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J Physiol. 2018 Aug;596(15):3341-3355. doi: 10.1113/JP275605. Epub 2018 Apr 17.

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

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Department of Medicine, University of Udine, Udine, Italy.
Department of Environmental Physiology, Swedish Aerospace Physiology Centre, Royal Institute of Technology, Stockholm, Sweden.
Department of Molecular Medicine, University of Pavia, Pavia, Italy.
Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany.
Department of Pediatrics and Adolescent Medicine, Medical Faculty, University of Cologne, Cologne, Germany.
Department of Automation, Biocybernetics and Robotics, Jožef Stefan Institute, Ljubljana, Slovenia.
Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada.
Institute of Bioimaging and Molecular Physiology, National Research Council, Milano, Italy.



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 O2 delivery, involving both the intramuscular matching between O2 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.


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 ( PIO2  = 133 mmHg; N-BR) and hypoxia ( PIO2  = 90 mmHg; H-BR). H-BR was aimed at simulating reduced gravity habitats. The effects of a 21 day hypoxic ambulatory confinement ( PIO2  = 90 mmHg; H-AMB) were also assessed. Pulmonary O2 uptake ( V̇O2 ), vastus lateralis fractional O2 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 O2 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. V̇O2peak decreased (P < 0.05) after N-BR (0.98 ± 0.13 L min-1 ) and H-BR (0.96 ± 0.17 L min-1 ) vs. BDC (1.05 ± 0.14 L min-1 ). In the presence of a decreased (by ∼6-8%) thigh muscle volume, V̇O2peak normalized per unit of muscle mass was not affected by both interventions. Δ[deoxy(Hb + Mb)]peak 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 V̇O2peak or Δ[deoxy(Hb + Mb)]peak . 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 O2 delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O2 supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone.


hypoxia; microgravity; mitochondrial respiration; planetary habitats; skeletal muscle oxidative metabolism

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