Dietary protein decreases exercise endurance through rapamycin-sensitive suppression of muscle mitochondria

Masanori Mitsuishi, Kazutoshi Miyashita, Ayako Muraki, Masanori Tamaki, Kumiko Tanaka, Hiroshi Itoh

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


Loss of physical performance is linked not only to decreased activity in daily life but also to increased onset of cardiovascular diseases and mortality. A highprotein diet is recommended for aged individuals in order to preserve muscle mass; however, the regulation of muscle mitochondria by dietary protein has not been clarified. We investigated the long-term effects of a high-protein diet on muscle properties, focusing especially on muscle mitochondria. Mice were fed a high-protein diet from the age of 8 wk and examined for mitochondrial properties and exercise endurance at the ages of 20 and 50 wk. Compared with normal chow, a high-protein diet significantly decreased the amount of muscle mitochondria, mitochondrial activity, and running distance at 50 wk, although it increased muscle mass and grip power. Inhibition of TORC1-dependent signal pathways by rapamycin from 8 wk suppressed the decline in mitochondria and exercise endurance observed when mice were fed the high-protein diet in association with preserved AMPK activity. Collectively, these findings suggest a role for dietary protein as a suppressor of muscle mitochondria and indicate that the age-associated decline in exercise endurance might be accelerated by excessive dietary protein through rapamycin-sensitive suppression of muscle mitochondria.

Original languageEnglish
Pages (from-to)E776-E784
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number7
Publication statusPublished - 2013 Oct 1


  • AMPK
  • Exercise endurance
  • Muscle mitochondria
  • Physical performance
  • Rapamycin
  • Skeletal muscle mass
  • TORC1

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)


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