Research Article

Biogerontology

, Volume 13, Issue 6, pp 621-631

First online:

PGC-1α transcriptional response and mitochondrial adaptation to acute exercise is maintained in skeletal muscle of sedentary elderly males

  • J. N. CobleyAffiliated withResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University
  • , J. D. BartlettAffiliated withResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University
  • , A. KayaniAffiliated withInstitute of Ageing and Chronic Disease, University of Liverpool
  • , S. W. MurrayAffiliated withCardiology Department, Liverpool Heart and Chest Hospital
  • , J. LouhelainenAffiliated withFaculty of Pharmacy and Biomolecular Sciences, Liverpool John Moores University
  • , T. DonovanAffiliated withSport and Exercise Sciences, Glyndwr University
  • , S. WaldronAffiliated withStepping Hill Hospital
  • , W. GregsonAffiliated withResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University
  • , J. G. BurnistonAffiliated withResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University
    • , J. P. MortonAffiliated withResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University
    • , G. L. CloseAffiliated withResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University Email author 

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Abstract

The aim of the present study was to examine the effects of ageing and training status on (1) markers of skeletal muscle mitochondrial content and (2) the ability to activate the acute signalling pathways associated with regulating exercise-induced mitochondrial biogenesis. Muscle biopsies were obtained from the vastus lateralis muscle of young untrained (24 ± 4 years, n = 6; YU), young trained (22 ± 3 years, n = 6; YT), old untrained (65 ± 6 years, n = 6; OU) and old trained (64 ± 3 years, n = 6; OT) healthy males before and after (3 h and 3 days post-exercise) completion of high-intensity interval cycling exercise. In resting muscle, lifelong training preserved mtDNA, PGC-1α and COXIV protein content such that muscles from OT individuals were comparable to muscles from both YU and YT individuals, whereas lifelong sedentary behaviour reduced such markers of mitochondrial content. Regardless of age or training status, acute exercise induced comparable increases in p38MAPK phosphorylation immediately post-exercise, PGC-1α and COXIV mRNA expression at 3 h post-exercise and COXIV protein at 3 days post-exercise. Data demonstrate that lifelong endurance training preserves skeletal muscle PGC-1α content and that despite the mitochondrial dysfunction typically observed with sedentary ageing, muscles from sedentary elderly individuals retain the capacity to activate the acute signalling pathways associated with regulating the early processes of mitochondrial biogenesis. We consider our data to have immediate translational potential as they highlight the potential therapeutic effects of exercise to induce skeletal muscle mitochondrial biogenesis persist late in adulthood, even after a lifetime of physical inactivity.

Keywords

p38MAPK Mitochondrial biogenesis mtDNA COXIV Exercise Training Ageing