Single bout of running exercise suppressed autophagy in the fasted state

饥饿引起的胰岛素和血清氨基酸的减少有效抑制了雷帕霉素（mTor）信号的靶细胞诱导自噬，这是骨骼肌（比目鱼肌、跖肌和腓肠肌）的细胞主要降解途径。研究了跑步机运动对饥饿小鼠骨骼肌mTor信号的影响。我发现mTor信号通路在饥饿条件下失活，在跑步机运动（12 m/min, 2 h）后重新激活，这是S6激酶和核糖体S6磷酸化状态的转变所揭示的。由此可见，运动后饥饿gfp转基因小鼠骨骼肌诱导的自噬体明显受到抑制。跑步机运动引起糖原素、半乳糖凝集素-1等表达的变化。然而，这些变化似乎与运动诱导的mTor再激活的机制无关。

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.