The increased plasma levels of αamino-n-butyric acid (AANB) and branched chain amino acids (BCA) are commonly observed after chronic ethanol consumption. These changes are respectively attributed to enhanced turnover of hepatic glutathione (GSH) and increased muscle protein catabolism. On the other hand, the ethanol-induced decrease in plasma level of alanine (ALA) is thought to be caused by enhanced hepatic production of lactate. The objective of this study was to investigate how these alterations can be exhibited in rats subjected to sustained ethanol intoxication and concomitant optimal nutrition. Plasma lactate levels and content of free amino acids in the liver and gastroenemius muscle were also determined to facilitate better understanding of factors involved in the aforementioned changes. Male Wistar rats were intragastrically infused with liquid diet plus ethanol or isocaloric glucose for 30 days. This regimen resulted in sustained blood alcohol levels and optimal nutrition as indicated by similar weight gains of ethanol or pair-fed animals to that of chow-fed rats. Hepatic content and plasma concentrations of ALA were not decreased in the ethanol-fed group, and the plasma lactate levels in these animals were not different from those in the controls. Levels of BCA (valine, isoleucine, leucine) were increased by 42–44% in plasma and 15–23% in the muscle of the ethanol-fed rats. AANB concentrations were significantly increased by 5-fold in the muscle and by 4-fold in plasma with only a 2-fold increase in the liver. These data indicate that the reported ethanol-induced depression in the plasma level and liver content of ALA can be prevented by optimal nutrition. Furthermore, the increased plasma levels of AANB seem to be associated more closely with increased protein turnover in the muscle than with the enhanced GSH metabolism in the liver. The elevated BCA levels in plasma are also likely to be specific effects of ethanol stimulating the muscle protein turnover.