Muscle disuse leads to rapid loss of muscle mass and development of insulin resistance, which may be ameliorated by beta2-agonist administration. Here, we tested the impact of the fast-acting beta2-agonist salbutamol during immobilization. In humans, salbutamol enhanced insulin-stimulated glucose disposal on the whole-body level, but not in immobilized muscle. Salbutamol decreased the efflux of amino acids from the immobilized forearm, indicating increased muscle protein synthesis and/or inhibition of breakdown, but did not affect amino acid net balance. In agreement, in mice salbutamol increased cumulative muscle protein synthesis, but did not result in a net gain of muscle mass upon immobilization, due to an accompanying increase in muscle protein turnover. Molecular analyses revealed immobilization inhibited salbutamol’s effects on muscle-transcriptome. In conclusion, salbutamol can increase muscle mass and glucose uptake, but not as effectively in inactive muscle, demonstrating that the mechanism of action and efficacy of beta2-adrenoreceptor signaling is muscle contraction dependent.
New Perspectives on the Physiological Basis of Muscle Loss (University of Exeter, UK) (2024) Proc Physiol Soc 60, SA08
Research Symposium: Effects of beta2-agonist salbutamol on muscle mass maintenance are mediated by muscle contraction
Jelle de Jong1, Tom Jameson1, Rob Andrews1, Mandy Dunlop1, Doaa Abdelrahman1, Andrew Murton1, Martien Caspers1, Nicole Worms1, Nanda Keijzer1, Qihan Cheng1, Bruno Guigas1, Esther van Duijn1, Wouter Vaes1, Arie Nieuwenhuizen1, Jaap Keijer1, Benjamin Wall1, Lars Verschuren1, Francis Stephens1, Anita van den Hoek1, Marlou Dirks1,
1Texas University Galveston United States, 2Wageningen University Wageningen Netherlands, 3TNO Leiden Netherlands, 4University of Exeter Exeter United Kingdom, 5Leiden University Leiden Netherlands, 6Wagenigen University Wageningen Netherlands,
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Where applicable, experiments conform with Society ethical requirements.