title: Long-term resistance exercise-induced muscular hypertrophy is associated with autophagy modulation in rats.
abstract: Elevation of anabolism and concurrent suppression of catabolism are critical metabolic adaptations for muscular hypertrophy in response to resistance exercise (RE). Here, we investigated if RE-induced muscular hypertrophy is acquired by modulating a critical catabolic process autophagy. Male Wistar Hannover rats (14 weeks old) were randomly assigned to either sedentary control (SC, n = 10) or resistance exercise (RE, n = 10). RE elicited significant hypertrophy of flexor digitorum profundus (FDP) muscles in parallel with enhancement in anabolic signaling pathways (phosphorylation of AKT, mTOR, and p70S6K). Importantly, RE-treated FDP muscle exhibited a significant decline in autophagy evidenced by diminished phosphorylation levels of AMPK, a decrease in LC3-II/LC3-I ratio, an increase in p62 level, and a decline in active form of lysosomal protease CATHEPSIN L in the absence of alterations of key autophagy proteins: ULK1 phosphorylation, BECLIN1, and BNIP3. Our study suggests that RE-induced hypertrophy is achieved by potentiating anabolism and restricting autophagy-induced catabolism.
authors.affiliation: Molecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, College of Health, University of West Florida, Pensacola, FL, USA.
authors.forename: Insu
authors.initials: I
authors.lastname: Kwon
authors.affiliation: Molecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, College of Health, University of West Florida, Pensacola, FL, USA.
authors.forename: Yongchul
authors.initials: Y
authors.lastname: Jang
authors.affiliation: Exercise Biochemistry Laboratory, Korea National Sport University, Seoul, Korea.
authors.forename: Joon-Yong
authors.initials: JY
authors.lastname: Cho
authors.affiliation: School of Applied Physiology and Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA, USA.
authors.forename: Young C
authors.initials: YC
authors.lastname: Jang
authors.affiliation: Molecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, College of Health, University of West Florida, Pensacola, FL, USA. ylee1@uwf.edu.
authors.forename: Youngil
authors.initials: Y
authors.lastname: Lee
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D000071189:Autophagy-Related Protein-1 Homolog / Q000378:metabolism; D000071186:Beclin-1 / Q000378:metabolism; D006984:Hypertrophy / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism / Q000503:physiopathology*; D010766:Phosphorylation / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000502:physiology
chemical_list: D000071186:Beclin-1; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins; D000071189:Autophagy-Related Protein-1 Homolog
keywords: Autophagy; Hypertrophy; Resistance exercise; Skeletal muscle