Font Size: a A A

Study On The Changes Of Bax, Bcl-2 And LDH-2 In Myocardium Of Rats With Continuous Weight Loading In Excessive Fatigue

Posted on:2016-06-06Degree:MasterType:Thesis
Country:ChinaCandidate:T T GuoFull Text:PDF
GTID:2207330470464427Subject:Human Movement Science
Abstract/Summary:PDF Full Text Request
Objective: according to the "glycolysis motion 36 h overload recovery interval" model and energy supply research interval theory over restoration movement in the process of glycolysis, to 36 h the best excess recovery interval based on sports fatigue, recovery process from fifth to six 36 h of excess recovery area between fatigue recovery extent the highest point, then restore the body’s ability to form the ability to recover gradually decreased, negative superposition state, fatigue accumulation, cause airframe fatigue. The body to exercise training in negative superposition, fatigue cumulative, have great effects on the body function condition. At present, about the body changes in the existing state of fatigue visceral organs many reports. However, the research on the dynamic change under the condition of excessive fatigue, the body organs is rare. Therefore, this paper uses "glycolysis Yun Gong 36 h overload recovery interval" intermittent swimming training mode to reach the state of fatigue in rats, to study the change regularity of the expression of LDH-2 and serum Bax and Bcl-2 protein in myocardial pathology, swimming rats in continuous in excessive fatigue state; through the study of fatigue accumulated continuously in the process of the index of heart, have a certain theoretical and practical significance to guide the national fitness movement, athlete protect the health, sports medical supervision, sports practice. Methods: Thirty male SD 56 rats, 7 were randomly selected recorded as blank control group(group N, n=7); the rest rats by "glycolysis model of exercise fatigue", using small, large amount of exercise for swimming, weight for rats 12% of body weight, the establishment of fatigue model after the modeling; stochastic killed 7 rats blood and left ventricular myocardial recorded as experimental control group(group S, n =7). After using a large amount of exercise training period in accordance with 36 h to rats continuously exhaustive swimming exercise to fatigue state. In the first 5-6 36 h recovery, recovery of rat ability appears negative superposition, after seventh 36 h after training were randomly killed 7 rats blood and left ventricular recorded as negative superposition starting group(group M, n=7). Each 36 h were randomly killed 7 rats blood and myocardium of left ventricle, denoted as A, B, C, D, E...... Group. The serum concentrations of LDH were measured by enzyme-linked immunosorbent assay, HE staining to observe the changes of myocardial do phase morphology structure and immunohistochemical staining and determination of its Bax and Bcl-2 protein expression changes observed. Results: 1, the blank control group, N group and experimental control group of normal myocardial tissue in S group, M group, excessive fatigue test under the condition of(seventh 36h) to the experimental group E(twelfth 36h) phase gradually appeared myocardial fiber slender, fracture part of myocardial fiber, focal myocardial vascular congestion and bleeding, extensive myocardial vascular congestion and hemorrhage, myocardial vascular extreme expansion, myocardial fiber fracture and severe necrosis, myocardial fibers dissolved necrosis and hemorrhage and necrosis, myocardial vascular widely old hemorrhage and hemosiderin. Each packet of cardiac damage the relationship between the N=S M=A=B ’C=D=E’. The higher expression of Bax protein 2, rat swimming to fatigue process, compared with the N group increased the expression of Bax protein in M, A, B, C, D, E group rats in heart tissue, with significant difference(P<0.05), and increased; compared with S group increased but there was no significant difference in Bax protein expression of M, A, B, C, D, E group rats in heart tissue(P>0.05). 3, the rat swimming to fatigue in the process of Bcl-2 expression decreased, Bcl-2 protein content was lower than that of N group M, A, B, C, D, E group rats in heart tissue, with significant difference(P<0.01), and a decreasing trend. 4, the rat swimming to fatigue process, M, A, B, C, D, E group rats serum LDH-2 was significantly elevated compared to N group, with significant difference(P<0.05); A, B, C, D, LDH-2 content in serum of E group than in S group increased significantly, and has significant differences(P<0.05). Conclusion: 1, continuous swimming rat myocardium in under the condition of excessive fatigue damage is larger, and with the continuous accumulation of fatigue damage is the deepening of heart. 2, under the condition of excessive fatigue, continuous swimming Rat Myocardium Apoptosis change promotion and inhibition. Inhibition of apoptosis protein Bcl-2 content decreased tendency is obvious, and promote apoptosis protein Bax content significantly, myocardial intracellular Bcl-2 and abnormal expression of Bax protein is the main cause of myocardial tissue injury. 3, under the condition of excessive fatigue, increase continuous swimming rats blood lactate dehydrogenase 2 content. The content of LDH-2 in serum increased direct aggravate myocardial injury.
Keywords/Search Tags:continuous loading, fatigue, Bax, Bcl-2, LDH-2
PDF Full Text Request
Related items