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Metabolic effects of induced alkalosis during progressive forearm exercise to fatigue

¹Department of Medical Biophysics, The University of Western Ontario, London N6A 5C1; ²Imaging Division, The Lawson Health Research Institute, and Department of Radiology, St. Joseph's Health Care, London N6A 4V2; ³School of Kinesiology, The University of Western Ontario, London N6A 3K7; ⁴Canadian Centre for Activity and Aging, London N6G 2M3; and ⁵Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada N6A 5C1

Submitted 24 November 2003 ; accepted in final form 28 January 2004

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 (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 NaHCO₃ (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, PCO₂, and [Lac^-]_pl, and plasma was calculated from pH and PCO₂. NaHCO₃ ingestion resulted in an increased (P < 0.05) plasma pH and 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 [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, 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.

sodium bicarbonate; intracellular pH; lactate; phosphorus-31 magnetic resonance spectroscopy; skeletal muscle; ergogenic aid

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