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Submaximal cycling exercise stimulates mTOR signaling pathway in human skeletal muscle
Author(s) -
Kakigi Ryo,
Naito Hisashi,
Yoshihara Toshinori,
Ozaki Hayao,
Kobayashi Hiroyuki,
Okada Takao
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb817
Subject(s) - pi3k/akt/mtor pathway , skeletal muscle , medicine , endocrinology , phosphorylation , autophagy , p70 s6 kinase 1 , protein kinase b , contraction (grammar) , chemistry , muscle contraction , signal transduction , biochemistry , apoptosis
It is known that eccentric muscle contraction promotes muscle protein synthesis. However, effects of concentric contraction on muscle protein synthesis are not clear. We determined whether high repetition of concentric contraction by cycling exercise stimulates mTOR signaling pathway in human skeletal muscle. Six young subjects (21±1 years) performed 90% VO 2 max cycling exercise at 90rpm for 5 minutes on bicycle ergometer. Muscle biopsies ( vastus lateralis ) were obtained before exercise and, at 1 and 3 h post‐exercise. mTOR signaling and markers of autophagy (LC3BI and LC3BII protein) were analyzed by using western blotting. Plasma GH, IGF‐1 and insulin levels significantly increased in post‐exercise period (p<0.05). Akt phosphorylation, upstream of mTOR, significantly increased at 1 h post‐exercise (p<0.05). S6K1 phosphorylation, a marker of mTOR activity, significantly increased at 3 h post‐exercise (p<0.05). At the same time point, LC3BII to I ratio were significantly decreased (p<0.05). These data suggest that high repetition of concentric contraction such as cycling exercise can stimulate mTOR signaling in human skeletal muscle, which might leads to promotion of protein synthesis and attenuation of autophagic protein degradation. This study was partly supported by the Sasakawa Scientific Research Grant from the Japan Science Society, and a Grant‐in‐Aid for Young Scientists (B) No. 24700703 .