Congestive heart failure is a condition associated with increased plasma norepinephrine levels, which have been demonstrated to impair glucose handling. In the present study, 10 patients suffering from congestive heart failure and 10 healthy age- and body mass index-matched subjects were submitted to a hyperinsulinemic (insulin infusion rate, 0.5 mU/kg · min⁻¹) glucose clamp, while simultaneous d-³H-glucose infusion and indirect calorimetry allowed for determination of glucose turnover parameters and substrate oxidation, respectively. On a separate day, basal local (myocardial) indirect calorimetry was also performed. Our data demonstrate that in congestive heart failure, fasting myocardial glucose oxidation (Gox) was inhibited with a simultaneous increase in lipid oxidation (Lox). In our patients, a significant decrease in total-body insulin-stimulated glucose metabolism (31.0 ± 0.5 v 20.3 ± 0.4 μmol/kg · min⁻¹, P < .01) and nonoxidative glucose metabolism (18.9 ± 1.1 v 11.0 ± 0.5 μmol/kg · min⁻¹, P < .05) was also found. Such latter changes were also associated with a simultaneous overdrive of Lox (0.4 ± 0.2 v 1.9 ± 0.2 μmol/kg · min⁻¹, P < .02) that was correlated with an enhanced availability of plasma free fatty acids (FFAs).