Purpose This study aimed to determine whether (i) a plasma acidosis contributes to a reduction of mechanical performance and (ii) bicarbonate supplementation blunts plasma acidosis and arterial oxygen desaturation to resist fatigue during the end spurt of a supramaximal trial in elite sprint and endurance cyclists. Methods Elite/world-class cyclists (n = 6 sprint, n = 6 endurance) completed two randomized, double-blind, crossover trials at 105%VO2peak simulating 3 min of a 4-km individual pursuit, 90 min after ingestion of 0.3 g·kg-1 BM sodium bicarbonate (BIC) or placebo (PLA). Peak power output (PPO), optimal cadence and optimal peak torque, and fatigue were assessed using a 6-s "all-out sprint" before (PPO1) and after (PPO2) each trial. Plasma pH, bicarbonate, lactate-, K+, Na+, Ca2+, and arterial hemoglobin saturation (SpO2(%)), were measured. Results Sprint cyclists exhibited a higher PPO, optimal pedal torque, and anaerobic power reserve (APR) than endurance cyclists. The trial reduced PPO (PLA) more for sprint (to 47% initial) than endurance cyclists (to 61% initial). Optimal cadence fell from ~151 to 92 rpm and cyclists with higher APR exhibited a reduced optimal peak torque. Plasma pH fell from 7.35 to 7.13 and plasma [lactate-] increased from 1.2 to 19.6 mM (PLA), yet neither correlated with PPO loss. Sprint cyclists displayed a lesser plasma acidosis but greater fatigue than endurance cyclists. BIC increased plasma [HCO3-] (+6.8 mM) and plasma pH after PPO1 (+0.09) and PPO2 (+0.07) yet failed to influence mechanical performance. SpO2 fell from 99% to 96% but was unrelated to the plasma acidosis and unaltered with BIC. Conclusions Plasma acidosis was not associated with the decline of PPO in a supramaximal trial with elite cyclists. BIC attenuated acid-base disturbances yet did not improve arterial oxygen desaturation or mechanical performance at the end-spurt stage.
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