method; Humans; Hypertrophy; Knee Joint; Leg; Male; Muscle, Skeletal; Resistance Training; Sodium Bicarbonate; Weight Lifting; Young Adult

Organ malfunction often occurs following cardiac arrest and resuscitation. Renal function, inulin clearance (Cln), was examined in 27 dogs before and after (days 2, 4, and 6) cardiac arrest and resuscitation. Group A (n = 7) had no ventricular fibrillation (VF), but cardiopulmonary support was applied for 20 min, and three transthoracic countershocks were delivered. In groups B (n = 7), C (n = 7), and D (n = 6) VF was induced for 2.5, 5.0, and 7.5 min, respectively, followed by cardiopulmonary support for 20, 20, and 15 min, respectively. When necessary, epinephrine and sodium bicarbonate were given during resuscitation. Countershock was applied for defibrillation. Kidneys were examined histologically in groups C and D. Following cardiac arrest, Cln was significantly less in the arrested groups compared to the nonarrested group. Within group C, which received the most epinephrine, Cln correlated negatively with epinephrine administration, and with the energy applied for defibrillation. Histologically, group C showed the highest incidence of cortical tubular cytoplasmic vacuolization, regeneration, inflammation, and tubular casts. Groups C and D showed outer medullary tubular cytoplasmic vacuolization, renal vascular changes, and calcification. In conclusion, cardiac arrest and resuscitation may precipitate acute renal hypofunction as well as reversible and irreversible morphological changes in normal functioning canine kidneys. The confounding effect of pre-existing renal disease remains to be examined experimentally.

Topics: Animals; Cardiopulmonary Resuscitation; Dogs; Electric Countershock; Epinephrine; Heart Arrest; Hypertrophy; Insulin; Kidney; Sodium Bicarbonate