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Enzyme activities of energy supplying metabolism were measured in muscle specimens of the brachial biceps or anterior tibial muscles both of alcoholic patients without neuropathy and of alcoholic patients with clinical manifestations of peripheral disease. Clinical, electromyographic, and nerve conduction studies were performed before the beginning of the biochemical measurements. Our electrophysiologic results suggest that an axonal lesion of peripheral nerves in chronic alcoholics occurs first, and that the distal ends of the motor nerve fibres are early affected. The enzyme activities of glycogen phosphorylase, triosephosphate dehydrogenase, and lactate dehydrogenase were significantly decreased in both tibial anterior muscles of chronic alcoholics with peripheral neuropathy and in the biceps brachial muscles of alcoholics without any clinical signs of neurogenic damage. The decrease of these activities seemed to be a more sensitive indicator of the beginning of an alcoholic neuropathy than the electromyographic findings. The activities of a-glycerophosphate dehydrogenase, 3-hydroxyacyl-CoA-dehydrogenase, citrate synthase, and succinate dehydrogenase were slightly decreased and the activities of hexokinase and 6-phosphogluconate dehydrogenase slightly increased in patients with alcoholic neuropathy. Both changes of enzyme activities and pathologic signs in the EMG pattern appeared to be more extensive in the tibial anterior muscles than in the biceps brachial muscles. A muscle enzyme pattern showing decreased activities of lactate dehydrogenase and triosephosphate dehydrogenase, as well as unchanged or slightly increased activity of a-glycerophosphate dehydrogenase, might be an indication of chronic alcohol abuse.