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*

*この研究の対応する著者

研究成果: Article査読

98 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)R127-R134
ジャーナルAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
303
2
DOI
出版ステータスPublished - 2012 7 15
外部発表はい

ASJC Scopus subject areas

  • 生理学
  • 生理学(医学)

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