| Objective: Exercise-induced fatigue of athletes is often appearance in dailytraining and games, and it leads to reduce the learning and memory, exerciseskill and competition results. Many studies have show that exercise-inducedfatigue have a negative impact on the function of the central nervous systemactivity, which including learning, memory, emotion and so on.As the mainhigher nervous function of the brain activity, learning and memory function isone of the important physiological foundation engaged in exercise. All kinds ofsporting events are implemented in the process of learning and memory functionany of these absenced will greatly reduce the exercise ability and technologylevel of athletes, and impair the training effectivenessand results of thecompetition seriously. So it is very necessary to study the exercise-inducedfatigue resulting in a decline in learning and memory.At present, thephenomenon ofexercise-induced fatigue resulting in a decline in learning andmemory has been confirmed, but its mechanism is notclear. There were some studies have shown that exercise-induced fatigue stress would active the HPAaxis and sympathetic nervous system, which lead to the immune cells in thebrain (mainly including the microglia and astrocytes) and secret inflammatoryfactora(such as interleukin1beta, tumor necrosis factoer alpha, etc.) and causeneuroinflammation. Recent research shows that under the condition of stress,neuroinflammation mediated bythe activation of the brain astrocytes andmicroglia and proinflammatory factor may damage the brain cognitive function.As a kind of typical fatigue stress, exercisemay be also activated brainmicroglial and astrocytes and cause the neuroinflammation, andneuroinflammation is involved in the sport fatigue caused by the learning andmemory ability of neural regulation also did not see in the literature. In thisstudy, we observed the effect of exercise-induced fatigue on the expressionof glial cells, inflammatorycytokines, inflammatory signalingpathway andmolecular protein related to learning and memory in rathippocampus, discussed the mechanism ofexercise-induced fatigueimpairedlearning and memory. The aim of this study is to provide a new explaination inthe mechanism ofexercise-induced fatigueimpaired learning and memory, andthe same time, it also provide an important theoretical basis in the developmentof anti fatigue medicine, the athlete’s athletic ability and competitionresults.Methods: Male Wistar rats, weight200±20g, were randomly divided intocontrol group (CG) and exercise-induced group (EG). EG rats were seven dayrepeated exhaustive treadmill training, which load is divided into three levels, each level of running speed are respectively8.2m/min,15m/min,20m/min, thetime of first and second load are15min, the third load is no time until exhaustion,CG was not intervention. After the exercise-induced fatigue model, the Y maze,including Y maze independent alternately, Y maze spatial recognition, Y mazeactive avoidanc was used to detect the ability of learning and memory behaviorin rats; then the electrophysiological in vivo was used to observe the change oflong-term potentiation in the area of hippocampal CA1; finally the molecularbiology technology was used to observe:①the expression of microglia (MG)and astrocyte (AS) in hippocampal after exercise with immunohistochemicaltest;②the expression of protein and mRNA levels of inflammatory cytokines,interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in rathippocampus with the semi quantitative PCR test and the enzyme linkedimmunosorbent assay;③the expression of inflammatiory signaling pathwayspecific proteins, including c-Jun N-terminal kinase (JNK), P38mitogenactivated protein kinases (P38MAPK) and nuclear transcription factor kappaB(NF-κB) in rat hippocampus; and the expression of learning and memory relatedmolecules, such as calcium/camodulin-dependent protein kinase Ⅱ (CaMK-Ⅱ)and cAMP-response element binding protein (CREB) in rat hippocampus withThe date using mean±standard error (Mean±SEM) representation. The SPSS18.0software was used to statistical analysis, differences between groups werecompared using independent sample T-test, P<0.05indicates that there was asignificant differences between the two group, P<0.01indicates that there was a very significant differences between the two group.Result:1. Y maze test results show that, in Y maze independent alternately, thealternation of EG rats was very significantly lower than the CG (P<0.01); theY mazespatial recognition shows that the duration of novel arm visits of EG ratswas significantly shorten and the number of arm visits was also decreased (P <0.01), and the duration of novel arm visits of EG rats was also significantly lessthan the starting arm and other arm (P <0.05); in Y maze active avoidance, theactive avoidance error number, identify the error times and training time of EGrats were significantly higher than CG (P <0.05, P <0.01), while the memorynumber right were significantly lower than CG (P <0.01).2. The electrophysiological experiments show that compared with CG, theslop of field excitatory postsynaptic potentialsof EG rats were significantlydecreased (P<0.01) and the long-term potentiation of EG rats in the area ofhippocampal CA1was inhibited.3. The molecular biology experimental results show that①theimmunohistochemicaltest reavels that, compared with CG, the volume ofmicroglia cells was larger, the soma became round, the protuberance wasincreased and the stained was darker. Statistical analysis that the area of positivecells and the staining gray level were significantly higher than in control group(P<0.05, P<0.01)；the astrocyte cell become swelling, mast and prominences,the area of positive cells and the staining gray level were significantly higher than in control group (P<0.05).②the expression of IL-1β, TNF-αmRNA wassignificantly higher than the control group(P<0.01), and the expression of IL-1β,TNF-α protein levels were alsosignificantly increased(P<0.01, P<0.05).③compared with CG group, the expression of inflammation signaling pathwayspecific proteins, including JNK, P38MAPK, NF-κB, were significantlyincreased (P<0.05, P<0.01); while the CaMK-Ⅱand CREB protein, thelearning and memory related molecules, were significantly decreased (P<0.01).Conclusions: After repeated exhaustive exercise, the learning and memoryability of rat was declined and the E-LTP and L-LTP of rats in hippocampusCA1area inhibited. These were indicated that exercise-induced fatigue not onlyled to a decline in short-term memory, but also led to a decline in long-termmemory.And the same time, the microglia cells and astrocyte cells wereactivated, their numbers, morphology were changed. Moreover, the levels ofinflammation factors in rat hippocampus were also increased. This was showthat exercised-induced fagitue may mediate the activation of glial cells in thebrain and lead the neuroinflammation.In addition, the specific proteins oninflammatory signaling pathway were also activated, suggested that theneuroinflammationmediated by glial cells may involve in the process ofinflammatory signaling pathway activated. And the expression of learning andmemoryrelated molecules were also declined, which are suggested thatneuroinflammation may participate in the neural mechanismofexercise-inducedfatigue impair learning and memory ability. |
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