Beta2 -agonist increases skeletal muscle interleukin 6 production and release in response to resistance exercise in men.

Abstract

ObjectiveSeveral tissues produce and release interleukin‐6 (IL‐6) in response to beta2‐adrenergic stimulation with selective agonists (beta2‐agonists). Moreover, exercise stimulates muscle IL‐6 production, but whether beta2‐agonists regulate skeletal muscle production and release of IL‐6 in humans in association with exercise remains to be clarified. Thus, we investigated leg IL‐6 release in response to beta2‐agonist salbutamol in lean young men at rest and in recovery from resistance exercise.DesignThe study employed a randomized controlled crossover design, where 12 men ingested either salbutamol (16 mg) or placebo for 4 days, followed by the last dose (24 mg) administered 1½ h before exercise. Arterial and femoral venous plasma IL‐6 as well as femoral artery blood flow was measured before and ½–5 h in recovery from quadriceps muscle resistance exercise. Furthermore, vastus lateralis muscle biopsies were collected ½ and 5 h after exercise for determination of mRNA levels of IL‐6 and Tumor Necrosis Factor (TNF)‐α.ResultsAverage leg IL‐6 release was 1.7‐fold higher (p = 0.01) for salbutamol than placebo, being 138 ± 76 and 79 ± 66 pg min−1 (mean ± SD) for salbutamol and placebo, respectively, but IL‐6 release was not significantly different between treatments within specific sampling points at rest and after exercise. Muscle IL‐6 mRNA was 1.5‐ and 1.7‐fold higher (p = 0.001) for salbutamol than placebo ½ and 5 h after exercise, respectively, whereas no significant treatment differences were observed for TNF‐α mRNA.ConclusionsBeta2‐adrenergic stimulation with high doses of the selective beta2‐agonist salbutamol, preceeded by 4 consecutive daily doses, induces transcription of IL‐6 in skeletal muscle in response to resistance exercise, and increases muscle IL‐6 release in lean individuals.