Pesta 2010 Abstract IOC60

From Bioblast
Pesta D, Macek C, Hoppel F, Faulhaber M, Burtscher M, Gnaiger E, Schocke M (2010) The impact of endurance training on muscle oxidative capacity. MiPNet15.10.


Pesta D, Macek C, Hoppel F, Faulhaber M, Burtscher M, Gnaiger E, Schocke M (2010)

Event: MiPNet15.10_IOC60

Skeletal muscle is a highly adaptable tissue that can adjust to different stimuli [1,2]. In the present study we investigated the impact of endurance training on muscle oxidative capacity with high resolution respirometry [3] and 31P magnetic resonance spectroscopy (31P MRS) [4]. 40 healthy untrained subjects (UG) who performed an endurance training program 3 times a week lasting for 10 weeks were included in the study. Spatially-resolved dynamic 31P MRS measurements were obtained from the upper leg and biopsy samples were taken from the vastus lateralis to assess mitochondrial capacity with high-resolution respirometry. Subsequently, endurance and strength capacities of the subjects were determined via motor performance tests. After 10 weeks, the initial tests and muscle biopsies were repeated. We observed a significant increase in mass specific OXPHOS flux with training in the UG from 78.97 Β± 16.05 to 101.39 Β± 19.19 (p<0.01). The capacity of the mitochondria to oxidize MCFA was significantly increased with training, observed as an increase in absolute flux (from 12.79 Β± 4.67 pre-training to 29.58 Β± 7.25 post-training, p<0.01) and in the flux control ratio (FCR=fraction of a given flux relative to the maximal flux) of octanoyl-carnitine (0.14 Β± 0.05 pre-training to 0.28 Β± 0.04 post-training, p<0.01). The FCR of OXPHOS was increased after training (0.95 Β± 0.09, p<0.01). To date, analysis of the 31P MRS was still in progress. In conclusion, mitochondria seem to adapt to endurance training in a quantitative and qualitative way. The qualitative adaptations can most prominently be observed in the capacity of MCFA oxidation, which is increased due to training. The limitation of the OXPHOS system seems to be decreased temporarily in untrained subjects exposed to exercise training. Yet, the exact reason for this decreased limitation due to training is unknown.

1. Desplanches D, Hoppeler H, TΓΌscher L, Mayet MH, Spielvogel H, Ferretti G, et al. (1996) Muscle tissue adaptations of high-altitude natives to training in chronic hypoxia or acute normoxia. J Appl Physiol 81:1946-51. 2. Hoppeler H, Klossner S, Vogt M (2008) Training in hypoxia and its effects on skeletal muscle tissue. Scand J Med Sci Sports 18 Suppl 1:38-49. 3. Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle: new perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41:1837-45. 4. Schocke MF, Esterhammer R, Arnold W, Kammerlander C, Burtscher M, Fraedrich G, et al. (2005) High-energy phosphate metabolism during two bouts of progressive calf exercise in humans measured by phosphorus-31 magnetic resonance spectroscopy. Eur J Appl Physiol 93:469-79.

β€’ Keywords: Exercise Training, Respiration, Permeabilized Fibres, Skeletal Muscle

β€’ O2k-Network Lab: AT Innsbruck Oroboros, AT Innsbruck Burtscher M


Stress:Ischemia-reperfusion  Organism: Human 

Preparation: Enzyme  Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase  Regulation: Fatty acid  Coupling state: OXPHOS 

HRR: Oxygraph-2k 

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