4.6 Article

Plasma Acidosis and Peak Power after a Supramaximal Trial in Elite Sprint and Endurance Cyclists: Effect of Bicarbonate

Journal

MEDICINE & SCIENCE IN SPORTS & EXERCISE
Volume 55, Issue 5, Pages 932-944

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0000000000003104

Keywords

ACIDOSIS; LACTATE; BICARBONATE; FATIGUE; SKELETAL MUSCLE; ANAEROBIC POWER RESERVE

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This study aimed to investigate the effect of plasma acidosis on mechanical performance and whether bicarbonate supplementation can attenuate plasma acidosis and arterial oxygen desaturation in elite cyclists. The results showed that plasma acidosis was not associated with the decline of peak power output, and bicarbonate supplementation failed to improve arterial oxygen desaturation or mechanical performance.
MILDENHALL, M. J., E. MAUNDER, D. J. PLEWS, M. I. LINDINGER, and S. P. CAIRNS. Plasma Acidosis and Peak Power after a Supramaximal Trial in Elite Sprint and Endurance Cyclists: Effect of Bicarbonate. Med. Sci. Sports Exerc., Vol. 55, No. 5, pp. 932-944, 2023. 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%V. O-2peak simulating 3 min of a 4-km individual pursuit, 90 min after ingestion of 0.3 g center dot kg(-1) BMsodium 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 (SpO(2)(%)), 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 similar to 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. SpO(2) 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 acidbase disturbances yet did not improve arterial oxygen desaturation or mechanical performance at the end-spurt stage.

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