Effect Of Exercise Precondition On Myocardium By Mitochondrial Biogenesis And Respiratory Function After Exhaustive Exercise Injury In Rats

ObjectiveExercise preconditioning can strengthen the heart for a long time of ischemia hypoxia tolerance through intermittent repeated of moderate intensity exercise to protect the heart,formerly we know the mechanism from anti-inflammatory,anti-apoptosis,anti-oxidative stress,but from the point of view there are few studies on energy metabolismbut the mechanism of EP has not been identified to date.Mitochondrial biogenesis is an important mechanism for the maintenance of energy metabolism in cardiomyocytes,and peroxisome proliferator-activated receptor γ coactivator-1α,is the core factor of the mitochondrial biology process,mitochondrial transcription factor A,Estrogen Related Receptor-α,can moderate mitochondrial genes replication and expression of transcription factors,induced mitochondrial precursor growth and differentiation,maintaining normal mitochondrial respiratory function,so as to ensure the full function of mitochondrial respiratory and mitochondrial biology process.The establishment of injury model of exercise preconditioning and exhaustion exercise rats,can probe the preliminary protection of EP through the PGC-1α,NRF1/NRF2,TFAM,ERRα to protect mitochondria function in exhaustion exercise rats,and the influence to the mitochondrial respiratory function.Methods1.Male Sprague Dawley rats were randomly divided into four groups: control group,exhausted group,short-term EP exhausted group,long-term EP exhausted group.The short-term EP underwent 3 days of intermittent swimming exercise,and the long-term exercise preconditioning group 3 weeks some as above.Except for sedentary control group,the exhausted exercise group and EP group underwent exhausted exercise.12 rats were taken from each group,except the C group,the rats were killed 30 minutes after exhausted exercise(Thomas exhausted standardization),besides sedentary control group which were killed in resting state during the same period.The myocardial tissue was taken as pathological section,and the microstructure was observed under light microscope after HE staining.2.The myocardial tissue was taken as pathological section,and the microstructure was observed under light microscope after HE staining.3.The content of CK and CK-MB was detected by ELISA.4.The left ventricular myocardium of rats muscle bundle was in BIOPS mechanical separation,solution in saponin,after weighing use the Oxygraph-2k high resolution mitochondrial respiratory apparatus to determine the rate of myocardial mitochondrial respiratory chain complexes Ⅰ,Ⅱ,state 3 respiration.Ⅳ5.Application of the double antibody clamp method to determine the specimen the rate of mitochondria permeability transition pore.6.The content of the expression of PGC-1α,NRF1,NRF2,TFAM,ERRα was detected by Western Blot.Results:1.Histomorphology of myocardium samples observed by light microscopy: cardiac sarcomeres of control group rats were arranged in neat rows,the density was uniform and there was no organelle edema.Myocardium of Group Exhausted suffered a high degree of edema,and muscle fibers rupture.In Groups of 3D and 3W group part of myocardium edema,furthermore,3D is more close to the control group.2.The comparision of CK、CK-MB、in rats serum of different groups(1)Compared with the sedentary control group,exhaustive group,short-term EP and long-term EP CK and CK-MB levels were significantly increased(P<0.05).(2)Compared with the exhaustive group,long-term EP group,the serum levels of CK,CK-MB,content not decreased significantly,there is not significant difference(P<0.05).4.The respiratory rate of myocardial mitochondrial respiratory chain complex I,II and IV of the state:(1)compared with C group,in addition to short-term and long-term exercise preconditioning group of respiratory chain complex II complexes,the respiration rate decreased significantly more than breathing groups(P<0.05);(2)compared with EE group,the long-term exercise adapt to short-term respiratory complex II and group IV grouplong-term respiration rate compound significantly increased(P< 0.05);(3)and the short term group long-term exercise preconditioning group of mitochondrial respiratory chain complexes of the respiratory rate increased significantly(P < 0.05).5.The myocardial mitochondrial MPTP opening condition:(1)compared with the control group,exhaustive group,short-term exercise preconditioning myocardial mitochondria of rats in MPTP group were significantly increased,with statistical significance(P<0.05);(2)long-term group than in the control group MPTP was not significant,no statistical significance(P >0.05);(3)long-term group than short-term exercise preconditioning group,exhaustive exercise group significantly decreased,with statistical significance(P <0.05).6.Expression levels of PGC-1α、NRF1、NRF2、TFAM、ERRα in The myocardial tissue:(1)compared with group C,in addition to the long-term exercise preconditioning groupPGC-1α,the expression of PGC-1α、NRF1、NRF2、TFAM、ERRα were significantly decreased,with statistical significance(P<0.05);(2)compared with exhaustion group,the short term and long term exercise preconditioning group rats,the content of myocardial PGC-1α、NRF1、NRF2、TFAM、ERRαsignificantly increased,with statistical significance(P<0.05);(3)in addition to PGC-1α group,long-term exercise preconditioning group than short-term rise more apparent,with statistical significance(P <0.05).Conclusion:1.Myocardial enzyme increased significantly after exhaustion exercise that exhaustion exercise can cause myocardial injury in rats.2.Cut mitochondria exhaustion exercise by biogenic key signaling pathways of expression of PGC-1α-NRF1/NRF2-TFAM,and to lower expression of ERRα,reduce mitochondrial respiratory complex activity,reduce myocardial ATP energy supply,causing myocardial energy hungry and myocardial damage.3.Movement preadaptation through the mitochondrial biology key signaling pathways in PGC-1α-NRF1/NRF2-TFAM expression,increase the expression of ERRα,stimulate mitochondrial biology,increased mitochondrial respiratory complex Ⅰ,Ⅱ,Ⅳactivity,hereby reducing the energy supply of mitochondria,so as to achieve the purpose of protecting myocardial.The role of longer duration of EP is more significant.