As the level of the sports competition constantly hightens, training intensity comes to the limit and this exercise stress causes excessive fatigue among the athletes. The research on the exercise fatigue, especially on the mechanism of the fatigue and the recovery of the fatigue based on its theory is the focus all over the world. The Central Nervous System (CNS) plays an important role in causing the exercise fatigue, but now the central mechanism of the exercise fatigue or the central fatigue of the exercise has not been correctly explained. It is very important in delay and recovery of the central fatigue to find out the mechanism of the central fatigue of the exercise.
The researchers of physiology chair, basic medicine faculty, Pyongyang Medical College,
First, we have made experiments with C57/6J mice(aged 8 weeks, weight 18～22g, male)undergoing forced treadmill training and evaluated body weight, serum lactate, blood urea nitrogen(BUN), creatine kinase(CK) and serum cortisol, the evaluating indicators to demonstrate that our model is significant exercise fatigue one.
Second, we examined changes of the hippocampal neurogenesis and learning and memory capacity during the exercise fatigue. Neurogenesis was examined by using Brdu+ staining. The numbers of Brdu+ cells in the model of exercise fatigue were greater than control (P<0.01), this result suggest that the exercise fatigue developing by the excess exercise impair the hippocampus and results from the compensatory regulation. Learning and memory capacity was assessed using MWM(Morris water maze), RAM(Radial arm maze).In the Morris spatial probe capacity exam, the latency of the exercise fatigue model was significantly increased than control group and exercise control(P<0.05), the numbers of crossing platform quadrant was decreased (P<0.05), and the correct percent was significantly decreased than control group and exercise control (P<0.05), indicating that spatial memory capacity becomes lower during the exercise fatigue.
The serum cortisol in the model of exercise fatigue was significantly increased than the exercise control, this results from decreased hippocampal inhibitory regulation on hypothalamus-hypophysis- adrenal gland axis.
The change of the hippocampal brain-drived nerotrophic factor(BDNF) and insulin-liked growth factor-1(IGF-1) level were measured to explore the molecular mechanism of the these functional changes of hippocampus during the exercise fatigue. BDNF and IGF-1 were quantified using enzyme-liked immnosorbent assay(ELISA). Hippocampal BDNF and IGF-1 level in the model of exercise fatigue were significantly higher than control group and exercise control (P<0.05), these results suggest that the exercise fatigue developed by the excess exercise improve the recovery function on the hippocampal impact.
Our study on the mechanism of central fatigue of the exercise is kept on in detail.
