mTOR signaling and the molecular adaptation to resistance exercise

被引:127
作者
Bodine, Sue C. [1 ]
机构
[1] Univ Calif Davis, Sect Neurobiol Physiol & Behav, Davis, CA 95616 USA
关键词
skeletal muscle; hypertrophy; protein translation; protein kinase B/Akt;
D O I
10.1249/01.mss.0000233797.24035.35
中图分类号
G8 [体育];
学科分类号
04 ; 0403 ;
摘要
Skeletal muscle size is dynamic and responsive to extracellular signals such as mechanical load, neural activity, hormones, growth factors, and cytokines. The signaling pathways responsible for regulating cell size in adult skeletal muscle under growth and atrophy conditions are poorly understood. However, recent evidence suggests a role for the PI3K/Akt/mTOR pathway. Protein translation is regulated through the phosphorylation of initiation factors that are controlled by signaling pathways downstream of PI3K/Akt. Recent work in mammals has suggested that activation of Akt/PKB, a Ser-Thr phosphatidylinositol-regulated kinase, and its downstream targets, glycogen synthase kinase-3 (GSK3) and the mammalian target of rapamycin (mTOR), may be critical regulators of postnatal cell size in multiple organ systems, including skeletal muscle. This paper will review some of the recent data that demonstrate the critical role of Akt/mTOR signaling in the regulation of postnatal muscle size, especially under conditions of increased external loading.
引用
收藏
页码:1950 / 1957
页数:8
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