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Physical activity changes the regulation of mitochondrial respiration in human skeletal muscle

J. Zoll, H. Sanchez *, B. N'Guessan, F. Ribera, E. Lampert, X. Bigard *, B. Serrurier *, D. Fortin †, B. Geny, V. Veksler †, R. Ventura-Clapier † and B. Mettauer

This study explores the importance of creatine kinase (CK) in the regulation of muscle mitochondrial respiration in human subjects depending on their level of physical activity. Volunteers were classified as sedentary, active or athletic according to the total activity index as determined by the Baecke questionnaire in combination with maximal oxygen uptake values (peak _O2, expressed in ml min^-1 kg^-1). All volunteers underwent a cyclo-ergometric incremental exercise test to estimate their peak _O2 and _O2 at the ventilatory threshold (VT). Muscle biopsy samples were taken from the vastus lateralis and mitochondrial respiration was evaluated in an oxygraph cell on saponin permeabilised muscle fibres in the absence (₀) or in the presence (_max) of saturating [ADP]. While ₀ was similar, _max differed among groups (sedentary, 3.7 ± 0.3, active, 5.9 ± 0.9 and athletic, 7.9 ± 0.5 µmol O₂ min^-1 (g dry weight)^-1). _max was correlated with peak _O2 (P < 0.01, r = 0.63) and with _T (P < 0.01, r = 0.57). There was a significantly greater degree of coupling between oxidation and phosphorylation (_max/₀) in the athletic individuals. The mitochondrial K_m for ADP was significantly higher in athletic subjects (P < 0.01). Mitochondrial CK (mi-CK) activation by addition of creatine induced a marked decrease in K_m in athletic individuals only, indicative of an efficient coupling of mi-CK to ADP rephosphorylation in the athletic subjects only. It is suggested that increasing aerobic performance requires an enhancement of both muscle oxidative capacity and mechanisms of respiratory control, attesting to the importance of temporal co-ordination of energy fluxes by CK for higher efficacy.

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