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Skeletal muscle is one of the most abundant and metabolically active tissues in mammals. The enormous plasticity of muscle is linked to the relative levels of physical activity and pathological conditions (e.g., cancer), in which skeletal muscle atrophy and weakness exacerbate morbidity and mortality. Inversely, exercise enhances skeletal muscle integrity and function and thereby lowers the risk for many chronic diseases. Resistance training is of particular importance in the context of muscle disuse and aging. The adaptive response of muscle to resistance exercise in regard to muscle mass and strength differs from developmental growth. Molecularly, the activation of the mammalian target of rapamycin complex 1 (mTORC1) is considered an essential step in mechanical overload-mediated skeletal muscle hypertrophy. However, both the upstream control as well as the downstream effect of mTORC1 remain poorly understood, as are the mTORC1-independent processes that control protein synthesis. Therefore, the aim of this chapter is to discuss the main mechanisms involved in resistance exercise-mediated skeletal muscle hypertrophy, including mTORC1 activation, ribosomal biogenesis, and the potential role of satellite cells in this process.
