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。

IF 1.2 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Behnam Heidari, Mohammad Reza Zolfaghari, Kamal Khademvatani, Amir Fattahi, Reza Zarezadeh
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引用次数: 0

摘要

组织钾likrein-kinin系统是一种内源性稳态通路,其刺激与心脏保护有关。本研究旨在确定运动训练对血浆组织激肽肽(TK)和缓激肽(BK)的影响及其与心肌肥厚的关系。方法:22名非运动员和22名运动员分别进行急性(布鲁斯试验)和慢性(12周游泳训练)锻炼。采用二维超声心动图评价心脏形态和功能特征。ELISA法测定血浆TK、BK浓度。结果:运动员左心室舒张末期直径指数(LVEDDI)和左心室质量指数(LVMI)明显高于非运动员。运动干预对两个研究组的超声心动图特征均无影响。慢性运动训练显著提高血浆TK和BK水平,其中运动员的升高更为明显。血浆TK与非运动员组LVEDDI (r=-0.64, P=0.036, r=-0.58, P=0.027)、LVMI (r=-0.51, P=0.032, r=-0.63, P=0.028)呈负相关。相反,非运动员血浆TK与左心室射血分数呈正相关(r=0.39, P=0.049),运动员血浆TK与左心室射血分数呈正相关(r=0.53, P=0.019)。结论:组织钾likrein-kinin系统的上调可能是对抗慢性运动训练引起的过度心肌肥厚的保护机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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来源期刊
Journal of Cardiovascular and Thoracic Research
Journal of Cardiovascular and Thoracic Research CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
2.00
自引率
0.00%
发文量
22
审稿时长
7 weeks
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