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Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats

Elevated salt intake induces changes in the extracellular matrix collagen, leading to myocardial stiffness and impaired relaxation. Resistance training (RT) has been used as a remarkably successful strategy in the treatment of heart disease. Therefore, the aim of this study was to investigate the ef...

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Autores principales: Barretti, D.L.M., Melo, S.F.S., Oliveira, E.M., Barauna, V.G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Associação Brasileira de Divulgação Científica 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572849/
https://www.ncbi.nlm.nih.gov/pubmed/28793051
http://dx.doi.org/10.1590/1414-431X20176146
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author Barretti, D.L.M.
Melo, S.F.S.
Oliveira, E.M.
Barauna, V.G.
author_facet Barretti, D.L.M.
Melo, S.F.S.
Oliveira, E.M.
Barauna, V.G.
author_sort Barretti, D.L.M.
collection PubMed
description Elevated salt intake induces changes in the extracellular matrix collagen, leading to myocardial stiffness and impaired relaxation. Resistance training (RT) has been used as a remarkably successful strategy in the treatment of heart disease. Therefore, the aim of this study was to investigate the effects of RT on preventing pathological adaptation of the left ventricle (LV) induced by salt overload. Male Wistar rats (10 weeks old) were distributed into four groups (n=8/group): control (CO), control+1% salt (CO+SALT), RT and RT+1% salt (RT+SALT). The RT protocol consisted of 4×12 bouts of squat training, 5/week for 8 weeks, with 80% of one repetition maximum (1RM). Echocardiographs were analyzed and interstitial collagen volume fraction (CVF) was determined in the LV. The 1RM tests in the RT and RT+SALT groups increased 145 and 137%, respectively, compared with the test performed before the training program. LV weight-to-body weight ratio and LV weight-to-tibia length ratio were greater in the RT and RT+SALT groups, respectively, compared with the CO group. Although there was no difference in the systolic function between groups, diastolic function decreased 25% in the CO+SALT group compared with the CO group measured by E/A wave ratio. RT partially prevented this decrease in diastolic function compared with the CO+SALT group. A 1% salt overload increased CVF more than 2.4-fold in the CO+SALT group compared with the CO group and RT prevented this increase. In conclusion, RT prevented interstitial collagen deposition in LV rats subjected to 1% NaCl and attenuated diastolic dysfunction induced by salt overload independent of alterations in blood pressure.
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spelling pubmed-55728492017-08-31 Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats Barretti, D.L.M. Melo, S.F.S. Oliveira, E.M. Barauna, V.G. Braz J Med Biol Res Research Articles Elevated salt intake induces changes in the extracellular matrix collagen, leading to myocardial stiffness and impaired relaxation. Resistance training (RT) has been used as a remarkably successful strategy in the treatment of heart disease. Therefore, the aim of this study was to investigate the effects of RT on preventing pathological adaptation of the left ventricle (LV) induced by salt overload. Male Wistar rats (10 weeks old) were distributed into four groups (n=8/group): control (CO), control+1% salt (CO+SALT), RT and RT+1% salt (RT+SALT). The RT protocol consisted of 4×12 bouts of squat training, 5/week for 8 weeks, with 80% of one repetition maximum (1RM). Echocardiographs were analyzed and interstitial collagen volume fraction (CVF) was determined in the LV. The 1RM tests in the RT and RT+SALT groups increased 145 and 137%, respectively, compared with the test performed before the training program. LV weight-to-body weight ratio and LV weight-to-tibia length ratio were greater in the RT and RT+SALT groups, respectively, compared with the CO group. Although there was no difference in the systolic function between groups, diastolic function decreased 25% in the CO+SALT group compared with the CO group measured by E/A wave ratio. RT partially prevented this decrease in diastolic function compared with the CO+SALT group. A 1% salt overload increased CVF more than 2.4-fold in the CO+SALT group compared with the CO group and RT prevented this increase. In conclusion, RT prevented interstitial collagen deposition in LV rats subjected to 1% NaCl and attenuated diastolic dysfunction induced by salt overload independent of alterations in blood pressure. Associação Brasileira de Divulgação Científica 2017-08-07 /pmc/articles/PMC5572849/ /pubmed/28793051 http://dx.doi.org/10.1590/1414-431X20176146 Text en http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Barretti, D.L.M.
Melo, S.F.S.
Oliveira, E.M.
Barauna, V.G.
Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats
title Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats
title_full Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats
title_fullStr Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats
title_full_unstemmed Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats
title_short Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats
title_sort resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572849/
https://www.ncbi.nlm.nih.gov/pubmed/28793051
http://dx.doi.org/10.1590/1414-431X20176146
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