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

Abstract

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 ₂ delivery, involving both the intramuscular matching between O ₂ 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 ₂ uptake ( ), vastus lateralis fractional O ₂ 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 ₂ delivery) carried outmore » 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 ⁻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, 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 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 O ₂ delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O ₂ supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone.« less

Authors:

Salvadego, Desy ^[1]; Keramidas, Michail E.  ^[2];

• Search DOE PAGES for author "Keramidas, Michail E."
• Search DOE PAGES for ORCID "0000-0002-7440-2171"

Kölegård, Roger ^[2]; Brocca, Lorenza  ^[3];

• Search DOE PAGES for author "Brocca, Lorenza"
• Search DOE PAGES for ORCID "0000-0003-1048-0573"

Lazzer, Stefano ^[1]; Mavelli, Irene ^[1]; Rittweger, Jörn ^[4]; Eiken, Ola ^[2]; Mekjavic, Igor B.  ^[5];

• Search DOE PAGES for author "Mekjavic, Igor B."
• Search DOE PAGES for ORCID "0000-0001-5930-2159"

Grassi, Bruno  ^[6]

• Search DOE PAGES for author "Grassi, Bruno"
• Search DOE PAGES for ORCID "0000-0003-3188-1659"

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+ Show Author Affiliations

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

Publication Date:

Tue Apr 17 00:00:00 EDT 2018

Sponsoring Org.:

USDOE

OSTI Identifier:

1433444

Resource Type:

Publisher's Accepted Manuscript

Journal Name:

Journal of Physiology

Additional Journal Information:

Journal Name: Journal of Physiology Journal Volume: 596 Journal Issue: 15; Journal ID: ISSN 0022-3751

Publisher:

Wiley

Country of Publication:

United Kingdom

Language:

English