BMB Reports 2019; 52(1): 64-69  
Sarcopenia targeting with autophagy mechanism by exercise
Sung Sup Park1,2,#, Young-Kyo Seo1,# & Ki-Sun Kwon1,2,*
1Aging Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, 2Department of Life Science, University of Science and Technology (UST), Daejeon 34113, Korea
Correspondence to: Tel: +82-42-860-4143; Fax: +82-42-879-8596; E-mail: kwonks@kribb.re.kr
#These authors contributed equally to this work.
Received: October 30, 2018; Published online: January 31, 2019.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
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.
Keywords:

Autophagy, Exercise, Remodeling, Sarcopenia, Skeletal muscle

Figures
Fig. 3. Role of autophagy in skeletal muscle performance. Autophagy might carry out basic functions such as component recycling and energy support in skeletal muscle. Aging inhibits autophagy formation in skeletal muscle through multiple factors such as accumulation of misfolded proteins or dysfunctional mitochondria. In order to repair muscle damage, the exercise is required to induce autophagy, which results satellite cell activation, muscle mass maintenance, fiber type switching, and muscle adaptation. Autophagy formation might be beneficial event for the muscle performance through regeneration and remodeling in skeletal muscle.


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