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Skeletal muscle is a highly adaptable tissue that can adjust to different external stimuli [1,2]. In the present study we investigated the impact of altered environmental conditions (normoxia and hypoxia) as well as training regimes (strength and endurance training) on parameters of muscle metabolism including mitochondrial respiration ([[OXPHOS]] and [[ET-pathway]] capacities) with different substrates and substrate combinations.
For assessing these parameters, 40 healthy and not specifically trained subjects enrolled in a strength and endurance training program lasting for 10 weeks, and split into a normoxic and a normobaric intermittent hypoxic (''F''<sub>iO2</sub>=0.12) training group. At baseline, subjects performed an in-vivo phosphorus-31 magnetic resonance spectroscopy (<sup>31</sup>P MRS) test of the quadriceps muscles during dynamic leg-extension exercise . Subsequently, endurance and strength capacities of the subjects were determined via motor performance tests. Biopsy samples from the vastus lateralis were obtained from the subjects for fibre type distribution with ATPase staining and measurement of mitochondrial performance with [[high-resolution respirometry]] to examine oxidative capacity of the muscle tissue [4,5]. After 10 weeks, the initial tests and muscle biopsies were repeated.
The Figure  shows superimposed traces of oxygen flux per mg tissue wet weight, from two subsamples of the same subject (Oroboros Oxygraph-2k; 37 °C; [[MiR06]] ; [O2] above 220 µM and below 360 µM with intermittent reoxygenations). The additive effect of [[CI+II]] substrate combinations  was pronounced, and an increase of [ADP] from 2.5 to 5.0 mM stimulated respiration significantly, thus reducing the apparent limitation by the [[phosphorylation system]] (stimulation by FCCP titration to induce the non-coupled state of [[electron transport system]] (ET-pathway) capacity. [[Residual oxygen consumption]] (ROX) is overestimated after short periods of inhibition of CII and CIII, with a further decline proceeding gradually as in the case of inhibition of CII in the presence of succinate. Our results will permit to evaluate physiological, biochemical, and molecular responses to a change in muscle metabolism resulting from a normoxic and hypoxic training regime.
Supported by OeNB Jubiläumsfond Austria project 13476; contribution to [[Mitofood]] COST Action FAO602.
1. Desplanches D, Hoppeler H, Tüscher 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. 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.
4. [[Gnaiger 2009 Int J Biochem Cell Biol|Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle: new perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41:1837-45.]]
5. [[Pesta 2012 Methods Mol Biol|Pesta D, Gnaiger E (2012) High-resolution respirometry. OXPHOS protocols for human cells and permeabilized fibres from small biopsies of human muscle. Methods Mol Biol 810:25-58.]]
6. [[MiPNet14.13|Fasching M, Renner-Sattler K, Gnaiger E (2009). Mitochondrial respiration medium – MiR06. Mitochondr Physiol Network 14.13:1-4. - www.oroboros.at]]
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