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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. |
- Nielsen, Joachim, et al.
(författare)
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Skeletal muscle glycogen content and particle size of distinct subcellular localizations in the recovery period after a high-level soccer match
- 2012
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Ingår i: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 112:10, s. 3559-3567
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Tidskriftsartikel (refereegranskat)abstract
- Whole muscle glycogen levels remain low for a prolonged period following a soccer match. The present study was conducted to investigate how this relates to glycogen content and particle size in distinct subcellular localizations. Seven high-level male soccer players had a vastus lateralis muscle biopsy collected immediately after and 24, 48, 72 and 120 h after a competitive soccer match. Transmission electron microscopy was used to estimate the subcellular distribution of glycogen and individual particle size. During the first day of recovery, glycogen content increased by ~60% in all subcellular localizations, but during the subsequent second day of recovery glycogen content located within the myofibrils (Intramyofibrillar glycogen, a minor deposition constituting 10–15% of total glycogen) did not increase further compared with an increase in subsarcolemmal glycogen (−7 vs. +25%, respectively, P = 0.047). Conversely, from the second to the fifth day of recovery, glycogen content increased (53%) within the myofibrils compared to no change in subsarcolemmal or intermyofibrillar glycogen (P < 0.005). Independent of location, increment in particle size preceded increment in number of particles. Intriguingly, average particle size decreased; however, in the period from 3 to 5 days after the match. These findings suggest that glycogen storage in skeletal muscle is influenced by subcellular localization-specific mechanisms, which account for an increase in number of glycogen particles located within the myofibrils in the period from 2 to 5 days after the soccer match.
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