Actions of a beta-adrenergic agonist on muscle protein metabolism in intact, adrenalectomized, and dexamethasone-supplemented adrenalectomized rats

Abstract The objectives were to investigate the possibility that glucocorticoids potentiate actions of beta-adrenergic agonists in skeletal muscle and to elucidate mechanisms by which glucocorticoids and beta-adrenergic agonists effect control of muscle growth. Forty-eight male rats were assigned to one of six treatments, which consisted of a sham-adrenalectomized control, sham-adrenalectomized supplemented with cimaterol, adrenalectomized, adrenalectomized supplemented with cimaterol, adrenalectomized supplemented with dexamethasone, and adrenalectomized supplemented with cimaterol and dexamethasone. After 8 days, muscle samples were collected for assay of nucleic acid contents and proteinase (cathepsins and calpains) and calpastatin activities. Both glucocorticoid status and cimaterol influenced muscle growth and metabolism. Adrenalectomy reduced muscle RNA content and dexamethasone restored RNA. Cimaterol increased RNA levels, increased total DNA content, reduced calpain activities, and increased calpastatin activity. This implies that cimaterol has potential to regulate both protein synthesis and degradation. We did not find evidence for glucocorticoids potentiating actions of cimaterol. Instead, we determined that cimaterol antagonized certain growth-inhibiting properties of the glucocorticoids. Effects of cimaterol on muscle growth and on metabolic parameters were highly dependent on glucocorticoid status suggesting that the variations in muscle responses to beta-adrenergic agonists, which have been detected in other studies, may be due to variations in glucocorticoid status of experimental animals. ( J. Nutr. Biochem. 5:43–49, 1994 .)