| In order to discuss the central mechanism of exercise-induced fatigue, we investigated the influence of exercise on antioxidant capacity and lipid per oxidative damage , cell electrical activity and neurotrophic factor's changes in rats.The rusults showed that:1. After ten days loading increasing swimming exercise, the rats showed the condition of fatigue and on the 7th and 10th day the body weight is decreased significantly (p<0.05, p<0.01) . In the 12SG and 24SG the CK are increased significantly (p<0.01) . In the OSG and 12SG the BU are increased significantly (p<0.05 ). Both the behavior and chemical index showed that the rats are in the condition of fatigue. The model is suitable for the use of the following experiments.2. Extracellular records in vivo were made from striatal neurons hi male rats after ten days loading increasing swimming exercise. The results showed that 1) In control group 94% neostriatal neurons spontaneous firing frequency is below 10Hz, while in exercise group 19% neurons spontaneous firing frequency is above lOHz. There is significant difference between them(p<0.05). 2) In control group 90% action-potential time is between l-3ms, while in exercise group 22% above 3ms. In the exercise group we recorded regular firing, irregular and regular irregular firing but also regular bursting firing and the time between the bursts is 140-210ms. 3) In exercise group the high frequency neurons are mainly focused in the dorsal part of the neostriatum. From the results we concluded that the neostriatal neurons discharge frequency is changed after exercise-induced fatigue and these neurons distribution is regular.3. Observed the expression of BDNF and GFAP in brain of rats after swimming. They were detected with SABC and analyzed with CMIAS8 image analysis system at hippocampi and striatum. Results showed that there was BDNF expression at hippocampi and striatum, and the expression was mainly in the neuron. Compared with CG, BDNF expression of 12SG athippocampi was increased significantly (p<0.01) , 24SG at hippocampi and striatum was significantly increased individually (p<0.01, p<0.05). Compared with CG, OSG, 12SG and 24SG at hippocampi and striatum was significantly changed (p<0.01, p<0.05) .Conclusions: Exercise induced fatigue can induce neuron damage and the changes of BDNF expression at hippocampus and striatum. The mechanism of these effects may be related with the NMD A receptor and TrkB. It is probably one of the reasons that make the changes of spontaneous activity. The increased GFAP can protect the damage cells.4. By setting up anaerobic training model in mice, effect of interval anaerobic training on antioxidant capacity and lipid peroxidative damage of brain, heart, muscles in mice were observed. The results showed that SOD activity and T-AOC and MDA contents appeared an increasing tendency after interval training, especially in muscles (p <0.05, p <0.01, p<0.001) .The changes of SOD and T-AOC in heart were similar to muscles (p <0.05, p <0.01, p <0.001) , but there was no difference in MDA content between TG and CG (p >0.05) . And T-AOC content in brain significantly increased (p<0.05 , p<0.01) .The change of most indexes in STG and LTG remarkably related to time lasting and density enhancing (p<0.05, p<0.01, p<0.001) . Interval training delayed natural growth of mice weight. Exercise capacity fall into a decline with time lasting and density enhancing. Conclusions: Antioxidant capacity and lipid peroxidative level induced by anaerobic exercise were significantly different in various tissues. In our experiment, fatigue could result from training-aggravated oxidative damage.
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