{"title":"PO-161不同运动方式对心肌梗死大鼠线粒体稳态的影响","authors":"Hai Bo, Yong Zhang","doi":"10.14428/ebr.v1i4.11883","DOIUrl":null,"url":null,"abstract":"Objective To investigate the different effect of moderate-intensity continuous training (MCT) and high-intensity interval exercise training (HIT) on ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction (AMI). \nMethods The AMI rat model was achieved by ligating coronary artery. The AMI and sham operation rats were randomly divided into four groups: sham operation group (Sham), AMI control group (AMI), AMI MCT group (AMI+M), and AMI HIT group (AMI+H). Animals in the AMI+M and AMI+H groups underwent 4 weeks MCT and HIT respectively. Five weeks after AMI, hemodynamic changes, mitochondrial bioenergetics, and PINK1, Beclin1, Mfn2, Drp1, Tfam, COXⅣ, PGC-1α were detected. \nResults Comparing with AMI group, in AMI+M and AMI+H groups, Beclin1 (146.33±18.47, 143.28±16.96.vs. 123.27±13.27, P<0.05), PINK1 (150.33±20.54, 152.28±18.34.vs. 125.27±17.67, P<0.05), Mfn2 (122.28±18.81, 117.19±17.04.vs. 46.27±6.72, P<0.01), and PGC-1α (82.15±16.58, 102.25±13.27.vs. 60.27±9.36, P<0.05~0.01) expression elevated significantly, whereas ROS generation (122.28±18.81, 117.19±17.04.vs. 46.27±6.72, P<0.01) and Drp1 expression (9.58±1.40, 10.18±1.37.vs. 15.85±1.61, P<0.05) showed dramatic decrease. In addition, in AMI+H group, +dp/dt max (6326±325.vs. 5368±271, P<0.05), -dp/dt max (-5312±246.vs. -4457±250, P<0.05), mitochondrial membrane potential (85.24±11.94.vs. 71.28±8.34, P<0.05), ATP synthesis activity (38.77±5.16.vs. 32.33±4.14, P<0.05), Tfam (95.25±12.05.vs. 78.27±12.22, P<0.05) and COXⅣ (89.25±14.06.vs. 67.27±13.71, P<0.05) expression improved significantly. Comparing with AMI+M group, in AMI+H group, +dp/dt max (6326±325.vs. 5775±310, P<0.05), -dp/dt max (-5312±246.vs. -4778±305, P<0.05), PGC-1α (102.25±13.27.vs. 82.15±16.58 1, P<0.05), Tfam (95.25±12.05.vs. 80.15±11.99, P<0.05) and COXⅣ(89.25±14.06.vs. 72.15±10.89, P<0.05) expression improved significantly. \nConclusions High-intensity interval exercise training is superior to moderate-intensity continuous training for ameliorating ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction.","PeriodicalId":12276,"journal":{"name":"Exercise Biochemistry Review","volume":"28 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"PO-161 Effect of different type of exercise on mitochondrial homeostasis in rats with myocardial infarction\",\"authors\":\"Hai Bo, Yong Zhang\",\"doi\":\"10.14428/ebr.v1i4.11883\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective To investigate the different effect of moderate-intensity continuous training (MCT) and high-intensity interval exercise training (HIT) on ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction (AMI). \\nMethods The AMI rat model was achieved by ligating coronary artery. The AMI and sham operation rats were randomly divided into four groups: sham operation group (Sham), AMI control group (AMI), AMI MCT group (AMI+M), and AMI HIT group (AMI+H). Animals in the AMI+M and AMI+H groups underwent 4 weeks MCT and HIT respectively. Five weeks after AMI, hemodynamic changes, mitochondrial bioenergetics, and PINK1, Beclin1, Mfn2, Drp1, Tfam, COXⅣ, PGC-1α were detected. \\nResults Comparing with AMI group, in AMI+M and AMI+H groups, Beclin1 (146.33±18.47, 143.28±16.96.vs. 123.27±13.27, P<0.05), PINK1 (150.33±20.54, 152.28±18.34.vs. 125.27±17.67, P<0.05), Mfn2 (122.28±18.81, 117.19±17.04.vs. 46.27±6.72, P<0.01), and PGC-1α (82.15±16.58, 102.25±13.27.vs. 60.27±9.36, P<0.05~0.01) expression elevated significantly, whereas ROS generation (122.28±18.81, 117.19±17.04.vs. 