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Journal article
Long-term resistance exercise-induced muscular hypertrophy is associated with autophagy modulation in rats
The journal of physiological sciences : JPS, Vol.68(12), pp.269-280
68
2018
PMCID: PMC3701192
PMID: 28213823
Web of Science ID: WOS:000320704000006
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.
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- Title
- Long-term resistance exercise-induced muscular hypertrophy is associated with autophagy modulation in rats
- Publication Details
- The journal of physiological sciences : JPS, Vol.68(12), pp.269-280
- Resource Type
- Journal article
- Publisher
- Springer Japan; Tokyo
- Series
- 68
- Number of pages
- 13
- Grant note
- T32HL007444 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) T32GM007198 / NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of General Medical Sciences (NIGMS) R01HL087023; R01HL101217 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA American Heart Association's Western States Affiliate
- Copyright
- The Physiological Society of Japan and Springer Japan 2017 All articles published by The Journal of Physiological Sciences are made freely and permanently accessible online immediately upon publication, without subscription charges or registration barriers.
- Identifiers
- WOS:000320704000006; 99380090641306600
- Academic Unit
- Movement Sciences and Health; Usha Kundu, MD College of Health
- Language
- English