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1 Medical Biophysics, The University of Western Ontario, London, Ontario, Canada; Imaging Division, Lawson Health Research Institute, London, Ontario, Canada
2 Medical Biophysics, The University of Western Ontario, London, Ontario, Canada; Imaging Division, Lawson Health Research Institute, London, Ontario, Canada; Kinesiology, The University of Western Ontario, London, Ontario, Canada
3 Kinesiology, The University of Western Ontario, London, Ontario, Canada; The Canadian Centre for Activity and Aging, London, Ontario, Canada; Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada
* To whom correspondence should be addressed. E-mail: graymer{at}lri.sjhc.london.on.ca.
Metabolic alkalosis induced by sodium bicarbonate (NaHCO3) 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 (Lacpl) accumulation. Together, these changes would imply a shift towards 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 NaHCO3 (ALK: 0.3 g. kg; 1.5 hrs prior to testing) to evaluate muscle metabolism over a complete range of exercise intensities. 31Phosphorus magnetic resonance spectroscopy was used to continuously monitor intracellular pH, [PCr], [Pi], and [ATP]. Blood samples drawn from a deep arm vein were analyzed with a blood gas-electrolyte analyzer to measure plasma pH, PCO2, and [Lac-]pl, and plasma [HCO3-] was calculated from pH and PCO2. NaHCO3 ingestion resulted in an increased (P < 0.05) plasma pH and [HCO3-] throughout rest and exercise. Time to fatigue and peak power output were increased (P < 0.05) by ~ 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 [Pi]/[PCr] ratio (1.21 ± 0.30 vs. 1.30 ± 0.30 W) were observed in ALK. No differences in total [H+], [Pi], or [Lac-]pl accumulation was detected. In conclusion, NaHCO3 ingestion was shown to increase plasma pH at rest, which resulted in a delayed onset of intracellular acidification during incremental exercise. Conversely, NaHCO3 was not associated with increased [Lac-]pl accumulation or PCr breakdown.
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