Derangements of muscle composition, ion transport, and oxygen consumption in chronically alcoholic dogs.

Abstract

Muscle ion composition, Na-K-ATPase activity, tissue respiration, and transmembrane potential differences were measured after 28 and 56 days of ethanol consumption (6.2 g X kg-1 X day-1) or an isocaloric amount of glucose in 12 and 4 dogs, respectively. Ethanol and glucose were given as supplements to an otherwise nutritious diet. After 28 and 56 days of alcohol consumption, skeletal muscle contents of phosphorus, magnesium, and potassium were significantly reduced as compared with either the control values or those in glucose-fed animals. In alcohol-fed animals, muscle sodium chloride, and calcium were significantly elevated. Ethanol consumption also resulted in hyperpolarization of the resting transmembrane potential of skeletal muscle fibers and a significant increase in Na-K-ATPase activity. No change was noted in Mg-ATPase activity. The increase in Na-K-ATPase activity was accompanied by increased sodium transport-dependent respiration. These results indicate that a subclinical myopathy may be induced by alcohol in the dog. Malnutrition did not appear to be a factor in this study, and thus the changes observed are believed to be due to ethanol per se. The magnitude and direction of these changes are similar to those observed in the skeletal muscle of chronically alcoholic humans. The changes in Na-K-ATPase activity and sodium transport-dependent respiration may represent adaptive responses of the muscle cell to ion transport or membrane disorders induced by ethanol.