The effects of hypoxic training on sea-level performance is equivocal (Wilber 2001) Potential mechanisms underlying any observed performance enhancements include changes in a multitude of central (enhanced O2 transport) and peripheral (enhanced muscle oxidative capacity) responses. The effects of hypoxic training on mitochondrial respiration in permeabilized fibres of well-trained humans has not been studied. Furthermore, it is possible that the intrinsic properties of mitochondrial function, such as substrate preference can be altered by intense exercise in hypoxia. Methods Ten well-trained endurance athletes completed a three weeks hypoxic training program, consisting of two interval-training sessions at 90 to 100% of V&O2max and three steady work sessions at 60% of V&O2max each week. All training sessions were performed under hypoxic conditions (simulated altitude of 3000 m, PIO2 . 100 mmHg, Altitrainer 200.). Prior and after the training period, four cycling tests were performed: an incremental test to exhaustion in normoxic and hypoxic conditions, an all-out anaerobic exercise (. 2 min), and a ten minutes time trial (TT). Gas exchanges and heart rate were measured during exercise by a breath-by-breath analyzer (K4b2, Cosmed, Rome, Italy). All the tests were performed on a bicycle equipped with a eSRMR road professional f powermeter (Schoberer Rad Messtechnik, Julich, Welldorf, Germany). Blood samples at rest were taken before, at the end of each week and after the training program and analyzed, following standard procedures, by the Pentra 120 Retic (abx, Montpellier, France). Muscles biopsy samples were taken from vastus lateralis before and after the training period and mitochondrial respiration in permeabilized muscle fibres was measured. The biopsies were performed using the technique of Bergstrom with suction. The muscle sample was used for preparation of skinned muscle fibres by permeabilisation of sarcolemma with saponin (Veksler, Kuznetsov et al. 1987). Oxygen consumption was measured using a Clark-type electrode in a water-jacketed glass chamber of 3 ml capacity at 30 C. Mitochondrial respiration was analyzed in a medium containing glutamate or palmitate and measured in the absence of ADP and after several progressive additions of ADP. Results No changes in hematological variables (Hemoglobin, hematocrit, mean cell volume, averaged globular content of hemoglobin, averaged corpuscular concentration of hemoglobin, red blood discs, reticulocytes and averaged reticulocytar volume) were observed. Maximal oxygen consumption (V&O2max, ml.kg-1.min-1) did not show any changes neither under normoxic, nor hypoxic condition. Peak power output (PPO) increased by 6.6% (339.0 } 48.8 to 361.5 } 44.1 W, mean } SD, P < 0.05) and 12.4% (282.5 } 34.1 to 317.5 } 39.3 W) under normoxic and hypoxic condition, respectively. Mean power output increased by 6.9% (P < 0.05) in the all-out anaerobic test, where a tendency to decrease in maximal end-exercise lactate concentration (14.2 } 2.5 versus 11.5 } 3.7 mmol.l-1, P = 0.07) was noticed. No changes were observed for the TT. Following training, maximal ADP-stimulated mitochondrial respiration (V&max) increased for glutamate (6.27 } 2.92 versus 8.56 } 2.6 nmolO2.min-1.mg-1 dry weight), and decreased for palmitate (8.39 } 5.83 versus 2.77 } 1.62 nmolO2.min-1.mg-1 dry weight). Discussion/Conclusion It is concluded that after three weeks of hypoxic training: (1) PPO increased in normoxic and hypoxic conditions without changes in V&O2max, nor hematological variables, (2) anaerobic capacity seems to be enhanced, (3) the intrinsic properties of mitochondrial function, i.e. the substrate preference is altered or otherwise expressed, qualitative changes of skeletal muscle mitochondrial respiration were observed.
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