PURPOSE: The aim of the present study was to investigate the effect of the beta2-agonist terbutaline (TER) on power output and muscle metabolism during maximal sprint cycling.
METHODS: In a randomized double-blind crossover design, nine moderately trained men (VO2max: 4.6±0.2 L[BULLET OPERATOR]min) conducted a 10-s cycle sprint after inhalation of either 15 mg TER or placebo (PLA). A muscle biopsy was collected before and <10 s after the sprint, and analyzed for metabolites.
RESULTS: Mean and peak power during the sprint were 8.3±1.1 and 7.8±2.5 % higher (P<0.05) in TER than in PLA, respectively. Moreover, net rate of glycogenolysis (6.5±0.8 vs. 3.1±0.7 mmol glucosyl units kg dw s) and glycolysis (2.4±0.2 vs. 1.6±0.2 mmol glucosyl units kg dw s) were higher (P<0.05) in TER than in PLA. After the sprint, ATP was reduced in PLA (P<0.05), but not in TER. During the sprint, there was no difference in breakdown of phosphocreatine (PCr) between treatments. Estimated anaerobic ATP utilization was 9.2 ±4.0 % higher (P<0.05) in TER than in PLA. After the sprint, ATP was lowered (P <0.05) by 25.7±7.3 % in type II fibers in PLA with no reduction in TER. Before the sprint, PCr was 24.5±7.2 % lower (P <0.05) in type II fibers in TER than in PLA. In PLA, breakdown of PCr was 50.2±24.8 % higher (P <0.05) in type II than in type I fibers with no difference in TER.
CONCLUSION: The present study shows that a terbutaline-induced increase in power output is associated with increased rates of glycogenolysis and glycolysis in skeletal muscles. Furthermore, as terbutaline counteracted a reduction in ATP in type II fibers, terbutaline may postpone fatigue development in these fibers.