Acute resistance exercise training does not augment mitochondrial remodelling in master athletes or untrained older adults

Ryan Neil Marshall, James McKendry, Benoit Smeuninx, Alex Peter Seabright, Paul T Morgan, Carolyn Greig, Leigh Breen

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Abstract

Background: Ageing is associated with alterations to skeletal muscle oxidative metabolism that may be influenced by physical activity status, although the mechanisms underlying these changes have not been unraveled. Similarly, the effect of resistance exercise training (RET) on skeletal muscle mitochondrial regulation is unclear.

Methods: Seven endurance-trained masters athletes ([MA], 74 ± 3 years) and seven untrained older adults ([OC]. 69 ± 6 years) completed a single session of knee extension RET (6 x 12 repetitions, 75% 1-RM, 120-s intra-set recovery). Vastus lateralis muscle biopsies were collected pre-RET, 1 h post-RET, and 48h post-RET. Skeletal muscle biopsies were analyzed for citrate synthase (CS) enzyme activity, mitochondrial content, and markers of mitochondrial quality control via immunoblotting.

Results: Pre-RET CS activity and protein content were ∼45% ( p < .001) and ∼74% greater in MA compared with OC ( p = .006). There was a significant reduction (∼18%) in CS activity 48 h post-RET ( p < .05) in OC, but not MA. Pre-RET abundance of individual and combined mitochondrial electron transport chain (ETC) complexes I-V were significantly greater in MA compared with OC, as were markers of mitochondrial fission and fusion dynamics (p-DRP-1Ser616, p-MFFSer146, OPA-1 & FIS-1, p < .05 for all). Moreover, MA displayed greater expression of p-AMPKThr172, PGC1α, TFAM, and SIRT-3 ( p < .05 for all). Notably, RET did not alter the expression of any marker of mitochondrial content, biogenesis, or quality control in both OC and MA.

 Conclusion: The present data suggest that long-term aerobic exercise training supports superior skeletal muscle mitochondrial density and protein content into later life, which may be regulated by greater mitochondrial quality control mechanisms and supported via superior fission-fusion dynamics. However, a single session of RET is unable to induce mitochondrial remodelling in the acute (1h post-RET) and delayed (48 h post-RET) recovery period in OC and MA.

Original languageEnglish
Article number1097988
Number of pages11
JournalFrontiers in Physiology
Volume13
DOIs
Publication statusPublished - 4 Jan 2023

Bibliographical note

Copyright © 2023 Marshall, McKendry, Smeuninx, Seabright, Morgan, Greig and Breen.

Keywords

  • Physiology
  • ageing
  • healthy ageing
  • mitochondria
  • resistance exercise
  • skeletal muscle

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