46.27±6.72, P<0.01) and Drp1 expression (9.58±1.40, 10.18±1.37.vs. 15.85±1.61, P<0.05) showed dramatic decrease. In addition, in AMI+H group, +dp/dt max (6326±325.vs. 5368±271, P<0.05), -dp/dt max (-5312±246.vs. -4457±250, P<0.05), mitochondrial membrane potential (85.24±11.94.vs. 71.28±8.34, P<0.05), ATP synthesis activity (38.77±5.16.vs. 32.33±4.14, P<0.05), Tfam (95.25±12.05.vs. 78.27±12.22, P<0.05) and COXⅣ (89.25±14.06.vs. 67.27±13.71, P<0.05) expression improved significantly. Comparing with AMI+M group, in AMI+H group, +dp/dt max (6326±325.vs. 5775±310, P<0.05), -dp/dt max (-5312±246.vs. -4778±305, P<0.05), PGC-1α (102.25±13.27.vs. 82.15±16.58 1, P<0.05), Tfam (95.25±12.05.vs. 80.15±11.99, P<0.05) and COXⅣ(89.25±14.06.vs. 72.15±10.89, P<0.05) expression improved significantly. \\nConclusions High-intensity interval exercise training is superior to moderate-intensity continuous training for ameliorating ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction.\",\"PeriodicalId\":12276,\"journal\":{\"name\":\"Exercise Biochemistry Review\",\"volume\":\"28 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-10-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Exercise Biochemistry Review\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.14428/ebr.v1i4.11883\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Exercise Biochemistry Review","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14428/ebr.v1i4.11883","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
PO-161 Effect of different type of exercise on mitochondrial homeostasis in rats with myocardial infarction
Objective To investigate the different effect of moderate-intensity continuous training (MCT) and high-intensity interval exercise training (HIT) on ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction (AMI).
Methods The AMI rat model was achieved by ligating coronary artery. The AMI and sham operation rats were randomly divided into four groups: sham operation group (Sham), AMI control group (AMI), AMI MCT group (AMI+M), and AMI HIT group (AMI+H). Animals in the AMI+M and AMI+H groups underwent 4 weeks MCT and HIT respectively. Five weeks after AMI, hemodynamic changes, mitochondrial bioenergetics, and PINK1, Beclin1, Mfn2, Drp1, Tfam, COXⅣ, PGC-1α were detected.
Results Comparing with AMI group, in AMI+M and AMI+H groups, Beclin1 (146.33±18.47, 143.28±16.96.vs. 123.27±13.27, P<0.05), PINK1 (150.33±20.54, 152.28±18.34.vs. 125.27±17.67, P<0.05), Mfn2 (122.28±18.81, 117.19±17.04.vs. 46.27±6.72, P<0.01), and PGC-1α (82.15±16.58, 102.25±13.27.vs. 60.27±9.36, P<0.05~0.01) expression elevated significantly, whereas ROS generation (122.28±18.81, 117.19±17.04.vs. 46.27±6.72, P<0.01) and Drp1 expression (9.58±1.40, 10.18±1.37.vs. 15.85±1.61, P<0.05) showed dramatic decrease. In addition, in AMI+H group, +dp/dt max (6326±325.vs. 5368±271, P<0.05), -dp/dt max (-5312±246.vs. -4457±250, P<0.05), mitochondrial membrane potential (85.24±11.94.vs. 71.28±8.34, P<0.05), ATP synthesis activity (38.77±5.16.vs. 32.33±4.14, P<0.05), Tfam (95.25±12.05.vs. 78.27±12.22, P<0.05) and COXⅣ (89.25±14.06.vs. 67.27±13.71, P<0.05) expression improved significantly. Comparing with AMI+M group, in AMI+H group, +dp/dt max (6326±325.vs. 5775±310, P<0.05), -dp/dt max (-5312±246.vs. -4778±305, P<0.05), PGC-1α (102.25±13.27.vs. 82.15±16.58 1, P<0.05), Tfam (95.25±12.05.vs. 80.15±11.99, P<0.05) and COXⅣ(89.25±14.06.vs. 72.15±10.89, P<0.05) expression improved significantly.
Conclusions High-intensity interval exercise training is superior to moderate-intensity continuous training for ameliorating ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction.