Muscle damage produced by chronic alcohol consumption.

The effects of chronic alcohol consumption on skeletal muscle, independent of nutritional factors, were studied. Chronic alcohol ingestion led to striking ultrastructural changes in skeletal muscle, including intracellular edema, enlarged and distorted mitochondria, dilatation of sarcoplasmic reticulum, and increased amounts of fat and glycogen. Actomyosin was isolated from skeletal muscle of baboons and volunteers fed alcohol. In this preparation, ATPase activity and the calcium sensitivity of ATPase were decreased. The isolated actomyosin displayed reduced contractility in vitro, measured by the association of actin and myosin and the response to adenosine diphosphate (ADP). In 2 of 3 volunteers, isolated membranes of the sarcoplasmic reticulum exhibited decreased calcium uptake. The pressure-rate product was increased in some of the volunteers after submaximal or maximal work. The changes decribed in this study were found after alcohol administration had been discontinued, and they may play a role in the development of alcoholic myopathy and cardiomyopathy.