Alcoholic myopathy is considered as multifactor desease. Mechanisms, leading to muscle pathology of excessive alcohol consumption, have several options for implementation. Thus, the development of alcoholic myopathy is accompanied by changes in oxidation-reduction status and antioxidant disbalance in skeletal muscle. Chronic alcohol intake and acute alcohol intoxication can reduce the rate of protein synthesis, including myofibrillar proteins. Alcohol abuse results in damage of signaling cascades, and increases the level of apoptosis in skeletal muscle.
