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Sökning: WAKA:ref > Gymnastik- och idrottshögskolan > Fritt online > Mogensen Martin

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1.
  • Mogensen, Martin, et al. (författare)
  • Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency
  • 2006
  • Ingår i: Journal of Physiology. - 0022-3751. ; 571:3, s. 669-681
  • Tidskriftsartikel (refereegranskat)abstract
    • The purpose of this study was to investigate the hypothesis that cycling efficiency in vivo is related to mitochondrial efficiency measured in vitro and to investigate the effect of training status on these parameters. Nine endurance trained and nine untrained male subjects ( , respectively) completed an incremental submaximal efficiency test for determination of cycling efficiency (gross efficiency, work efficiency (WE) and delta efficiency). Muscle biopsies were taken from m. vastus lateralis and analysed for mitochondrial respiration, mitochondrial efficiency (MEff; i.e. P/O ratio), UCP3 protein content and fibre type composition (% MHC I). MEff was determined in isolated mitochondria during maximal (state 3) and submaximal (constant rate of ADP infusion) rates of respiration with pyruvate. The rates of mitochondrial respiration and oxidative phosphorylation per muscle mass were about 40% higher in trained subjects but were not different when expressed per unit citrate synthase (CS) activity (a marker of mitochondrial density). Training status had no influence on WE (trained 28.0 +/- 0.5, untrained 27.7 +/- 0.8%, N.S.). Muscle UCP3 was 52% higher in untrained subjects, when expressed per muscle mass (P < 0.05 versus trained). WE was inversely correlated to UCP3 (r=-0.57, P < 0.05) and positively correlated to percentage MHC I (r= 0.58, P < 0.05). MEff was lower (P < 0.05) at submaximal respiration rates (2.39 +/- 0.01 at 50% ) than at state 3 (2.48 +/- 0.01) but was neither influenced by training status nor correlated to cycling efficiency. In conclusion cycling efficiency was not influenced by training status and not correlated to MEff, but was related to type I fibres and inversely related to UCP3. The inverse correlation between WE and UCP3 indicates that extrinsic factors may influence UCP3 activity and thus MEff in vivo.
2.
  • Mogensen, Martin, et al. (författare)
  • Mitochondrial efficiency in rat skeletal muscle: influence of respiration rate, substrate and muscle type.
  • 2006
  • Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 185, s. 229-236
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To investigate the hypothesis that mitochondrial efficiency (i.e. P/O ratio) is higher in type I than in type II fibres during submaximal rates of respiration.Methods: Mitochondria were isolated from rat soleus and extensor digitorum longus (EDL) muscles, representing type I and type II fibres, respectively. Mitochondrial efficiency (P/O ratio) was determined with pyruvate (Pyr) or palmitoyl-L-carnitine (PC) during submaximal (constant rate of ADP infusion) and maximal (Vmax, state 3) rates of respiration and fitted to monoexponential functions.Results: There was no difference in Vmax between PC and Pyr in soleus but in EDL Vmax with PC was only 58% of that with Pyr. The activity of 3-hydroxyacyl-CoA dehydrogenase (HAD) was 3-fold higher in soleus than in EDL. P/O ratio at Vmax was 8-9% lower with PC (2.33±0.02 (soleus) and 2.30±0.02 (EDL)) than with Pyr (2.52±0.03 (soleus) and 2.54±0.03 (EDL)) but not different between the two muscles (P>0.05). P/O ratio was low at low rates of respiration and increased exponentially when the rate of respiration increased. The asymptotes of the curves were similar to P/O ratio at Vmax. P/O ratio at submaximal respirations was not different between soleus and EDL neither with Pyr nor with PC.Conclusion: Mitochondrial efficiency, as determined in vitro, was not significantly different in the two fibre types neither at Vmax nor at submaximal rates of respiration. The low Vmax for PC oxidation in EDL may relate to low activity of β-oxidation.
3.
  • Sahlin, Kent, et al. (författare)
  • Repeated static contractions increase mitochondrial vulnerability towards oxidative stress in human skeletal muscle
  • 2007
  • Ingår i: Journal of applied physiology. - 8750-7587. ; 101, s. 833-839
  • Tidskriftsartikel (refereegranskat)abstract
    • Repeated static contractions (RSC) induce large fluctuations in tissue oxygen tension and increase the generation of reactive oxygen species (ROS). This study investigated the effect of RSC on muscle contractility, mitochondrial respiratory function, and in vitro sarcoplasmatic reticulum (SR) Ca2+-kinetics in human muscle. Ten male subjects performed 5 bouts of static knee extension with 10 min rest in between. Each bout of RSC (target torque 66% of maximal voluntary contraction torque, MVC) was maintained to fatigue. Muscle biopsies were taken pre-exercise and 0.3 and 24 h post-exercise from vastus lateralis. Mitochondria were isolated and respiratory function measured after incubation with H2O2 (HPX) or control medium (CON). Mitochondrial function was not affected by RSC during CON. However, RSC exacerbated mitochondrial dysfunction during HPX resulting in decreased respiratory control index, decreased mitochondrial efficiency (P/O ratio) and increased non-coupled respiration (HPX/CON post vs. pre-exercise). SR Ca2+ uptake rate was lower 0.3 h vs. 24 h post-exercise, whereas SR Ca2+ release rate was unchanged. RSC resulted in long-lasting changes in muscle contractility including reduced maximal torque, low frequency fatigue (LFF) and faster torque relaxation. It is concluded that RSC increases mitochondrial vulnerability towards ROS, reduces SR Ca2+ uptake rate and causes LFF. Although conclusive evidence is lacking we suggest that these changes are related to increased formation of ROS during RSC.
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  • Resultat 1-3 av 3
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