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Protein coingestion with alcohol following strenuous exercise attenuates alcohol-induced intramyocellular apoptosis and inhibition of autophagy
Smiles, William J. Parr, Evelyn B. Coffey, Vernon G. Lacham-Kaplan, Orly Hawley, John Alan Camera, Donny Michael
Smiles, William J.
Parr, Evelyn B.
Coffey, Vernon G.
Lacham-Kaplan, Orly
Hawley, John Alan
Camera, Donny Michael
Abstract
Alcohol ingestion decreases postexercise rates of muscle protein synthesis, but the mechanism( s ) ( e.g., increased protein breakdown ) underlying this observation is unknown. Autophagy is an intracellular “recycling” system required for homeostatic substrate and organelle turnover; its dysregulation may provoke apoptosis and lead to muscle atrophy. We investigated the acute effects of alcohol ingestion on autophagic cell signaling responses to a bout of concurrent ( combined resistance- and endurance-based ) exercise. In a randomized crossover design, eight physically active males completed three experimental trials of concurrent exercise with either postexercise ingestion of alcohol and carbohydrate ( 12 ± 2 standard drinks; ALC-CHO ), energy-matched alcohol and protein ( ALC-PRO ), or protein ( PRO ) only. Muscle biopsies were taken at rest and 2 and 8 h postexercise. Select autophagy-related gene ( Atg ) proteins decreased compared with rest with ALC-CHO ( P < 0.05 ) but not ALC-PRO. There were parallel increases ( P < 0.05 ) in p62 and PINK1 commensurate with a reduction in BNIP3 content, indicating a diminished capacity for mitochondria-specific autophagy ( mitophagy ) when alcohol and carbohydrate were coingested. DNA fragmentation increased in both alcohol conditions ( P < 0.05 ); however, nuclear AIF accumulation preceded this apoptotic response with ALC-CHO only ( P < 0.05 ). In contrast, increases in the nuclear content of p53, TFEB, and PGC-1α in ALC-PRO were accompanied by markers of mitochondrial biogenesis at the transcriptional ( Tfam, SCO2, and NRF-1 ) and translational ( COX-IV, ATPAF1, and VDAC1 ) level ( P < 0.05 ). We conclude that alcohol ingestion following exercise triggers apoptosis, whereas the anabolic properties of protein coingestion may stimulate mitochondrial biogenesis to protect cellular homeostasis.
Keywords
alcohol, exercise, autophagy, apoptosis, protein
Date
2016
Type
Journal article
Journal
American Journal of Physiology: Endocrinology and Metabolism
Book
Volume
311
Issue
5
Page Range
E836-E849
Article Number
ACU Department
Centre for Exercise and Nutrition
Faculty of Health Sciences
Mary MacKillop Institute for Health Research
Non-faculty
Faculty of Health Sciences
Mary MacKillop Institute for Health Research
Non-faculty
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Event URL
Open Access Status
License
File Access
Controlled