Inhaled Beta2-agonist increases power output and glycolysis during sprinting in men

TY - JOUR

T1 - Inhaled Beta2-agonist increases power output and glycolysis during sprinting in men

AU - Kalsen, Anders

AU - Hostrup, Morten

AU - Söderlund, Karin

AU - Karlsson, Sebastian

AU - Backer, Vibeke

AU - Bangsbo, Jens

N1 - CURIS 2016 NEXS 012

PY - 2016

Y1 - 2016

N2 - Purpose: The aim of the present study was to investigate the effects of the beta2-Agonist terbutaline (TER) on power output and muscle metabolism during maximal sprint cycling. Methods: In a randomized double-blind cross-over design, nine moderately trained men (VO2max = 4.6 ± 0.2 LIminj1) conducted a 10-s cycle sprint after inhalation of either 15 mg of TER or placebo (PLA). A muscle biopsy sample was collected before and G10 s after the sprint and was analyzed for metabolites. Results: The mean power and peak power during the sprint were 8.3% ± 1.1% and 7.8% ± 2.5% higher (P < 0.05) with TER than with PLA, respectively. Moreover, the net rates of glycogenolysis (6.5 ± 0.8 vs 3.1 ± 0.7 mmol glucosyl unitsIkg dry weightj1Isj1) and glycolysis (2.4 ± 0.2 vs 1.6 ± 0.2 mmol glucosyl unitsIkg dry weightj1Isj1) were higher (P < 0.05) with TER than with PLA. After the sprint, adenosine triphosphate (ATP) was reduced with PLA (P < 0.05) but not with TER. During the sprint, there was no difference in the breakdown of phosphocreatine (PCr) between treatments. Estimated anaerobic ATP utilization was 9.2% ± 4.0% higher (P < 0.05) with TER than with PLA. After the sprint, ATP in Type II fibers was lowered (P < 0.05) by 25.7% ± 7.3% with PLA but was not reduced with TER. Before the sprint, PCr in Type II fibers was 24.5% ± 7.2% lower (P < 0.05) with TER than with PLA. With PLA, breakdown of PCr was 50.2% ± 24.8% higher (P < 0.05) in Type II fibers (vs Type I fibers), whereas no difference was observed between fiber types with TER. Conclusion: The present study shows that a TER-induced increase in power output is associated with increased rates of glycogenolysis and glycolysis in skeletal muscles. Furthermore, as TER counteracts a reduction in ATP in Type II fibers, TER may postpone fatigue development in these fibers.

AB - Purpose: The aim of the present study was to investigate the effects of the beta2-Agonist terbutaline (TER) on power output and muscle metabolism during maximal sprint cycling. Methods: In a randomized double-blind cross-over design, nine moderately trained men (VO2max = 4.6 ± 0.2 LIminj1) conducted a 10-s cycle sprint after inhalation of either 15 mg of TER or placebo (PLA). A muscle biopsy sample was collected before and G10 s after the sprint and was analyzed for metabolites. Results: The mean power and peak power during the sprint were 8.3% ± 1.1% and 7.8% ± 2.5% higher (P < 0.05) with TER than with PLA, respectively. Moreover, the net rates of glycogenolysis (6.5 ± 0.8 vs 3.1 ± 0.7 mmol glucosyl unitsIkg dry weightj1Isj1) and glycolysis (2.4 ± 0.2 vs 1.6 ± 0.2 mmol glucosyl unitsIkg dry weightj1Isj1) were higher (P < 0.05) with TER than with PLA. After the sprint, adenosine triphosphate (ATP) was reduced with PLA (P < 0.05) but not with TER. During the sprint, there was no difference in the breakdown of phosphocreatine (PCr) between treatments. Estimated anaerobic ATP utilization was 9.2% ± 4.0% higher (P < 0.05) with TER than with PLA. After the sprint, ATP in Type II fibers was lowered (P < 0.05) by 25.7% ± 7.3% with PLA but was not reduced with TER. Before the sprint, PCr in Type II fibers was 24.5% ± 7.2% lower (P < 0.05) with TER than with PLA. With PLA, breakdown of PCr was 50.2% ± 24.8% higher (P < 0.05) in Type II fibers (vs Type I fibers), whereas no difference was observed between fiber types with TER. Conclusion: The present study shows that a TER-induced increase in power output is associated with increased rates of glycogenolysis and glycolysis in skeletal muscles. Furthermore, as TER counteracts a reduction in ATP in Type II fibers, TER may postpone fatigue development in these fibers.

U2 - 10.1249/MSS.0000000000000732

DO - 10.1249/MSS.0000000000000732

M3 - Journal article

C2 - 26197029

SN - 0195-9131

VL - 48

SP - 39

EP - 48

JO - Medicine and Science in Sports and Exercise

JF - Medicine and Science in Sports and Exercise

IS - 1

ER -