2013 Fiscal Year Final Research Report

Single bout of running exercise suppressed autophagy in the fasted state

Research Project

Project/Area Number	24700705
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Sports science
Research Institution	Juntendo University
Principal Investigator	ZHENG DONGMEI 順天堂大学, 医学(系)研究科(研究院), 非常勤助教 (10420829)
Project Period (FY)	2012-04-01 – 2014-03-31
Keywords	Autophagy / Endurance exercise / LC3 / muscle / mTOR / treadmill
Research Abstract	Starvation-induced decrease in insulin and serum amino acids effectively suppresses the mammalian target of rapamycin (mTor) signaling to induce autophagy, a cellular major degradative pathway, in skeletal muscles (soleus, plantaris, and gastrocnemius). I investigated effect of treadmill running exercise on mTor signaling of skeletal muscles of starved mice. I found that mTor signaling pathway once inactivated under starvation conditions was reactivated after treadmill running exercise (12 m/min, 2 h) as revealed by the transition of phosphorylation state of S6-kinase and ribosomal S6. In accordance with this, autophagosomes induced in the skeletal muscles of starved GFP-transgenic mice were markedly suppressed after exercise. Treadmill running exercise caused changes in the expression of glycogenin, galectin-1, etc. However, these changes do not seem to connect to the mechanism of exercise-induced mTor reactivation.