Male mice selected for rapid 3 to 6 wk postweaning gain (M16) and unselected controls (ICR) were ad libitum fed a stock diet containing 0, 50 or 200 ppm cimaterol, a beta-agonist, from 4 to 7 or 4 to 10 wk of age. Mortality rate was higher in M16 than in ICR mice fed cimaterol (12.5 vs 1.3%; P less than .01). No mortalities occurred in either line fed the control diet. Line M16 exceeded (P less than .01) ICR in growth rate, feed intake, feed efficiency and lean index. Line X cimaterol level interactions (P less than .01) were found for the first three of these traits, although cimaterol level did not change line ranking. Epididymal fat as a percentage of empty body weight decreased at a faster rate in M16 than in ICR as cimaterol level increased. At 0 and 50 ppm, M16 exceeded ICR (P less than .05), but at 200 ppm there was no line difference (P greater than .05). Line M16 exceeded (P less than .05) ICR in blood glucose (5%), nonesterified fatty acids (4%) and lactate at 7 wk (9%), but lactate was higher in ICR at 10 wk (13%). Lines were not different in blood urea-N. Compared to zero cimaterol level, at 50 and 220 ppm glucose decreased (14% and 23%; P less than .05), nonesterified fatty acids decreased (3% and 29%; P less than .05), lactate increased (9% and 11%; P less than .05) and blood urea-N increased (3% and 16%; P less than .05). There were no line X cimaterol level interactions for blood metabolites. Differences in mortality rate, growth, feed consumption, feed efficiency and epididymal fat pad percentage between the high-growth and control lines in response to cimaterol may reflect genetic differences in mechanisms of metabolic regulation.