Obesity-prone (OP) rodents are used as models of human obesity predisposition. The goal of the present study was to identify preexisting defects in energy expenditure components in OP rats. Two studies were performed. In the first one, male Wistar rats (n = 48) were fed a high-carbohydrate diet (HCD) for 3 wk and then a high-fat diet (HFD) for the next 3 wk. This study showed that adiposity gain under HCD was 2.9-fold larger in carbohydrate-sensitive (CS) than in carbohydrate-resistant (CR) rats, confirming the concept of "carbohydrate-sensitive" rats. Energy expenditure (EE), respiratory quotient (RQ), caloric intake (CI), and locomotor activity measured during HFD identified no differences in EE and RQ between fat-resistant (FR) and fat-sensitive (FS) rats, and indicated that obesity developed in FS rats only as the result of a larger CI not fully compensated by a parallel increase in EE. A specific pattern of spontaneous activity, characterized by reduced activity burst intensity, was identified in FS rats but not in CS ones. This mirrors a previous observation that under HCD, CS but not FS rats, exhibited bursts of activity of reduced intensity. In a second study, rats were fed a HFD for 3 wk, and the components of energy expenditure were examined by indirect calorimetry in 10 FR and 10 FS rats. This study confirmed that a low basal EE, reduced thermic effect of feeding, defective postprandial energy partitioning, or a defective substrate utilization by the working muscle are not involved in the FS phenotype.