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Skeletal muscle hypertrophy and anti‐atrophy effects of clenbuterol are mediated by the β2‐adrenergic receptor
Author(s) -
Hinkle Richard T.,
Hodge Karen M.B.,
Cody David B.,
Sheldon Russell J.,
Kobilka Brian K.,
Isfort Robert J.
Publication year - 2002
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.10092
Subject(s) - muscle hypertrophy , denervation , clenbuterol , medicine , endocrinology , atrophy , agonist , muscle atrophy , skeletal muscle , receptor , gastrocnemius muscle , adrenergic
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