Diabetologia

, Volume 60, Issue 8, pp 1491–1501 | Cite as

Bed rest and resistive vibration exercise unveil novel links between skeletal muscle mitochondrial function and insulin resistance

  • Helena C. Kenny
  • Floriane Rudwill
  • Laura Breen
  • Michele Salanova
  • Dieter Blottner
  • Tim Heise
  • Martina Heer
  • Stephane Blanc
  • Donal J. O’Gorman
Article

Abstract

Aims/hypothesis

Physical inactivity has broad implications for human disease including insulin resistance, sarcopenia and obesity. The present study tested the hypothesis that (1) impaired mitochondrial respiration is linked with blunted insulin sensitivity and loss of muscle mass in healthy young men, and (2) resistive vibration exercise (RVE) would mitigate the negative metabolic effects of bed rest.

Methods

Participants (n = 9) were maintained in energy balance during 21 days of bed rest with RVE and without (CON) in a crossover study. Mitochondrial respiration was determined by high-resolution respirometry in permeabilised fibre bundles from biopsies of the vastus lateralis. A hyperinsulinaemic–euglycaemic clamp was used to determine insulin sensitivity, and body composition was assessed by dual-energy x-ray absorptiometry (DEXA).

Results

Body mass (−3.2 ± 0.5 kg vs −2.8 ± 0.4 kg for CON and RVE, respectively, p < 0.05), fat-free mass (−2.9 ± 0.5 kg vs −2.7 ± 0.5 kg, p < 0.05) and peak oxygen consumption (\( \overset{\cdot }{V}{\mathrm{O}}_{2\mathrm{peak}} \)) (10–15%, p < 0.05) were all reduced following bed rest. Bed rest decreased insulin sensitivity in the CON group (0.04 ± 0.002 mg kgFFM−1 [pmol l−1] min−1 vs 0.03 ± 0.002 mg kgFFM−1 [pmol l−1] min−1 for baseline vs post-CON), while RVE mitigated this response (0.04 ± 0.003 mg kgFFM−1 [pmol l−1] min−1). Mitochondrial respiration (oxidative phosphorylation and electron transport system capacity) decreased in the CON group but not in the RVE group when expressed relative to tissue weight but not when normalised for citrate synthase activity. LEAK respiration, indicating a decrease in mitochondrial uncoupling, was the only component to remain significantly lower in the CON group after normalisation for citrate synthase. This was accompanied by a significant decrease in adenine nucleotide translocase protein content.

Conclusions/interpretation

Reductions in muscle mitochondrial respiration occur concomitantly with insulin resistance and loss of muscle mass during bed rest and may play a role in the adaptations to physical inactivity. Significantly, we show that RVE is an effective strategy to partially prevent some of the deleterious metabolic effects of bed rest.

Keywords

Bed rest Energy expenditure Exercise Insulin resistance Metabolism Mitochondrial function Skeletal muscle 

Abbreviations

ANT

Adenine nucleotide translocase

CHO

Carbohydrate

CON

Control

ETS

Electron transport system

FA

Fatty acid

OXPHOS

Oxidative phosphorylation

RMR

Resting metabolic rate

RVE

Resistive vibration exercise

SUIT

Substrate-uncoupler-inhibitor titration

TMPD

N,N,N′,N′-Tetramethyl-p-phenylenediamine dihydrochloride

UCP3

Uncoupling protein 3

\( \overset{\cdot }{V}{\mathrm{O}}_{2\mathrm{peak}} \)

Peak oxygen consumption

Supplementary material

125_2017_4298_MOESM1_ESM.pdf (561 kb)
ESM(PDF 560 kb)

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Copyright information

© Springer-Verlag Berlin Heidelberg 2017

Authors and Affiliations

  • Helena C. Kenny
    • 1
    • 2
  • Floriane Rudwill
    • 3
  • Laura Breen
    • 2
  • Michele Salanova
    • 4
  • Dieter Blottner
    • 4
  • Tim Heise
    • 5
  • Martina Heer
    • 5
    • 6
  • Stephane Blanc
    • 3
  • Donal J. O’Gorman
    • 1
    • 2
  1. 1.3U Diabetes Consortium, School of Health and Human PerformanceDublin City UniversityDublin 9Ireland
  2. 2.National Institute for Cellular and BiotechnologyDublin City UniversityDublinIreland
  3. 3.Université de Strasbourg, Institut Pluridisiplinaire Hubert Curien, Départment d’Ecologie, Physiologie et Ethologie, CNRS, UMR7178StrasbourgFrance
  4. 4.Charité Universitätsmedizin BerlinBerlinGermany
  5. 5.ProfilNeussGermany
  6. 6.Institute of Nutrition and Food SciencesUniversity of BonnBonnGermany

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