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

Cory Walter Baumann, Russell George Rogers, Jeffrey Scott Otis, Christopher Paul Ingalls

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)914-924
Number of pages11
JournalMuscle and Nerve
Issue number5
StatePublished - Nov 1 2016
Externally publishedYes


  • eccentric contractions
  • mouse
  • recovery
  • skeletal muscle
  • torque


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