Metabolic effects of induced alkalosis during progressive forearm exercise to fatigue

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Abstract
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], [Pi], 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 [Pi]-to-[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 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.