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1 STAPS, Université de Savoie, Le bourget du Lac, France
2 Institute of Molecular Biology and Physiology, Copenhagen Muscle Research Centre, Copenhagen, Denmark
3 Copenhagen, Denmark; Institute of Molecular Biology and Physiology, Copenhagen Muscle Research Centre, Copenhagen, Denmark
4 Laboratoire de Physiologie, unité PPEH, Université Jean Monnet, Saint Etienne, France
* To whom correspondence should be addressed. E-mail: laurent.messonnier{at}univ-savoie.fr.
We examine the influence of the cytosolic and membrane-bound contents of carbonic anhydrase (CAII, CAIII, CAIV and CAXIV) and the muscle content of proteins involved in lactate and proton transport (MCT1, MCT4 and NHE1) on work capacity during supramaximal exercise. Eight healthy sedentary subjects performed exercises at 120 % of the work rate corresponding to maximal oxygen uptake (Pamax) until exhaustion in placebo (CON) and metabolic alkalosis (ALK) conditions. The total (WTOT) and supramaximal (WSUP) work performed was measured. Muscle biopsies were obtained prior to and immediately after standardized exercises (se) at 120 % Pamax in both conditions to determine the content of the targeted proteins, the decrease in muscle pH and the muscle lactate accumulation per joule of supramaximal work performed (
pHm/Wsup-se and [Lac]m/Wsup-se) and the dynamic buffer capacity. In CON, WSUP was negatively correlated with pHm/Wsup-se, positively correlated with [Lac]m/Wsup-se and MCT1, and tended to be positively correlated with MCT4 and NHE1. CAII + CAIII were correlated positively with pHm/Wsup-se and negatively with [Lac]m/Wsup-se, while CAIV was positively related to WTOT. The changes in WSUP with alkalosis were correlated positively with those in dynamic buffer capacity and negatively with WSUP in CON. Performance improvement with ALK was greater in subjects having a low content of proteins involved in pH regulation and lactate/proton transport. These results show the importance of pH regulating mechanisms and lactate/proton transport on work capacity and the role of the CA to delay decrease in muscle pH and lactate accumulation during supramaximal exercise in humans.
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