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Biochem Biophys Res Commun. 2015 Jan 2;456(1):519-26. doi: 10.1016/j.bbrc.2014.11.118. Epub 2014 Dec 6.

A treadmill exercise reactivates the signaling of the mammalian target of rapamycin (mTor) in the skeletal muscles of starved mice.

Author information

1
Department of Biochemistry, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
2
Laboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
3
Sportology Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
4
Department of Biochemistry, Juntendo University School of Medicine, Tokyo 113-8421, Japan; Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
5
Department of Biochemistry, Juntendo University School of Medicine, Tokyo 113-8421, Japan; Laboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
6
Department of Biochemistry, Juntendo University School of Medicine, Tokyo 113-8421, Japan; Translational Research Center, Fukushima Medical University, Fukushima 960-1295, Japan. Electronic address: jezaki@fmu.ac.jp.

Abstract

It has been well established that a starvation-induced decrease in insulin/IGF-I and serum amino acids effectively suppresses the mammalian target of rapamycin (mTor) signaling to induce autophagy, which is a major degradative cellular pathway in skeletal muscles. In this study, we investigated the systematic effects of exercise on the mTor signaling of skeletal muscles. Wild type C57BL/6J mice were starved for 24h under synchronous autophagy induction conditions. Under these conditions, endogenous LC3-II increased, while both S6-kinse and S6 ribosomal protein were dephosphorylated in the skeletal muscles, which indicated mTor inactivation. Using GFP-LC3 transgenic mice, it was also confirmed that fluorescent GFP-LC3 dots in the skeletal muscles increased, including soleus, plantaris, and gastrocnemius, which clearly showed autophagosomal induction. These starved mice were then subjected to a single bout of running on a treadmill (12m/min, 2h, with a lean of 10 degrees). Surprisingly, biochemical analyses revealed that the exercise elicited a decrease in the LC3-II/LC3-I ratio as well as an inversion from the dephosphorylated state to the rephosphorylated state of S6-kinase and ribosomal S6 in these skeletal muscles. Consistently, the GFP-LC3 dots of the skeletal muscles were diminished immediately after the exercise. These results indicated that exercise suppressed starvation-induced autophagy through a reactivation of mTor signaling in the skeletal muscles of these starved mice.

KEYWORDS:

Autophagy; Exercise; GFP-LC3; Skeletal muscle; Treadmill; mTor

PMID:
25485704
DOI:
10.1016/j.bbrc.2014.11.118
[Indexed for MEDLINE]

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