Behnam Heidari, Mohammad Reza Zolfaghari, Kamal Khademvatani, Amir Fattahi, Reza Zarezadeh
{"title":"运动员和非运动员女性运动训练、心肌肥厚和组织钾激肽-激肽系统之间的相互关系。","authors":"Behnam Heidari, Mohammad Reza Zolfaghari, Kamal Khademvatani, Amir Fattahi, Reza Zarezadeh","doi":"10.34172/jcvtr.2022.28","DOIUrl":null,"url":null,"abstract":"<p><p><b><i>Introduction:</i></b> The tissue kallikrein-kinin system is an endogenous homeostatic pathway, which its stimulation is associated with cardioprotection. The present study aimed to determine the effect of exercise training on plasma tissue kallikrein (TK) and bradykinin (BK) and their association with cardiac hypertrophy. <b><i>Methods:</i></b> 22 non-athlete and 22 athlete women were exposed to acute (Bruce test) and chronic (12-week swimming training) exercises. 2D echocardiography was used to evaluate morphological and functional features of the heart. Plasma concentrations of TK and BK were quantified by ELISA. <b><i>Results:</i></b> Athletes had significantly higher values of left ventricle end-diastolic diameter index (LVEDDI) and left ventricle mass index (LVMI) than non-athletes. Exercise intervention affected echocardiographic features in neither of the study groups. Chronic exercise training notably increased plasma levels of TK and BK, which increase was more pronounced in the athletes. Plasma TK negatively correlated with LVEDDI (r=-0.64, <i>P</i>=0.036 and r=-0.58, <i>P</i>=0.027) and LVMI (r=-0.51, <i>P</i>=0.032 and r=-0.63, <i>P</i>=0.028) in the non-athlete and athlete groups. In opposition, there was a positive correlation between plasma TK and left ventricle ejection fraction in non-athletes (r=0.39, <i>P</i>=0.049) and athletes (r=0.53, <i>P</i>=0.019). <b><i>Conclusion:</i></b> The upregulation of the tissue kallikrein-kinin system may be a protective mechanism against excessive cardiac hypertrophy induced by chronic exercise training.</p>","PeriodicalId":15207,"journal":{"name":"Journal of Cardiovascular and Thoracic Research","volume":"14 3","pages":"159-165"},"PeriodicalIF":1.2000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617055/pdf/","citationCount":"0","resultStr":"{\"title\":\"Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women.\",\"authors\":\"Behnam Heidari, Mohammad Reza Zolfaghari, Kamal Khademvatani, Amir Fattahi, Reza Zarezadeh\",\"doi\":\"10.34172/jcvtr.2022.28\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b><i>Introduction:</i></b> The tissue kallikrein-kinin system is an endogenous homeostatic pathway, which its stimulation is associated with cardioprotection. The present study aimed to determine the effect of exercise training on plasma tissue kallikrein (TK) and bradykinin (BK) and their association with cardiac hypertrophy. <b><i>Methods:</i></b> 22 non-athlete and 22 athlete women were exposed to acute (Bruce test) and chronic (12-week swimming training) exercises. 2D echocardiography was used to evaluate morphological and functional features of the heart. Plasma concentrations of TK and BK were quantified by ELISA. <b><i>Results:</i></b> Athletes had significantly higher values of left ventricle end-diastolic diameter index (LVEDDI) and left ventricle mass index (LVMI) than non-athletes. Exercise intervention affected echocardiographic features in neither of the study groups. Chronic exercise training notably increased plasma levels of TK and BK, which increase was more pronounced in the athletes. Plasma TK negatively correlated with LVEDDI (r=-0.64, <i>P</i>=0.036 and r=-0.58, <i>P</i>=0.027) and LVMI (r=-0.51, <i>P</i>=0.032 and r=-0.63, <i>P</i>=0.028) in the non-athlete and athlete groups. In opposition, there was a positive correlation between plasma TK and left ventricle ejection fraction in non-athletes (r=0.39, <i>P</i>=0.049) and athletes (r=0.53, <i>P</i>=0.019). <b><i>Conclusion:</i></b> The upregulation of the tissue kallikrein-kinin system may be a protective mechanism against excessive cardiac hypertrophy induced by chronic exercise training.</p>\",\"PeriodicalId\":15207,\"journal\":{\"name\":\"Journal of Cardiovascular and Thoracic Research\",\"volume\":\"14 3\",\"pages\":\"159-165\"},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2022-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617055/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Cardiovascular and Thoracic Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.34172/jcvtr.2022.28\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2022/8/30 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cardiovascular and Thoracic Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.34172/jcvtr.2022.28","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/8/30 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women.
Introduction: The tissue kallikrein-kinin system is an endogenous homeostatic pathway, which its stimulation is associated with cardioprotection. The present study aimed to determine the effect of exercise training on plasma tissue kallikrein (TK) and bradykinin (BK) and their association with cardiac hypertrophy. Methods: 22 non-athlete and 22 athlete women were exposed to acute (Bruce test) and chronic (12-week swimming training) exercises. 2D echocardiography was used to evaluate morphological and functional features of the heart. Plasma concentrations of TK and BK were quantified by ELISA. Results: Athletes had significantly higher values of left ventricle end-diastolic diameter index (LVEDDI) and left ventricle mass index (LVMI) than non-athletes. Exercise intervention affected echocardiographic features in neither of the study groups. Chronic exercise training notably increased plasma levels of TK and BK, which increase was more pronounced in the athletes. Plasma TK negatively correlated with LVEDDI (r=-0.64, P=0.036 and r=-0.58, P=0.027) and LVMI (r=-0.51, P=0.032 and r=-0.63, P=0.028) in the non-athlete and athlete groups. In opposition, there was a positive correlation between plasma TK and left ventricle ejection fraction in non-athletes (r=0.39, P=0.049) and athletes (r=0.53, P=0.019). Conclusion: The upregulation of the tissue kallikrein-kinin system may be a protective mechanism against excessive cardiac hypertrophy induced by chronic exercise training.