Ethanol-Impaired Myogenic Differentiation is Associated With Decreased Myoblast Glycolytic Function.

During myoblast proliferation, EtOH decreased glycolytic metabolism and increased maximal OCR, suggesting that myoblast metabolic phenotype was dysregulated with EtOH. The EtOH-induced decrease in ECAR was associated with decreased differentiation. These findings suggest that EtOH-mediated shifts in metabolic phenotype may underlie impaired differentiation, which has important clinical implications for myogenesis in those affected by alcoholic myopathy.