Skeletal muscle hypertrophy and anti-atrophy effects of clenbuterol are mediated by the β2-adrenergic receptor

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Abstract

Analyses were performed to evaluate the roles of the β1- and β2-adrenergic receptors in the skeletal muscle hypertrophy and anti-atrophy response to the β-adrenergic agonist, clenbuterol. Treatment of wild-type mice with clenbuterol resulted in statistically significant hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles and inhibition of denervation-induced atrophy of these muscles. Treatment of β1-adenergic receptor knockout mice with clenbuterol also resulted in statistically significant hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles and inhibition of denervation-induced atrophy of these muscles. In contrast, in β2-adrenergic receptor knockout mice and in mice lacking both the β1- and β2-adrenergic receptors, clenbuterol treatment did not result in hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles, nor did it inhibit denervation-induced atrophy in these muscles. Together these data demonstrate that the β2-adrenergic receptor is responsible for both the skeletal muscle hypertrophy and anti-atrophy effects of the β-adrenergic agonist clenbuterol. © 2002 Wiley Periodicals, Inc. Muscle Nerve 25: 000–000, 2002

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