title: Recovery of strength is dependent on mTORC1 signaling after eccentric muscle injury.
abstract: 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.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
authors.affiliation: Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, 30302-3975, USA.
authors.forename: Cory Walter
authors.initials: CW
authors.lastname: Baumann
authors.affiliation: Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, 30302-3975, USA.
authors.forename: Russell George
authors.initials: RG
authors.lastname: Rogers
authors.affiliation: Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, 30302-3975, USA.
authors.forename: Jeffrey Scott
authors.initials: JS
authors.lastname: Otis
authors.affiliation: Muscle Biology Laboratory, Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, 30302-3975, USA. cingalls@gsu.edu.
authors.forename: Christopher Paul
authors.initials: CP
authors.lastname: Ingalls
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005260:Female; D007166:Immunosuppressive Agents / Q000633:toxicity; D051379:Mice; D008810:Mice, Inbred C57BL; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000187:drug effects / Q000502:physiology; D009135:Muscular Diseases / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology*; D038762:Ribosomal Protein S6 Kinases, 70-kDa / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D020123:Sirolimus / Q000633:toxicity; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*; D013997:Time Factors; D019415:Torque
chemical_list: D007166:Immunosuppressive Agents; C546843:mTOR protein, mouse; D038762:Ribosomal Protein S6 Kinases, 70-kDa; D058570:TOR Serine-Threonine Kinases; D020123:Sirolimus
keywords: eccentric contractions; mouse; recovery; skeletal muscle; torque