The effect of the beta-adrenergic agonist cimaterol on bovine and chicken primary myotubes was assessed. Cimaterol at 10-100 nM concentrations reduced cathepsin B benzyloxy-carbonyl-Arg-Arg-4-methyl-7-coumarylamide hydrolyzing activity, as well as benzyloxycarbonyl-Phe-Arg-4-methyl-7-coumarylamide hydrolysis, which is a substrate for both cathepsin B and cathepsin L. Maximum effect was observed after 6-16 h treatment. Cathepsin H Arg-4-methyl-7-coumarylamide hydrolyzing activity was low and not significantly affected by cimaterol treatment. Despite decreasing cathepsin activities, cimaterol also increased proteolysis rates but induced no detectable effect on protein synthesis rates. These observations suggest that beta-agonists, as a result of a direct action on muscle, can decrease cathepsin activities but that beta-agonist-induced muscle hypertrophy may not be due to a direct effect on muscle cells.