The effects of 10-day hypoxic (ambient PO₂ 12.5 kPa, corresponding to ~4,000 m asl) bed rest (H-BR) and 10-day normoxic bed rest (BR) on skeletal muscle oxidative metabolism were evaluated; H-BR was taken as a simulation of lunar habitats (pilot study, PlanHab Project [FP7 EU]).

Pulmonary gas exchange and vastus lateralis fractional O₂ extraction (by NIRS) were determined on 12 young males during incremental one-leg knee extension exercise. Mitochondrial respiration was evaluated by high-resolution respirometry in "skinned"vastus lateralis fibers.

Peak pulmonary O₂ uptake was lower in H-BR (0.84±0.10 L/min, x±SD) and BR (0.83±0.11) vs. baseline (CTRL) (0.90±0.10). Skeletal muscle peak fractional O₂ extraction was lower in H-BR (63±14%) and BR (58±10) vs. CTRL (68±12). No significant changes in maximal ADP-stimulated mitochondrial respiration were observed in H-BR (40.8±8.8 pmolO₂/s/mg ww) or BR (48.9±11.5) vs. CTRL (45.6±7.0). Oxidative phosphorylation coupling was also unaffected.

Skeletal muscle oxidative function in vivo was slightly but significantly impaired after 10-d H-BR and BR, whereas mitochondrial respiration in "skinned" fibers was preserved. Hypoxia does not modify the impairment of skeletal muscle oxidative metabolism in vivo induced by 10-d bed rest. The main constraints would be "downstream" of cardiovascular O₂ delivery, but "upstream" of oxidative phosphorylation (intramuscular O₂ delivery/O₂ utilization coupling, peripheral O₂ diffusion).

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