β₂-Adrenergic agonist salbutamol augments hypertrophy in MHCIIa fibers and sprint mean power output but not muscle force during 11 weeks of resistance training in young men

In this study, we examined the effect of β₂-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 yr; means ± SD) were randomized to daily intake of oral salbutamol (16 mg/day; RES+SAL) or placebo (RES) during 11 wk of full-body resistance training 3 times/wk. Mean power output during 10-s maximal cycling increased more (P = 0.027) in RES+SAL (+ 12%) than in RES ( þ 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 toward 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 was 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 iso-form 1 and 2 did not change with the intervention in either group (P ≥ 0.100). These observations indicate that the enhancement of sprint mean power output induced by salbutamol is at least partly attributed to greater hypertrophy of MHCIIa fibers and transition toward the MHCIIa isoform.