mTOR signaling and the molecular adaptation to resistance exercise

Sue C. Bodine

Research output: Contribution to journalArticle

113 Scopus citations

Abstract

Skeletal muscle size is dynamic and responsive to extracellular signals such as mechanical load, neural activity, hormones, growth factors, and cytokines. The signaling pathways responsible for regulating cell size in adult skeletal muscle under growth and atrophy conditions are poorly understood. However, recent evidence suggests a role for the PI3K/Akt/mTOR pathway. Protein translation is regulated through the phosphorylation of initiation factors that are controlled by signaling pathways downstream of PBK/Akt. Recent work in mammals has suggested that activation of Akt/PKB, a Ser-Thr phosphatidylinositol-regulated kinase, and its downstream targets, glycogen synthase kinase-3 (OSK3) and the mammalian target of rapamycin (mTOR), may be critical regulators of postnatal cell size in multiple organ systems, including skeletal muscle. This paper will review some of the recent data that demonstrate the critical role of Akt/mTOR signaling in the regulation of postnatal muscle size, especially under conditions of increased external loading.

Original languageEnglish (US)
Pages (from-to)1950-1957
Number of pages8
JournalMedicine and Science in Sports and Exercise
Volume38
Issue number11
DOIs
StatePublished - Nov 2006

Keywords

  • Hypertrophy
  • Protein kinase B/AKT
  • Protein translation
  • Skeletal muscle

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Physical Therapy, Sports Therapy and Rehabilitation
  • Orthopedics and Sports Medicine

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