Abnormalities in energy metabolism may play an important role in the development of hypertensive heart failure. However, the transition from compensated hypertrophy to heart failure is not fully understood in terms of energy metabolism. In Dahl salt-sensitive (DS) and salt-resistant (DR) rats, myocardial fatty acid and glucose uptakes were determined with ¹³¹I-9-methylpentadecanoic acid (9MPA) and ¹⁴C-deoxyglucose (DG), fatty acid -oxidation with a thin-layer chromatography, and insulin-stimulated glucose uptake with euglycemic hyperinsulinemic glucose clamp. The rats were fed a diet containing 8% NaCl after the age of 6 weeks that resulted in the development of compensated hypertrophy in the DS rats at 12 weeks of age, leading ultimately to heart failure by 18 weeks. Uptake of DG increased markedly with age in the DS rats, whereas 9MPA uptake was marginally but significantly increased only in animals aged 12 weeks. The ratio of 9MPA -oxidation metabolites to total uptake in the DS rats was significantly lower (p<0.05) at 12 (37%) and 18 weeks (34%) compared to at 6 weeks (45%). Insulin increased DG uptake more than two-fold in the DS rats at 6 weeks although this increase was markedly attenuated at 12 and 18 weeks (11% and 8%, respectively). Our data suggest that in a hypertrophied heart prior to heart failure, fatty acid oxidation is impaired and the capacity to increase glucose uptake during insulin stimulation markedly reduced. These changes in both glucose and fatty acid metabolism occurring in association with myocardial hypertrophy may have a pathogenic role in the subsequent development of heart failure.