We investigated stable cirrhotic patients f o r muscle glycogen content. Muscle biopsy samples were taken of 14 patients after overnight fasting. Electron microscopy showed normal intracellular distribution of glycogen (n = 8). Muscle glycogen concentration was 16.5 f 7.1 gm/kg wet muscle weight (normal range, 10 to 20 gmkg). Basal, early postabsorptive, exerciseinduced and insulin-induced respiratory quotients as well as insulin sensitivity (euglycemic clamp technique, 7.2 pmol insdidkg body weight/min) and glucose tolerance were assessed. T h e glucose disposal rate was 23.0 2 10.1 Fmol/kg/min (mean f S.D.), indicating moderate insulin resistance in these patients. We found no association between basal muscle glycogen content and basal o r postprandial respiratory quotient, insulin sensitivity, nutritional status or glucose tolerance. However, there was a positive correlation between muscle glycogen content and exercise, as well as insulin-induced respiratory quotient (r = 0.651, p < 0.03 and r = 0.587, p < 0.03, respectively). We conclude that postabsorptive muscle glycogen stores, which are effectively maintained in patients with cirrhosis, are one determinant of exercise-induced and insulin-induced whole body fuel metabolism in these patients. (HEPATOLOGY 1994;20: 135-141.) Patients with cirrhosis are frequently malnourished without obvious relation to the severity of liver disease. However, several metabolic abnormalities such as depleted liver glycogen stores, reduced hepatic glucose production, low basal respiratory quotients and hy-perinsulinemia, as well as insulin resistance, are frequently seen in cirrhotic patients (1-3). Because muscle glycogen stores are the main source of skeletal muscle carbohydrate supply, altered muscle glycogen content itself may contribute to the metabolic alterations in cirrhosis that finally affect nutritional status. No study has yet investigated the potential impact of altered skeletal