Muscle plasticity and β 2-adrenergic receptors: Adaptive responses of β 2-adrenergic receptor expression to muscle hypertrophy and atrophy

Shogo Sato, Ken Shirato, Kaoru Tachiyashiki, Kazuhiko Imaizumi

    Research output: Contribution to journalArticlepeer-review

    34 Citations (Scopus)


    We discuss the functional roles of β 2 -adrenergic receptors in skeletal muscle hypertrophy and atrophy as well as the adaptive responses of 2 -adrenergic receptor expression to anabolic and catabolic conditions. β 2-Adrenergic receptor stimulation using anabolic drugs increases muscle mass by promoting muscle protein synthesis and/or attenuating protein degradation. These effects are prevented by the downregulation of the receptor. Endurance training improves oxidative performance partly by increasing β 2-adrenergic receptor density in exercise-recruited slow-twitch muscles. However, excessive stimulation of β 2- adrenergic receptors negates their beneficial effects. Although the preventive effects of β 2-adrenergic receptor stimulation on atrophy induced by muscle disuse and catabolic hormones or drugs are observed, these catabolic conditions decrease β 2-adrenergic receptor expression in slow-twitch muscles. These findings present evidence against the use of β 2-adrenergic agonists in therapy for muscle wasting and weakness. Thus, β 2-adrenergic receptors in the skeletal muscles play an important physiological role in the regulation of protein and energy balance.

    Original languageEnglish
    Article number729598
    JournalJournal of Biomedicine and Biotechnology
    Publication statusPublished - 2011

    ASJC Scopus subject areas

    • Biotechnology
    • Molecular Medicine
    • Genetics
    • Molecular Biology
    • Health, Toxicology and Mutagenesis
    • Medicine(all)


    Dive into the research topics of 'Muscle plasticity and β <sub>2</sub>-adrenergic receptors: Adaptive responses of β <sub>2</sub>-adrenergic receptor expression to muscle hypertrophy and atrophy'. Together they form a unique fingerprint.

    Cite this