Age-associated declines in mitochondrial biogenesis and protein quality control factors are minimized by exercise training

Erika Koltai, Nikolett Hart, Albert W. Taylor, Sataro Goto, Jenny K. Ngo, Kelvin J.A. Davies, Zsolt Radak*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

110 Citations (Scopus)


A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial VO 2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome-c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.

Original languageEnglish
Pages (from-to)R127-R134
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number2
Publication statusPublished - 2012 Jul 15
Externally publishedYes


  • LON protease
  • Mitochondrial fission/fusion
  • Oxidative stress
  • Sirtuins

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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