Alcohol and Skeletal Muscle in Health and Disease.
alcohol
comorbidity
metabolism
mitochondria
muscles
protein synthesis
proteolysis
skeletal
Journal
Alcohol research : current reviews
ISSN: 2169-4796
Titre abrégé: Alcohol Res
Pays: United States
ID NLM: 101594475
Informations de publication
Date de publication:
2023
2023
Historique:
medline:
9
11
2023
pubmed:
8
11
2023
entrez:
8
11
2023
Statut:
epublish
Résumé
Alcohol-related myopathy is one of the earliest alcohol-associated pathological tissue changes that is progressively exacerbated by cumulative long-term alcohol misuse. Acute and chronic alcohol use leads to changes in skeletal muscle mass and function. As discussed in this evidence-based review, alcohol-mediated mechanisms are multifactorial with effects on anabolic and catabolic signaling, mitochondrial bioenergetics, extracellular matrix remodeling, and epigenomic alterations. However, systematic studies are limited, especially regarding the acute effects of alcohol on skeletal muscle. This review focuses on peer-reviewed manuscripts published between January 2012 and November 2022 using the search terms "alcohol" or "ethanol" and "skeletal muscle" in MEDLINE, PubMed, and Web of Science using EndNote reference management software. Eligible manuscripts included full-length research papers that discussed acute and chronic effects of alcohol on skeletal muscle mass and function in both clinical and preclinical studies. The review also includes alcohol-mediated skeletal muscle effects in the context of comorbidities. The three databases together yielded 708 manuscripts. Of these, the authors excluded from this review 548 papers that did not have "alcohol" or "muscle" in the title and 64 papers that were duplicates or did not discuss skeletal muscle. Thus, of all the manuscripts considered for this review, 96 are included and 612 are excluded. Additionally, relevant papers published earlier than 2012 are included to provide context to the review. Both acute and chronic alcohol use decrease protein synthesis and increase protein degradation. Alcohol also impairs mitochondrial function and extracellular matrix remodeling. However, there is a gap in the literature on the known alcohol-mediated mechanisms, including senescence, role of immune activation, and interorgan communication, on the development of alcohol-related myopathy. With increased life expectancy, changing alcohol use patterns, and increasing frequency of alcohol use among females, current observational studies are needed on the prevalence of alcohol-related myopathy. Additionally, the compounding effects of acute and chronic alcohol use on skeletal muscle with aging or exercise, in response to injury or disuse, and in the context of comorbidities including diabetes and human immunodeficiency virus (HIV), call for further investigation. Though evidence suggests that abstinence or reducing alcohol use can improve muscle mass and function, they are not restored to normal levels. Hence, understanding the pathophysiological mechanisms can help in the design of therapeutic strategies to improve skeletal muscle health.
Identifiants
pubmed: 37937295
doi: 10.35946/arcr.v43.1.04
pii: arcr-43-1-4
pmc: PMC10627576
doi:
Substances chimiques
Ethanol
3K9958V90M
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
04Subventions
Organisme : NIAAA NIH HHS
ID : F30 AA029358
Pays : United States
Organisme : NIAAA NIH HHS
ID : P60 AA009803
Pays : United States
Déclaration de conflit d'intérêts
Disclosures The authors declare no competing financial or nonfinancial interests.
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