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Muscle Nerve. 2016 Nov;54(5):914-924. doi: 10.1002/mus.25121. Epub 2016 Aug 22.

Recovery of strength is dependent on mTORC1 signaling after eccentric muscle injury.

Author information

1
Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, 30302-3975, USA.
2
Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, 30302-3975, USA. cingalls@gsu.edu.

Abstract

INTRODUCTION:

Eccentric contractions may cause immediate and long-term reductions in muscle strength that can be recovered through increased protein synthesis rates. The purpose of this study was to determine whether the mechanistic target-of-rapamycin complex 1 (mTORC1), a vital controller of protein synthesis rates, is required for return of muscle strength after injury.

METHODS:

Isometric muscle strength was assessed before, immediately after, and then 3, 7, and 14 days after a single bout of 150 eccentric contractions in mice that received daily injections of saline or rapamycin.

RESULTS:

The bout of eccentric contractions increased the phosphorylation of mTORC1 (1.8-fold) and p70s6k1 (13.8-fold), mTORC1's downstream effector, 3 days post-injury. Rapamycin blocked mTORC1 and p70s6k1 phosphorylation and attenuated recovery of muscle strength (∼20%) at 7 and 14 days.

CONCLUSION:

mTORC1 signaling is instrumental in the return of muscle strength after a single bout of eccentric contractions in mice. Muscle Nerve 54: 914-924, 2016.

KEYWORDS:

eccentric contractions; mouse; recovery; skeletal muscle; torque

PMID:
27015597
DOI:
10.1002/mus.25121
[Indexed for MEDLINE]

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