Skeletal muscle myopathy is caused by prolonged ethanol misuse and affects between half and two-thirds of chronic alcohol misusers. This chronic myopathy is characterized by a selective reduction in Type II (fast twitch) fibre area; Type I (slow twitch) fibres are relatively unaffected. The myopathy is not mediated by the patients' corticosteroid and nutritional status, liver dysfunction or neurological changes, and there is little correlation between alcoholic myopathy and alcohol intake. However, plasma alpha-tocopherol and selenium levels in myopathic alcoholics are reduced. The myopathy may in some way be related to the reduced fractional rates of skeletal muscle protein synthesis that occur in alcohol misusers and implicates free radical reactions in the pathogenesis of the myopathy. We have established a rat model of chronic alcoholic myopathy. In this model anatomically distinct skeletal muscles were taken to represent Type I (i.e. soleus) or Type II (i.e. plantaris) fibres. There were selective losses of Type II muscle protein at the end of 6 weeks of ethanol feeding. These changes were also not apparently mediated by nutritional limitations, neurological changes or liver dysfunction. Skeletal muscle protein synthesis was also reduced, as was plasma alpha tocopherol and selenium levels. Thus the rat model is amendable for further work to elucidate the molecular mechanisms responsible for alcohol-induced muscle loss.