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
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.