Activity, O2 consumption, and body composition were measured in female rats with lesions of the ventromedial hypothalamus (VMH). One group of lesioned rats was food restricted to maintain body weights at control levels. O2 consumption of these food-restricted VMH-lesioned rats was 13% lower than that of nonlesioned rats. About half this energy savings accrued from reduced activity; the remainder resulted from a decline in resting metabolic rate (RMR). Though matched in weight to controls, the body composition of the restricted VMH-lesioned rats was abnormal. Their carcass protein was reduced by 12%, whereas fat was elevated 200%. The replacement of lean metabolically active tissue by carcass fat appears to underlie the reduction in RMR, an interpretation supported by multiple-regression analysis of carcass composition. Ad libitum-fed VMH-lesioned rats did not show this carcass protein decline, though their fat was elevated 895%. These results confirm that reduced activity contributes to energy savings and weight gain after VMH lesions. Likewise, restricting weight of VMH-lesioned rats to control levels reduced RMR, apparently because carcass protein declines. But, since ad libitum-fed female VMH-lesioned rats do not display reduced carcass protein, the historic assumption that RMR reductions contribute to their obesity appears unwarranted.