The Generation Of Exercise-induced Reactive Oxygen Species And Its Regulation On Mitochondrial Energy Transformation In Skeletal Muscle

It is widely accepted and experimentally proven that exercise can induce oxygen free ridicals produced in mitochondria. In the past years, researchers primarily gave their attentions to damage by exercise–induced mitochondia ROS, but very little has been known about"early event"of balace between ROS generation and elimination, molecular mechanism of redox potential and balance of energy by regulating of ROS, and activation of uncoupling proteins by ROS and feedback regulated ROS generation by uncoupling proteins.SoWe should have anafresh foucus on the positive role of ROS in exercise. According to the Bedford's protocol, SD rats were forced to run on the treadmill. Animals were sacrificed at rest, 45min, 90min, 120min and 150min immediately during exercise respectively in untrained and trained groups.We observed the degree and efficiency of oxidative phosphorylation, ROS generation rate, transmembrane potential, ATP synthesis, the express of UCP3 and Mn-SOD, MDA, state 3 and 4 respiratory rate of skeletal muscle during acute exercise.The results and conclusions:1) Exercise-induced mitochondria ROS generation increase rapidly during acute exercise in untrained and trained SD rats.It indicated that ROS generation of mitochondria during acute exercise was an normal physiological event.2) Uncoupling protein 3 increased rapidly in skeletal muscle mitochondria during acute exercise.It showed that there is an UCP3 pool in skeletal muscle cellular cytoplasm.3) Acute exercise induced UCP3 increased rapidly, ROS generation increased primarily and decreased during acute exercise, increased ROS can activate UCP3 activty, which showed that there is a feedback loop of ROS→UCP3→proton leak→ROS.4) UCP3 expressed more rapidly than Mn-SOD during acute exercise, UCP-3 activation and/or induced-expression were an earlier event relative to Mn-SOD in the anti-oxidation defense.5) At the beginning of exercising, efficiency of oxidative phosphorylation increased gradually and ROS generated significantly. With the transmembrane potential descenting a little the ROS generation declined significantly. Mitochondrial transmembrane potential was responsible to ROS generation. ROS generation itself was the re-distribution of electron flux and a protection mechanism of the mitochondrial function. We speculated it was the initial effect of ROS generation in the regulation of mitochondrial energy transferring.6) With the increasing of the ROS generation, ROS, as an original induceor, could lead to a direct electric leak and indirect electric leak by activated proton conductance of UCP3, which was the followed effect of the ROS generation. It suggests that ROS may serve as a'Molecular Switch'in the exact regulation of mitochondrial energy transferring.7) Mn-SOD expression up-regulated after endurance training,which eliminated most ROS ,and UCP3 expression decreased .So ROS and UCP3 induced proton leak decreased ,which reduced energy waste, strengthen mitochondria supplying energy.