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Contribution à l'étude des effets de l'activité physique sur le fonctionnement mitochondrial et la production de radicaux libres - Etude sur mitochondries musculaires et hépatiques

Abstract : The aim of this work was to study hepatic and muscular mitochondria function in response to chronic or acute exercise. We have simultaneously studied the mitochondrial oxygen consumption and free radical production based on the H2O2 production with Amplex Red as a probe. We have shown that a single bout of exercise increases free radical production that was persistent for 2 hours in muscle while it was delayed in liver. This free radical production appears to be tolerated by the mitochondria through the antioxidant pool that remained unaffected. Measurements with specific substrates and inhibitors on the electron transport chain that are useful to functionally isolate the different respiratory complexes allowed us to determine specific sites of adaptations. In a second part, we tested the effect of moderate chronic exercise that induced increases in mitochondrial density in muscle and more originally in liver, along with functional adaptations. Muscle mitochondria seems to have a better efficiency to extract reduced equivalents from fatty acids through a process named metabolic slipping. Liver mitochondria displayed an enhanced oxidation yield in ADP-stimulated respiratory status with complex I substrates. Results suggest that the decrease in mitochondrial functioning is compensated by the increase in the tissue mitochondrial density, as shown by parallel increases in CS activity. The sites of ROS production appear to be tissue specific. In fact, exercise appears to affect mostly the H2O2 production from complex III in muscle mitochondria but complex I in liver mitochondria. The use of PGC-1α antisense oligonucleotides, in order to decrease the PGC-1α protein expression, doesn't affect mitochondrial biogenesis induced by endurance training in muscle but totally inhibit the training-induced mitochondrial biogenesis in liver. Functional adaptations (i.e. altered respiratory control and ROS production) linked to the absence of this protein seem to confirm the essential role of PGC-1α in tissue-specific mitochondrial adaptations to exercise. These results suggest that free radicals could play a role by feedback control of PGC-1α, on exercise-induced mitochondrial adaptations.
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https://tel.archives-ouvertes.fr/tel-00626716
Contributor : Tom Coisne <>
Submitted on : Monday, September 26, 2011 - 9:41:45 PM
Last modification on : Thursday, November 19, 2020 - 3:52:36 PM
Long-term archiving on: : Tuesday, December 27, 2011 - 2:35:45 AM

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  • HAL Id : tel-00626716, version 1

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Citation

Tom Coisne. Contribution à l'étude des effets de l'activité physique sur le fonctionnement mitochondrial et la production de radicaux libres - Etude sur mitochondries musculaires et hépatiques. Physiologie [q-bio.TO]. Université Joseph-Fourier - Grenoble I, 2007. Français. ⟨tel-00626716⟩

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