Sarcopenia Targeting With Autophagy Mechanism by Exercise

BMB Rep. 2019 Jan;52(1):64-69. doi: 10.5483/BMBRep.2019.52.1.292.


The loss of skeletal muscle, called sarcopenia, is an inevitable event during the aging process, and significantly impacts quality of life. Autophagy is known to reduce muscle atrophy caused by dysfunctional organelles, even though the molecular mechanism remains unclear. Here, we have discuss the current understanding of exercise-induced autophagy activation in skeletal muscle regeneration and remodeling, leading to sarcopenia intervention. With aging, dysregulation of autophagy flux inhibits lysosomal storage processes involved in muscle biogenesis. AMPK-ULK1 and the FoxO/PGC-1ɑ signaling pathways play a critical role in the induction of autophagy machinery in skeletal muscle, thus these pathways could be targets for therapeutics development. Autophagy has been also shown to be a critical regulator of stem cell fate, which determines satellite cell differentiation into muscle fiber, thereby increasing muscle mass. This review aims to provide a comprehensive understanding of the physiological role of autophagy in skeletal muscle aging and sarcopenia. [BMB Reports 2019; 52(1): 64-69].

Publication types

  • Review

MeSH terms

  • Adenylate Kinase
  • Aging
  • Animals
  • Autophagy / physiology
  • Autophagy-Related Protein-1 Homolog
  • Cell Differentiation
  • Exercise / physiology*
  • Forkhead Box Protein O1
  • Humans
  • Muscle Fibers, Skeletal
  • Muscle, Skeletal / physiology
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Physical Conditioning, Animal / physiology*
  • Sarcopenia / therapy*
  • Signal Transduction


  • Forkhead Box Protein O1
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Autophagy-Related Protein-1 Homolog
  • Adenylate Kinase