期刊
EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY
卷 118, 期 3, 页码 485-500出版社
SPRINGER
DOI: 10.1007/s00421-017-3792-9
关键词
Skeletal muscle; Resistance exercise; Myofibrillar protein synthesis; Edema; Soreness; Satellite cells
资金
- Sao Paulo Research Foundation (FAPESP) [2012/24499-1, 2013/21218-4, 2014/19594-0, 2016/24259-1, 2017/04299-1]
- National Council for Scientific and Technological Development (CNPq) [303085/2015-0, 448387/2014-0]
- Natural Science and Engineering Research Council (NSERC)
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [12/24499-1] Funding Source: FAPESP
Resistance training (RT)-induced skeletal muscle hypertrophy is a highly intricate process. Despite substantial advances, we are far from understanding exactly how muscle hypertrophy develops during RT. The aim of the present review is to discuss new insights related to the role of skeletal muscle damage and muscle protein synthesis (MPS) in mediating RT-induced hypertrophy. Specifically, the thesis that in the early phase of RT (<= 4 previous RT sessions) increases in muscle cross-sectional area are mostly attributable to muscle damage-induced muscle swelling; then (after similar to 10 sessions), a modest magnitude of muscle hypertrophy ensues; but only during a latter phase of RT (after similar to 18 sessions) is true muscle hypertrophy observed. We argue that the initial increases in MPS post-RT are likely directed to muscle repair and remodelling due to damage, and do not correlate with eventual muscle hypertrophy induced by several RT weeks. Increases in MPS post-RT session only contribute to muscle hypertrophy after a progressive attenuation of muscle damage, and even more significantly when damage is minimal. Furthermore, RT protocols that do not promote significant muscle damage still induce similar muscle hypertrophy and strength gains compared to conditions that do promote initial muscle damage. Thus, we conclude that muscle damage is not the process that mediates or potentiates RT-induced muscle hypertrophy.
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