Exercise Training Attenuates Cirrhotic Cardiomyopathy

Souza, Sérgio Luiz Borges de; Mota, Gustavo Augusto Ferreira; Gregolin, Carlo; Nascimento, Milena do; Luvizotto, Renata de Azevedo Melo; Bazan, Silméia Garcia Zanati; Sugizaki, Mário Mateus; Barbisan, Luı́s Fernando; Cicogna, Antônio Carlos; Nascimento, André Ferreira do

doi:10.1007/s12265-020-09997-0

Cited by 10 publications

(14 citation statements)

References 56 publications

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“…Here, we showed that (1) early exercise training had a protective effect against AS-induced pathological remodelling and cardiac dys- For this report, we adapted a training protocol from previous studies that found benefits in functional capacity and cardiac function with different experimental models of cardiac disease. 28,29,33 Both trained groups presented higher functional capacity than untrained Sham and AS groups, as shown by others. 14,17 Previous studies attempt to rescue deficient cardiac function in aortic stenosis rats using a late exercise program that resulted in inconsistent conclusions.…”

Section: Discussionsupporting

confidence: 76%

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Effects of early exercise on cardiac function and lipid metabolism pathway in heart failure

de Souza,

Mota,

da Silva

et al. 2023

J Cellular Molecular Medi

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We employed an early training exercise program, immediately after recovery from surgery, and before severe cardiac hypertrophy, to study the underlying mechanism involved with the amelioration of cardiac dysfunction in aortic stenosis (AS) rats. As ET induces angiogenesis and oxygen support, we aimed to verify the effect of exercise on myocardial lipid metabolism disturbance. Wistar rats were divided into Sham, trained Sham (ShamT), AS and trained AS (AST). The exercise consisted of 5‐week sessions of treadmill running for 16 weeks. Statistical analysis was conducted by anova or Kruskal–Wallis test and Goodman test. A global correlation between variables was also performed using a two‐tailed Pearson's correlation test. AST rats displayed a higher functional capacity and a lower cardiac remodelling and dysfunction when compared to AS, as well as the myocardial capillary rarefaction was prevented. Regarding metabolic properties, immunoblotting and enzymatic assay raised beneficial effects of exercise on fatty acid transport and oxidation pathways. The correlation assessment indicated a positive correlation between variables of angiogenesis and FA utilisation, as well as between metabolism and echocardiographic parameters. In conclusion, early exercise improves exercise tolerance and attenuates cardiac structural and functional remodelling. In parallel, exercise attenuated myocardial capillary and lipid metabolism derangement in rats with aortic stenosis‐induced heart failure.

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Section: Discussionsupporting

confidence: 76%

“…For this report, we adapted a training protocol from previous studies that found benefits in functional capacity and cardiac function with different experimental models of cardiac disease 28,29,33 . Both trained groups presented higher functional capacity than untrained Sham and AS groups, as shown by others 14,17 …”

Section: Discussionmentioning

confidence: 99%

Effects of early exercise on cardiac function and lipid metabolism pathway in heart failure

de Souza,

Mota,

da Silva

et al. 2023

J Cellular Molecular Medi

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“…LV function was evaluated by heart rate (HR), posterior wall shortening velocity (PWSV), ejection fraction (EF), mesocardial fraction shortening (MFS), early and late diastolic mitral inflow velocities (E and A waves), and E/A ratio, E-wave deceleration time (EDT), and isovolumetric relaxation time (IVRT). Additionally, was evaluated the tissue Doppler imaging (TDI) of systolic (s'), early (e'), and late (a') diastolic velocity of the mitral annulus (arithmetic average of the lateral and septal walls) and E/e' ratio [28,44].…”

Section: Echocardiographic Studymentioning

confidence: 99%

“…Exercise training (ET) has been prescribed as adjuvant therapy for cardiac disease and a remarkable attenuator of cardiovascular risk and disease progression [24][25][26][27][28]. Indeed, ET counteracts sympathetic hyperactivity in cardiac disease in humans [29] and animal models [30][31][32].…”

Section: Introductionmentioning

confidence: 99%

Adjustments in β-Adrenergic Signaling Contribute to the Amelioration of Cardiac Dysfunction by Exercise Training in Supravalvular Aortic Stenosis

Souza

Mota

Silva

et al. 2020

Cell Physiol Biochem

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“…In addition, exercise is a cost-effective way of preventing or improving certain heart diseases. For example, exercise attenuates HFD-induced cardiac fibrosis, reductions in the shortening fraction, and arrhythmias in rats and Drosophila [ 36 , 37 , 38 ]; improves cardiac dysfunction and lipid accumulation induced by Nmnat knockdown in Drosophila [ 39 ]; improves cardiac function and myocardial fibrosis in diabetic cardiomyopathy mice [ 40 ]; and prevents or ameliorates thioacetamide (TAA)-induced cardiac-dysfunctional pathological cardiac structural remodeling [ 41 ]. However, functional studies of MYOM2 in the heart and IFM are lacking, and the relationship between regular exercise and MYOM2 is unclear.…”

Section: Introductionmentioning

confidence: 99%

Regular Exercise Rescues Heart Function Defects and Shortens the Lifespan of Drosophila Caused by dMnM Downregulation

Ding

et al. 2022

IJERPH

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Although studies have shown that myomesin 2 (MYOM2) mutations can lead to hypertrophic cardiomyopathy (HCM), a common cardiovascular disease that has a serious impact on human life, the effect of MYOM2 on cardiac function and lifespan in humans is unknown. In this study, dMnM (MYOM2 homologs) knockdown in cardiomyocytes resulted in diastolic cardiac defects (diastolic dysfunction and arrhythmias) and increased cardiac oxidative stress. Furthermore, the knockdown of dMnM in indirect flight muscle (IFM) reduced climbing ability and shortened lifespan. However, regular exercise significantly ameliorated diastolic cardiac dysfunction, arrhythmias, and oxidative stress triggered by dMnM knockdown in cardiac myocytes and also reversed the reduction in climbing ability and shortening of lifespan caused by dMnM knockdown in Drosophila IFM. In conclusion, these results suggest that Drosophila cardiomyocyte dMnM knockdown leads to cardiac functional defects, while dMnM knockdown in IFM affects climbing ability and lifespan. Furthermore, regular exercise effectively upregulates cardiomyocyte dMnM expression levels and ameliorates cardiac functional defects caused by Drosophila cardiomyocyte dMnM knockdown by increasing cardiac antioxidant capacity. Importantly, regular exercise ameliorates the shortened lifespan caused by dMnM knockdown in IFM.

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Exercise Training Attenuates Cirrhotic Cardiomyopathy

Cited by 10 publications

References 56 publications

Effects of early exercise on cardiac function and lipid metabolism pathway in heart failure

Effects of early exercise on cardiac function and lipid metabolism pathway in heart failure

Adjustments in β-Adrenergic Signaling Contribute to the Amelioration of Cardiac Dysfunction by Exercise Training in Supravalvular Aortic Stenosis

Regular Exercise Rescues Heart Function Defects and Shortens the Lifespan of Drosophila Caused by dMnM Downregulation

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