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Autophagy is inhibited in hypertrophied skeletal muscle in response to 8 weeks of progressive resistance exercise
Author(s) -
kwon insu,
Jang yongchul,
Cho JoonYong,
Lee Youngil
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1245.30
Subject(s) - autophagy , anabolism , endocrinology , medicine , tfeb , muscle hypertrophy , skeletal muscle , chemistry , endurance training , lipofuscin , biochemistry , apoptosis
Although autophagy induced by endurance exercise is a catabolic adaptive process by which muscular biochemical and morphological alterations occur, the effects of resistance exercise used for enhancing anabolic processes on autophagy have not been clearly understood. Here, we showed that while 8 weeks of rigorous resistance exercise significantly increased muscle mass and strength, autophagy was repressed. Twenty male Wistar rats (age: 6 weeks) were randomly divided into two groups: sedentary control (SC, n=10) and resistance exercise (RE, n=10). After familiarized with ladder climbing, RE group performed the ladder climbing exercise as a resistance exercise (3 times/week for 8 weeks with progressively reinforced intensity). 48 hours after the last session of training, Flexor Digitorum Profundus (FDP) muscles were excised, weighed, and homogenized for western blot analysis. We found that the relative muscle mass in concordance with weight carrying capacity was significantly increased in RE group. Effective training stress was proved by increases in heat shock protein 72 (HSP72) and an antioxidant protein MnSOD levels, respectively. Intriguingly, we observed that RE antagonized an autophagic process evidenced by a decline in LC3 II/I ratio and an increase in p62 levels and that this phenomenon occurred without the alterations of Beclin‐1 and BNIP3 levels. To examine why RE dampened autophagic flux, we measured levels of LAMP2 and TFEB, a master regulator of lysosomal biogenesis and found that neither TFEB nor LAMP2 levels were changed. Interestingly, however, an active form of Cathepsin L level was markedly suppressed in RE group compared to SC. Taken together, our study suggests that muscular hypertrophy by RE is inversely related to autophagy possibly by inhibiting lysosomal degradation process. Support or Funding Information This project was supported by a grant from the University of west Florida through the Office of Research and Sponsored Programs.