NaHCO3-induced alkalosis reduces the phosphocreatine slow component during heavy-intensity forearm exercise.
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.
Forbes
S C
SC
School of Kinesiology, The University of Western Ontario, London, Ontario, Canada N6A-3K7.
Raymer
G H
GH
Kowalchuk
J M
JM
Marsh
G D
GD
D000136:Acid-Base Equilibrium / Q000187:drug effects / Q000502:physiology; D000140:Acidosis, Lactic / Q000378:metabolism / Q000503:physiopathology; D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D000471:Alkalosis / Q000378:metabolism* / Q000503:physiopathology; D015444:Exercise / Q000502:physiology*; D005542:Forearm / Q000502:physiology; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000502:physiology*; D010085:Oxidative Phosphorylation; D010725:Phosphocreatine / Q000378:metabolism*; D011522:Protons; D017693:Sodium Bicarbonate / Q000008:administration & dosage*
D011522:Protons; D010725:Phosphocreatine; D019344:Lactic Acid; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D017693:Sodium Bicarbonate