| Object: Over-exercise causes injury to the body and long-lasting, over-training induces damage to the heart. In this investigation, we over-trained the rats and induce damages in the myocardial cells and then observed changes in morphology and physiological function of cardiac cells. We discussed features and the repair process of exercise-induced myocardial damage for the purpose of providing evidence of monitoring this kind of damage and therefore suggesting preventive and curative measures for exercise-induced myocardial damage.Methods: In this investigation, 4-week-old male wistar rats are randomly divided into 10 groups: control, over-trained, and Phosphocreatine disodium salt treatment after being over-trained. All groups except the control group received the ascending over-load training for eight weeks according to the over-training procedure. Anesthesia the rats for UCG examination immediately after the training, 6 hours, 24 hours, 72 hours and a week after the training, respectively and then executed them and tested the Hb, BUN, and T to assess the exercise load of the experimental animal. We also tested the serum CK, CK-MB, LDH, LDH1, SOD and MDA in the myocardial tissue, and observed the morphology of the myocardium of each group of rats. TUNEL was utilized to test apoptosis and immunohistochemistry and immoblotting were used to assess the expression of Bcl-2 and Bax. We observed changes in these parameters at the time points mentioned above and processed the data obtained with SPSS for Windows 11.5, all results are presented in mean±SD( x±s). Data obtained between different groups are processed with one-way ANOVA and T test is used to process data within the same group. P<0.05 is considered to have statistical significance.Result:1. Over-training group and drug-treated over-training group manifested decreased motor ability and deterioration in general condition. The parameters reflecting physiological conditions changes significantly as well: compared with control group, Hb and serum T decreased dramatically (p<0.01), BUN level increased significantly (p<0.01).2. After over-training, the myocardial fibers degenerated, cloudy and swelling, and ballooning change can be seen in some areas. A large amount of inflammatory cells infiltrated in the interstitial tissue.3. Compared with the control group, the LVID(s) of the rats in the over-training group enlarged significantly (p<0.01), the heart rate increased and the LVEF%,LVFS%数decreased significantly. As the recovering time increased, parameters reflecting the systolic function of myocardial cells gradually restored. 1 week after the training, the UCG data restored to a normal level.4. After the training, the levels of myocardial enzymes elevated significantly (p<0.01). The serum CK amounted to peak level immediately after the training and as the recovering time increased, the CK level declined gradually. The serum CK-MB, LDH, LDH1 show also the similar changes. Over training leads to increased MDA in the myocardium and decreased SOD activity (p<0.01). As the recovering time increased, MDA content in the myocardium decreased gradually while the SOD activity increased. 5. The apoptosis rate and the expression of Bax (gene that promotes apoptosis) increased significantly after being over-trained (p<0.01). While the expression of Bcl-2, which inhibits apoptosis, decreased significantly (p<0.05). Therefore the Bcl-2/Bax ratio decreased significantly (p<0.01). As the recovering time increased, the apoptosis rate and the expression of Bax declined gradually and the Bcl-2/ Bax ratio increased gradually.6. Compared with the control group, the level of LDH, CK-MB and LDH1 in the myocardial cells in drug treated over trained group decreased significantly 6 hours after being over-trained (p<0.01). While the LVEF%,LVFS% increased significantly 24 and 72 hours after being trained compared with the control group (p<0.01). The myocardial MDA level of the drug treated over trained group and the over trained group differ significantly 24 and 72 hours after receiving the training (p<0.05). 24 hours after the training, drug treated group showed significant increase in Bcl-2/Bax ratio compared with the over trained group.Conclusion:1. Our experiment successfully built over training model in rats.2. The morphology of the myocardial is damaged after being over trained.3. The systolic function of the left ventricle declines after being over trained and restores 1 week after receiving the training.4. After being over trained, the myocardial mitochondria produce more free radicals, yet the ability of eliminating these free radicals decreases. The level of increases considerably and membranous damage happens. The myocardial enzymes escape from the cells, thus the enzyme parameters are changed. Some of these parameters elevated at first and then declined. The reason for this phenomenon may lies in the fact that over training causes transient ischemia and hypoxia in the myocardial cells and after the training, the cells are damaged due to ischemic-reperfusion injury. As the recovering time increased, the trend of the free radical and enzyme changes become similar.5. After being over trained, the apoptosis rate in the rat myocardium increases and as the recovering time increases, the expression of the apoptosis promoting gene Bax decreases and the Bcl-2/Bax ratio increases, indicating decreased apoptosis of the myocardium.6. Differences in parameters reflecting the level of myocardial damage repair exist between over trained group and drug treated group, indicating that Phosphocreatine disodium salt treatment after over training may accelerate the repair rate of damaged myocarium.
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