| Objective Excessive fatigue is a very commen phenomenon in the practice of sports. We should adjust the way of our sports or training promptly and have a rest in time when we are In the event of excessive fatigue in order to avoid the irreversible injury caused by disorder of the body internal environment what is the result of excessive fatigue. Motor cortex is the nerve center of controlling the body motion. If its morphologiy, structure or function changes, the ability of the body’s movement and other functional state will be affected. We explore the regulation mechanisms of apoptosis in the motor cortex when the body is excessive fatigue and try to find the time node of balance between self-protection and stimulation of injury is broken in motor cortex under that state through studying the dynamic changes of morphological structure and expression of Bax, Bcl-2 protein and BDNF in motor cortex of the rats that did loaded swimming continuously under the state of excessive fatigue caused by the high intensity swimming what based in glycolysis for energy.Methods We bought 72 purebred male sprague dawley rats of specific pathogen free. 7rats were randomly selected as the control group to be fed normally, the others were be used for experiments conducted in two phases. In the first stage, fatigue model was established in 6 days according to glycolysis for energy sport fatigue model. All rats performed swimming training loaded 12% of their own body weight in the 6days according to small, medium, large, small, medium, large amount of exercise in turn. And we trained the rats for two groups in the morning and two groups in the afternoon. The large amount of exercise was four times for a group, medium amount of exercise was three times for a group and small amount of exercise was two times for a group. The rest time between two times was 5 min and that between two groups was 15 min, the time of each swimming end in the rats’ noses sank below the water surface. In the second stage,we trained the rats according to the excess recovery model of 36 h with loaded 12% of their own body weight, the training was large amount of exercise and the rest time referenced above. And we trained the rats every 36 h. Yin Jin’s studies have found that the recovery of rats’ s fatigue reached its limit after 5′36h and the turning point of fatigue recovery appeared after5′36h. Then, the ability of fatigue recoverying decreased so that fatigue accumulated and the rats reached the state of excessive fatigue. After the 6′36h training, killed 7 rats after each training immediately until all rats were killed and the rats were recorded as group A, B, D, E, F?.Result On the whole, all rats’ s brain motor cortex had pathological changes except control group and had a tend of increasing constantly with the fatigue increased. The expression of Bax protein expression in the motor cortex of control group is weak. And that of group B、D、E、F、G、H were increased gradually and all were significantly higher than that in group C(p <0.05). Compared to group A, group D, E, F, G, H had significant differences from it. And it also had significant differences between group H and group C,A, B, D. The expression level of Bcl-2 protein was low, that of group B, D, E, F, G, H were significantly higher than that in group C. The expression of Bcl-2 protein increased gradually from group C to group F, decreased from group F to group H, and it exsited significant differences between group F and group C, A, B, D. The expression of BDNF in group A, B, D, E, F,G, H were all significantly higher than that of group C. Expression of BDNF increased gradually from group C to Group F and decreased from group F to group H, and it exsited significant differences between group F and group C, A, B, D, E.Conclusion 1. In the glycolytic energy supplying conditions, the fatigue of rats with continuous loaded-swimming accumulate for their ability of recovery and the injury in their brain motor cortex increase. 2. As for the increased injury in the motor cortex, the body resists the cell apoptosis in motor cortex by regulating the expression of Bax, Bcl-2and BDNF. Expression of BDNF and Bcl-2 protein increase at first and then drop.Expression of Bax protein increased gradually with the injury increased in motor cortex.3. 13 ′ 36 h may be the time point that the balance between self-protection and injury stimulation in motor cortex is broken. |