Chronic administration of some beta-adrenergic agonists markedly stimulates hypertrophy of skeletal muscles. It appears that type II fibers are more responsive to beta-adrenergic agonists than type I fibers. The hypertrophic effect of beta-adrenergic agonists is transient, with the effect diminishing during prolonged treatment. Similarly, some cellular responses including the increase in RNA concentration and the decrease in calpain I activity are also short-lived. Recent evidence suggests that the temporal response is associated with decreased beta-adrenoceptor density. Both increased rate of protein synthesis and/or decreased protein degradation have been suggested as the mechanism of action of these compounds on hypertrophy of skeletal muscles. It is important to consider the temporal nature of cellular responses to chronic treatment of beta-adrenergic agonists as well as the differential effects of these compounds on protein metabolism among skeletal muscle fiber types when investigating the mechanism(s) of action of these compounds.