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Skeletal muscle hypertrophy is promoted in vivo by administration of beta-adrenergic receptor (betaAR) agonists. Chicken skeletal muscle cells were treated with 1 microM isoproterenol, a strong betaAR agonist, between days 7 and 10 in culture. betaAR population increased by approximately 40% during this treatment; however, the ability of the cells to synthesize cyclic adenosine monophosphate (cAMP) was diminished by twofold. Neither the basal concentration of cAMP nor the quantity of myosin heavy chain (MHC) was affected by the 3-d exposure to isoproterenol. To understand further the relationship between intracellular cAMP levels, betaAR population, and muscle protein accumulation, intracellular cAMP levels were artificially elevated by treatment with 0-10 betaM forskolin for 3 d. The basal concentration of cAMP in forskolin-treated cells increased up to sevenfold in a dose-dependent manner. Increasing concentrations of forskolin also led to an increase in betaAR population, with a maximum increase of approximately 40-60% at 10 microM forskolin. A maximum increase of 40-50% in the quantity of MHC was observed at 0.2 microM forskolin, but higher concentrations of forskolin reduced the quantity of MHC back to control levels. At 0.2 microM forskolin, intracellular levels of cAMP were higher by approximately 35%, and the betaAR population was higher by approximately 30%. Neither the number of muscle nuclei fused into myotubes nor the percentage of nuclei in myotubes was affected by forskolin at any of the concentrations studied.