more potential benefits from exercise

Last week's NY Times notes that exercise creates brown fat in rats ... it is a long jump to claim it would happen in humans, but it is very interesting.

The current issue of Nature reports that exercise also promotes cellular autophagy in rats.  A long jump to humans, but the lead researcher said this was enough information enough to get her to get into a regular exercise routine.  If it pans out it might explain several benefits of exercise.

 

Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis

•  
  • Congcong He,
  • Michael C. Bassik,
  • Viviana Moresi,
  • Kai Sun,
  • Yongjie Wei,
  • Zhongju Zou,
  • Zhenyi An,
  • Joy Loh,
  • Jill Fisher,
  • Qihua Sun,
  • Stanley Korsmeyer,
  • Milton Packer,
  • Herman I. May,
  • Joseph A. Hill,
  • Herbert W. Virgin,
  • Christopher Gilpin,
  • Guanghua Xiao,
  • Rhonda Bassel-Duby,
  • Philipp E. Scherer
  • &Beth Levine

Nature (2012) doi:10.1038/nature10758

Received 22 September 2010 Accepted 06 December 2011  published online 18 January 2012

Exercise has beneficial effects on human health, including protection against metabolic disorders such as diabetes¹. However, the cellular mechanisms underlying these effects are incompletely understood. The lysosomal degradation pathway, autophagy, is an intracellular recycling system that functions during basal conditions in organelle and protein quality control². During stress, increased levels of autophagy permit cells to adapt to changing nutritional and energy demands through protein catabolism³. Moreover, in animal models, autophagy protects against diseases such as cancer, neurodegenerative disorders, infections, inflammatory diseases, ageing and insulin resistance^4, 5, 6. Here we show that acute exercise induces autophagy in skeletal and cardiac muscle of fed mice. To investigate the role of exercise-mediated autophagy in vivo, we generated mutant mice that show normal levels of basal autophagy but are deficient in stimulus (exercise- or starvation)-induced autophagy. These mice (termed BCL2 AAA mice) contain knock-in mutations in BCL2 phosphorylation sites (Thr69Ala, Ser70Ala and Ser84Ala) that prevent stimulus-induced disruption of the BCL2–beclin-1 complex and autophagy activation. BCL2 AAA mice show decreased endurance and altered glucose metabolism during acute exercise, as well as impaired chronic exercise-mediated protection against high-fat-diet-induced glucose intolerance. Thus, exercise induces autophagy, BCL2 is a crucial regulator of exercise- (and starvation)-induced autophagy in vivo, and autophagy induction may contribute to the beneficial metabolic effects of exercise.