Format

Send to

Choose Destination
Eur J Appl Physiol. 2018 Mar;118(3):485-500. doi: 10.1007/s00421-017-3792-9. Epub 2017 Dec 27.

The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis.

Author information

1
School of Physical Education and Sport, University of São Paulo, Av. Prof. Mello Moraes, 65, São Paulo, SP, 05508-030, Brazil. felipedamas@usp.br.
2
Laboratory of Neuromuscular Adaptations to Resistance Training-MUSCULAB, Department of Physical Education, Federal University of São Carlos, Rod. Washington Luiz, km 235-SP310, São Carlos, SP, 13565-905, Brazil. felipedamas@usp.br.
3
Laboratory of Neuromuscular Adaptations to Resistance Training-MUSCULAB, Department of Physical Education, Federal University of São Carlos, Rod. Washington Luiz, km 235-SP310, São Carlos, SP, 13565-905, Brazil.
4
School of Physical Education and Sport, University of São Paulo, Av. Prof. Mello Moraes, 65, São Paulo, SP, 05508-030, Brazil.

Abstract

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 ~ 10 sessions), a modest magnitude of muscle hypertrophy ensues; but only during a latter phase of RT (after ~ 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.

KEYWORDS:

Edema; Myofibrillar protein synthesis; Resistance exercise; Satellite cells; Skeletal muscle; Soreness

PMID:
29282529
DOI:
10.1007/s00421-017-3792-9
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center