Send to

Choose Destination
Am J Physiol Endocrinol Metab. 2013 Oct 1;305(7):E776-84. doi: 10.1152/ajpendo.00145.2013. Epub 2013 Jul 23.

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

Author information

Department of Internal Medicine, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan; and.


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 high-protein 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.


AMPK; TORC1; exercise endurance; muscle mitochondria; physical performance; rapamycin; skeletal muscle mass

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center