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- Hostrup, Morten, et al.
(författare)
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Mechanisms underlying enhancements in muscle force and power output during maximal cycle ergometer exercise induced by chronic beta(2)-adrenergic stimulation in men
- 2015
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 119:5, s. 475-486
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Tidskriftsartikel (refereegranskat)abstract
- The study was a randomized placebo-controlled trial investigating mechanisms by which chronic beta(2)-adrenergic stimulation enhances muscle force and power output during maximal cycle ergometer exercise in young men. Eighteen trained men were assigned to an experimental group [oral terbutaline 5 mg/30 kg body weight (bw) twice daily (TER); n = 9] or a control group [placebo (PLA); n = 9] for a 4-wk intervention. No changes were observed with the intervention in PLA. Isometric muscle force of the quadriceps increased (P <= 0.01) by 97 +/- 29 N (means +/- SE) with the intervention in TER compared with PLA. Peak and mean power output during 30 s of maximal cycling increased (P <= 0.01) by 32 +/- 8 and 25 +/- 9 W, respectively, with the intervention in TER compared with PLA. Maximal oxygen consumption ((V) over dotO(2)max) and time to fatigue during incremental cycling did not change with the intervention. Lean body mass increased by 1.95 +/- 0.8 kg (P <= 0.05) with the intervention in TER compared with PLA. Change in single fiber cross-sectional area of myosin heavy chain (MHC) I (1,205 +/- 558 mu m(2); P <= 0.01) and MHC II fibers (1,277 +/- 595 mu m(2); P <= 0.05) of the vastus lateralis muscle was higher for TER than PLA with the intervention, whereas no changes were observed in MHC isoform distribution. Expression of muscle proteins involved in growth, ion handling, lactate production, and clearance increased (P <= 0.05) with the intervention in TER compared with PLA, with no change in oxidative enzymes. Our observations suggest that muscle hypertrophy is the primary mechanism underlying enhancements in muscle force and peak power during maximal cycling induced by chronic beta(2-)adrenergic stimulation in humans.
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| 2. |
- Kalsen, Anders, et al.
(författare)
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Inhaled Beta2-agonist Increases Power Output and Glycolysis during Sprinting in Men.
- 2016
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Ingår i: Medicine & Science in Sports & Exercise. - 0195-9131 .- 1530-0315. ; 48:1, s. 39-48
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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