Whole-body oxidation rates of branched chain amino acids (BCAA) are increased during catabolic diseases. A significant role for muscle in this feature has been suggested and, therefore, activities of the rate limiting enzyme in the degradative pathway of the BCAA in muscle were investigated in a catabolic rat model (intraperitoneal zymosan injection). Both actual and total activities of the branched chain alpha-keto acid dehydrogenase complex zymosan treated rats and compared with values measured in pair fed and ad libitum fed controls. The actual activity and the percentage of the enzyme in the active form were increased 2 and 6 days after the zymosan challenge. Total activity of the BC-complex and the activities of mitochondrial marker enzymes were reduced 2 days after zymosan treatment. We conclude that zymosan treatment leads to (1) a reduction of the mitochondrial content in skeletal muscle and (2) a prolonged activation of the BC-complex in muscle which may explain enhanced oxidation of BCAA during catabolic diseases.