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1 Service de Physiologie Clinique et des EFR, Departement de Physiologie, Hopital Civil, Strasbourg, France, Metropolitan
2 Institute of Anatomy, University of Bern, Bern, Switzerland
3 Service de Physiologie Clinique et des EFR, Departement de Physiologie, Hopital Civil, Strasbourg, France, Metropolitan; Service de Cardiologie, Hopitaux Civils de Colmar, Colmar, France, Metropolitan
4 U-446 INSERM, Faculte de Pharmacie, Chatenay-Malabry, France, Metropolitan
* To whom correspondence should be addressed. E-mail: Ruddy.Richard{at}physio-ulp.u-strasbg.fr.
This study investigates whether adaptations of mitochondrial function accompany the improvement of endurance performance capacity observed in well-trained athletes after an intermittent hypoxic training program (IHT). Fifteen endurance trained athletes performed two weekly training sessions on treadmill at vVT2 (velocity associated to the second ventilatory threshold) with FiO2=14.5% (HYP, n=8) or with FiO2=21% (NOR, n=7), integrated into their usual training, for 6 weeks. Before and after training, oxygen uptake and speed at VT2, maximal oxygen uptake (VO2max), time to exhaustion (Tlim) at vVO2max (minimal speed associated with VO2max) were measured and muscle biopsies of Vastus Lateralis were harvested. Muscle oxidative capacities (Vmax) and sensitivity of mitochondrial respiration to ADP (Km) were evaluated on permeabilized muscle fibers. Tlim, VO2 at VT2 and VO2max were significantly improved in HYP (+42%, +8%, +5% respectively) but not in NOR. No increase in muscle oxidative capacity was obtained with either training protocol. However, mitochondrial regulation shifted to a more oxidative profile in HYP only as shown by the increased Km for ADP (NOR: before 476±63, after 524±62µM, ns; HYP: before 441±59, after 694±51µM, p<0.05). Thus, including hypoxia sessions into the usual training of athletes qualitatively ameliorates mitochondrial function by increasing the respiratory control by creatine, providing a tighter integration between ATP demand and supply.
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