Metabolic effects of induced alkalosis during progressive forearm exercise to fatigue.
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.
Raymer
Graydon H
GH
Department of Medical Biophysics, The University of Western Ontario, London, Ontario, Canada. graymer@lri.sjhc.london.on.ca
Marsh
Greg D
GD
Kowalchuk
John M
JM
Thompson
R Terry
RT
D000251:Adenosine Triphosphatases; D000328:Adult; D000471:Alkalosis / Q000378:metabolism* / Q000503:physiopathology*; D001639:Bicarbonates / Q000097:blood; D002245:Carbon Dioxide / Q000097:blood; D015444:Exercise; D005542:Forearm; D006801:Humans; D007773:Lactates / Q000097:blood; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D018763:Muscle Fatigue / Q000502:physiology*; D010313:Partial Pressure; D010725:Phosphocreatine / Q000378:metabolism
D001639:Bicarbonates; D007773:Lactates; D010725:Phosphocreatine; D002245:Carbon Dioxide; D000251:Adenosine Triphosphatases