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Research progress on molecular mechanism of resistance training-induced skeletal muscle hypertrophy: the crucial role of mTOR signaling

ZHAO Yong-Cai¹, HUANG Tao^2,*

¹College of Exercise and Health, Tianjin University of Sport, Tianjin 301617, China；²Department of Physical Education, Shanghai Jiao Tong University, Shanghai 200240, China

Abstract

Resistance training promotes protein synthesis and hypertrophy, enhancing strength of skeletal muscle through the activation of the mammalian target of rapamycin (mTOR) and the subsequent increases of ribosome biogenesis and translation capacity. Recent studies indicate that resistance training has positive effects on physical fitness and illness treatment, yet the mechanisms underlying hypertrophic adaptation remain insufficiently understood. Human studies focused on the correlation between mTOR signals and hypertrophy-related protein production, while animal research demonstrated that mTOR complex 1 (mTORC1) is the main regulator of resistance training induced-hypertrophy. A number of upstream factors of mTORC1 have been identified, while the downstream mechanisms involved in the resistance training induced-hypertrophy are rarely studied. mTORC1 regulates the activation of satellite cells, which fuse with pre-existing fibers and contribute to hypertrophic response to resistance training. This article reviews the research progress on the mechanism of skeletal muscle hypertrophy caused by resistance training, analyzes the role of mTOR-related signals in the adaptation of skeletal muscle hypertrophy, and aims to provide a basis for basic research on muscle improvements through resistance training.

Key words: resistance training; skeletal muscle; muscle hypertrophy; ribosome

Received: 　　Accepted:

Corresponding author: 黄涛　　E-mail:

DOI: 10.13294/j.aps.2025.0048

Citing This Article：

ZHAO Yong-Cai, HUANG Tao. Research progress on molecular mechanism of resistance training-induced skeletal muscle hypertrophy: the crucial role of mTOR signaling. Acta Physiol Sin 2025; 77 (3): 573-586 (in Chinese with English abstract).