Beta2-agonist salbutamol augments hypertrophy in MHCIIa fibers and sprint power output but not muscle force during 11 weeks of resistance training in young men
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In this study, we examined the effect of beta2-agonist salbutamol at oral doses during a period of resistance training on sprint performance, quadriceps contractile function, skeletal muscle hypertrophy, fiber-type composition, maximal activity of enzymes of importance for anaerobic energy turnover, and sarcoplasmic reticulum Ca2+-handling in young men. Twenty-six men (23±2 years;mean±SD) were randomized to daily intake of oral salbutamol (16 mg/d;RES+SAL) or placebo (RES) during 11 weeks full-body resistance training 3 times/week. Mean power output during 10s maximal cycling increased more (P=0.027) in RES+SAL (+12%) than in RES (+7%), whereas peak power output increased similarly (RES+SAL:+8%;RES:+7%;P=0.400). Quadriceps dynamic peak torque and maximal voluntary isometric torque increased by 13 and 14% (P≤0.001) in RES+SAL and 13 and 13% (P≤0.001) in RES, respectively. Myosin heavy chain (MHC) isoform distribution transitioned from MHCI and MHCIIx towards MHCIIa in RES+SAL (P=0.002), but not in RES (P=0.323). MHCIIa cross-sectional-area increased more (P=0.040) in RES+SAL (+35%) than RES (+21%). Sarcoplasmic reticulum Ca2+-release rate increased in both groups (RES+SAL:+9%,P=0.048;RES:+13%,P=0.008), whereas Ca2+-uptake rate increased only in RES (+12%,P=0.022) but not different from the non-significant change in RES+SAL (+2%,P=0.484). Maximal activity of lactate dehydrogenase increased only in RES+SAL (+13%,P=0.008). Muscle content of the dihydropyridine receptor, ryanodine receptor 1, and sarcoplasmic reticulum Ca2+-ATPase isoform 1 and 2 did not change with the intervention in either group (P≥0.100). These observations suggest that salbutamol is a muscle anabolic drug, which induces greater sprint mean power output, without affecting peak power output and muscle strength when ingested during a period of resistance training.
|Tidsskrift||Journal of Applied Physiology|
|Status||Accepteret/In press - 24 dec. 2020|
Afventer publicering som [Epub ahead of print] samt tildeling af CURIS-nummer.
- Det Natur- og Biovidenskabelige Fakultet