Dubouchaud 2017 MITOEAGLE Obergurgl

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COST Action MitoEAGLE
Effects of a single bout of exercise on the production of reactive oxygen species in muscle and liver isolated mitochondria.

Link: MitoEAGLE

Dubouchaud H, Quiclet C, Le Guen M, Coisne T, Batandier C, Hininger-Favier I, Couturier K (2017)

Event: MitoEAGLE Obergurgl 2017

COST Action MitoEAGLE

Acute exercise is often associated with tissue damages from oxidative stress due to limitations in antioxidant capacities or to enhanced reactive oxygen species (ROS) production. In addition, ROS could also have a regulatory role as signaling molecules. In most cells, mitochondria are the major source of ROS but the effect of exercise on such mitochondrial ROS production has not been studied in details. The aim of this study was therefore to measure both the mitochondrial oxygen consumption (JO2) and the mitochondrial H2O2 production, as an index of ROS production, after a single bout of treadmill exercise in rats sacrificed immediately after a 1-hour exercise bout (E0) or after a 2-hour recovery (E2) compared to controls (C). We observe differences between liver and muscle mitochondria in response to acute exercise. While there is no change in mitochondrial JO2 in liver, we show that mitochondrial JO2 is increased in muscle right after exercise when the respiratory chain is energized with both complex I and II substrates. These changes disappear after a 2-hour recovery period. In muscle, mitochondrial H2O2 production is increased after exercise (from 50 % to several times, depending on the conditions tested). These changes remain significant after a 2-hour recovery period in muscle, whatever the substrate used to energize the respiratory chain. In liver, there is also an increase in H2O2 production (+ 20%) in response to exercise that is limited to non-phosphorylating conditions. The use of specific combinations of substrates and inhibitors of the respiratory chain suggests that a single bout of exercise alters ROS production at the complex III level in muscle but at the complex I level in liver. Future studies should focus now on the physiological role of such ROS as signals for muscle and liver adaptations to exercise.


Bioblast editor: Kandolf G


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Oxidative stress;RONS  Organism: Rat  Tissue;cell: Skeletal muscle, Liver  Preparation: Isolated mitochondria 


Pathway: NS 

Event: A1, Oral 


Affiliation

LBFA, INSERM U1055, Univ Grenoble Alpes.- herve.dubouchaud@univ-grenoble-alpes.fr