Separate and combined effects of a 10-d exposure to hypoxia and inactivity on oxidative function in vivo and mitochondrial respiration ex vivo in humans.

An integrative evaluation of oxidative metabolism was carried out in 9 healthy young men (age: 24.1±1.7 years [mean±SD]) prior to (CTRL) and following a 10-day horizontal bed rest, carried out in normoxia (N-BR) or hypoxia (F_IO₂=0.147; H-BR). H-BR was aimed to simulate planetary habitats. Pulmonary O₂ uptake (V'O₂) and vastus lateralis fractional O₂ extraction (changes in deoxygenated hemoglobin+myoglobin concentration, [deoxy(Hb+Mb)]; near-infrared spectroscopy) were evaluated, in normoxia, during an incremental cycle ergometer exercise (CE) and one-leg knee extension exercise (KE) (aimed at reducing cardiovascular constraints to oxidative function). Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers. During CE V'O₂peak and [deoxy(Hb+Mb)]peak were lower (P<0.05) after both N-BR and H-BR vs. CTRL; during KE the variables were lower after N-BR, but not after H-BR. During CE the "overshoot" of [deoxy(Hb+Mb)] during constant work rate exercise was greater in N-BR and H-BR vs. CTRL, whereas during KE a significant difference vs. CTRL was observed only after N-BR. Maximal mitochondrial respiration determined ex vivo was not affected by both interventions. In N-BR, a significant impairment of oxidative metabolism occurred downstream of central cardiovascular O₂ delivery and upstream of mitochondrial function, possibly at the level of the intramuscular matching between O₂ supply and utilization (see the [deoxy(Hb+Mb)] overshoot) and peripheral O₂ diffusion. Superposition of H on BR did not aggravate, and partially reversed, the impairment of muscle oxidative function in vivo induced by BR. The effects of longer exposures will have to be determined.

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