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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 cardi...

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Autores principales: Heidari, Behnam, Zolfaghari, Mohammad Reza, Khademvatani, Kamal, Fattahi, Amir, Zarezadeh, Reza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Tabriz University of Medical Sciences 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617055/
https://www.ncbi.nlm.nih.gov/pubmed/36398053
http://dx.doi.org/10.34172/jcvtr.2022.28
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author Heidari, Behnam
Zolfaghari, Mohammad Reza
Khademvatani, Kamal
Fattahi, Amir
Zarezadeh, Reza
author_facet Heidari, Behnam
Zolfaghari, Mohammad Reza
Khademvatani, Kamal
Fattahi, Amir
Zarezadeh, Reza
author_sort Heidari, Behnam
collection PubMed
description 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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spelling pubmed-96170552022-11-16 Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women Heidari, Behnam Zolfaghari, Mohammad Reza Khademvatani, Kamal Fattahi, Amir Zarezadeh, Reza J Cardiovasc Thorac Res Original Article 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. Tabriz University of Medical Sciences 2022 2022-08-30 /pmc/articles/PMC9617055/ /pubmed/36398053 http://dx.doi.org/10.34172/jcvtr.2022.28 Text en © 2022 The Author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Heidari, Behnam
Zolfaghari, Mohammad Reza
Khademvatani, Kamal
Fattahi, Amir
Zarezadeh, Reza
Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women
title Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women
title_full Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women
title_fullStr Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women
title_full_unstemmed Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women
title_short Interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women
title_sort interrelation among exercise training, cardiac hypertrophy, and tissue kallikrein-kinin system in athlete and non-athlete women
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617055/
https://www.ncbi.nlm.nih.gov/pubmed/36398053
http://dx.doi.org/10.34172/jcvtr.2022.28
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