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Muscle damage produced by chronic alcohol consumption.

E Rubin, A M Katz, C S Lieber

    The American Journal of Pathology
    |June 1, 1976
    PubMed
    Summary

    Chronic alcohol consumption damages skeletal muscle structure and function, leading to reduced contractility and impaired calcium regulation. These alcohol-induced muscle changes persist even after cessation, potentially contributing to alcoholic myopathy.

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    Area of Science:

    • Biochemistry
    • Cell Biology
    • Physiology

    Background:

    • Chronic alcohol consumption is a significant health concern.
    • Alcohol's impact on skeletal muscle, independent of nutrition, requires detailed investigation.
    • Understanding these effects is crucial for addressing alcoholic myopathy and cardiomyopathy.

    Purpose of the Study:

    • To investigate the ultrastructural and functional effects of chronic alcohol ingestion on skeletal muscle.
    • To assess the impact on actomyosin function and sarcoplasmic reticulum calcium handling.
    • To determine if observed changes persist after alcohol withdrawal.

    Main Methods:

    • Electron microscopy to observe skeletal muscle ultrastructure.
    • Isolation and biochemical analysis of actomyosin from baboon and human skeletal muscle.

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  • Measurement of ATPase activity, calcium sensitivity, and contractility of actomyosin.
  • Assessment of calcium uptake by isolated sarcoplasmic reticulum membranes.
  • Evaluation of cardiovascular response (pressure-rate product) during exercise.

    • Main Results:

    • Chronic alcohol ingestion caused significant ultrastructural damage, including intracellular edema and mitochondrial distortion.
    • Isolated actomyosin exhibited decreased ATPase activity, reduced calcium sensitivity, and impaired contractility.
    • Sarcoplasmic reticulum calcium uptake was diminished in a majority of subjects.
    • Cardiovascular function showed altered pressure-rate product during exertion.

    Conclusions:

    • Chronic alcohol consumption induces severe ultrastructural and functional deficits in skeletal muscle.
    • These alcohol-related muscle impairments, including reduced contractility and calcium dysregulation, persist post-cessation.
    • The findings suggest a direct role for alcohol-induced myopathy in the pathogenesis of alcoholic myopathy and cardiomyopathy.