TY - JOUR
T1 - Strength training improves heart function, collagen and strength in rats with heart failure
AU - Dias, Leisiane G.
AU - Reis, Carlos H.O.
AU - Dos Santos, Leonardo
AU - Krause Neto, Walter
AU - Lima-Leopoldo, Ana Paula
AU - Baker, Julien S.
AU - Leopoldo, André S.
AU - Bocalini, Danilo S.
N1 - Thanks to Fundação de Amparo à Pesquisa do Espírito Santo (FAPES, grant numbers 1007/2022, 637/2022, 625/2022, 1099/2022) and Conselho Nacional de Desenvolvimento Científico and Tecnológico (CNPq) for financial assistance.
Publisher Copyright:
© 2024. The Author(s).
PY - 2024/2/16
Y1 - 2024/2/16
N2 - BACKGROUND/OBJECTIVES: Myocardial infarction (MI) frequently leads to cardiac remodeling and failure with impaired life quality, playing an important role in cardiovascular deaths. Although physical exercise is a well-recognized effective non-pharmacological therapy for cardiovascular diseases, the effects of strength training (ST) on the structural and functional aspects of cardiac remodeling need to be further documented. In this study, we aimed to investigate the role of a linear block ST protocol in the rat model of MI.METHODS AND RESULTS: After 6 weeks of MI induction or sham surgery, male adult rats performed ST for the following 12 weeks. The ladder-based ST program was organized in three mesocycles of 4 weeks, with one load increment for each block according to the maximal carrying load test. After 12 weeks, the infarcted-trained rats exhibited an increase in performance, associated with reduced cardiac hypertrophy and pulmonary congestion compared with the untrained group. Despite not changing MI size, the ST program partially prevented cardiac dilatation and ventricular dysfunction assessed by echocardiography and hemodynamics, and interstitial fibrosis evaluated by histology. In addition, isolated cardiac muscles from infarcted-trained rats had improved contractility parameters in a steady state, and in response to calcium or stimuli pauses.CONCLUSIONS: The ST in infarcted rats increased the capacity to carry mass, associated with attenuation of cardiac remodeling and pulmonary congestion with improving cardiac function that could be attributed, at least in part, to the improvement of myocardial contractility.
AB - BACKGROUND/OBJECTIVES: Myocardial infarction (MI) frequently leads to cardiac remodeling and failure with impaired life quality, playing an important role in cardiovascular deaths. Although physical exercise is a well-recognized effective non-pharmacological therapy for cardiovascular diseases, the effects of strength training (ST) on the structural and functional aspects of cardiac remodeling need to be further documented. In this study, we aimed to investigate the role of a linear block ST protocol in the rat model of MI.METHODS AND RESULTS: After 6 weeks of MI induction or sham surgery, male adult rats performed ST for the following 12 weeks. The ladder-based ST program was organized in three mesocycles of 4 weeks, with one load increment for each block according to the maximal carrying load test. After 12 weeks, the infarcted-trained rats exhibited an increase in performance, associated with reduced cardiac hypertrophy and pulmonary congestion compared with the untrained group. Despite not changing MI size, the ST program partially prevented cardiac dilatation and ventricular dysfunction assessed by echocardiography and hemodynamics, and interstitial fibrosis evaluated by histology. In addition, isolated cardiac muscles from infarcted-trained rats had improved contractility parameters in a steady state, and in response to calcium or stimuli pauses.CONCLUSIONS: The ST in infarcted rats increased the capacity to carry mass, associated with attenuation of cardiac remodeling and pulmonary congestion with improving cardiac function that could be attributed, at least in part, to the improvement of myocardial contractility.
KW - Contractility
KW - Exercise
KW - Myocardial fibrosis
KW - Myocardial remodeling
KW - Resistance training
UR - http://www.scopus.com/inward/record.url?scp=85185393769&partnerID=8YFLogxK
UR - https://jps.biomedcentral.com/articles/10.1186/s12576-024-00899-3#article-info
U2 - 10.1186/s12576-024-00899-3
DO - 10.1186/s12576-024-00899-3
M3 - Journal article
C2 - 38365576
AN - SCOPUS:85185393769
SN - 1880-6546
VL - 74
JO - The journal of physiological sciences : JPS
JF - The journal of physiological sciences : JPS
M1 - 10
ER -