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.
School of Kinesiology, The University of Western Ontario, London, Ontario, Canada N6A-3K7.
S C
SC
Forbes
G H
GH
Raymer
J M
JM
Kowalchuk
G D
GD
Marsh
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