PlanHab : hypoxia does not worsen the impairment of skeletal muscle oxidative function induced by bed rest alone.

KEY POINTS

Superposition of hypoxia on 21 day bed rest did not worsen the impairment of skeletal muscle oxidative function induced by bed rest alone. A significant impairment of maximal oxidative performance was identified downstream of cardiovascular O delivery, involving both the intramuscular matching between O supply and utilization and mitochondrial respiration. These chronic adaptations appear to be relevant in terms of exposure to spaceflights and reduced gravity habitats (Moon or Mars), as characterized by low gravity and hypoxia, in patients with chronic diseases characterized by hypomobility/immobility and hypoxia, as well as in ageing.

ABSTRACT

Skeletal muscle oxidative function was evaluated in 11 healthy males (mean ± SD age 27 ± 5 years) prior to (baseline data collection, BDC) and following a 21 day horizontal bed rest (BR), carried out in normoxia (  = 133 mmHg; N-BR) and hypoxia (  = 90 mmHg; H-BR). H-BR was aimed at simulating reduced gravity habitats. The effects of a 21 day hypoxic ambulatory confinement (  = 90 mmHg; H-AMB) were also assessed. Pulmonary O uptake ( ), vastus lateralis fractional O extraction (changes in deoxygenated haemoglobin + myoglobin concentration, Δ[deoxy(Hb + Mb)]; near-infrared spectroscopy) and femoral artery blood flow (ultrasound Doppler) were evaluated during incremental one-leg knee-extension exercise (reduced constraints to cardiovascular O delivery) carried out to voluntary exhaustion in a normoxic environment. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibres. decreased (P < 0.05) after N-BR (0.98 ± 0.13 L min ) and H-BR (0.96 ± 0.17 L min ) vs. BDC (1.05 ± 0.14 L min ). In the presence of a decreased (by ∼6-8%) thigh muscle volume, normalized per unit of muscle mass was not affected by both interventions. Δ[deoxy(Hb + Mb)] decreased (P < 0.05) after N-BR (65 ± 13% of limb ischaemia) and H-BR (62 ± 12%) vs. BDC (73 ± 13%). H-AMB did not alter or Δ[deoxy(Hb + Mb)] . An overshoot of Δ[deoxy(Hb + Mb)] was evident during the first minute of unloaded exercise after N-BR and H-BR. Arterial blood flow to the lower limb during both unloaded and peak knee extension was not affected by any intervention. Maximal ADP-stimulated mitochondrial respiration decreased (P < 0.05) after all interventions vs. control. In 21 day N-BR, a significant impairment of oxidative metabolism occurred downstream of cardiovascular O delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone.