scholarly journals Exercise Training and Cardiac Remodeling

2020 ◽  
Author(s):  
Dayanne Borges ◽  
Suzilene Ormond ◽  
Murilo Nogueira ◽  
Keemilyn Silva ◽  
Jeeser Almeida
Keyword(s):  
Exercise Training ◽  
Cardiac Remodeling

Exercise training in adverse cardiac remodeling

2014 ◽  
Author(s):  
Dirk J. Duncker ◽  
Elza D. van Deel ◽  
Monique C. de Waard ◽  
Martine de Boer ◽  
Daphne Merkus ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Remodeling

scholarly journals Impact of Leucine Supplementation on Exercise Training Induced Anti-Cardiac Remodeling Effect in Heart Failure Mice

Nutrients ◽  
2015 ◽  
Vol 7 (5) ◽  
pp. 3751-3766 ◽  
Author(s):  
Wilson de Moraes ◽  
Thaís Melara ◽  
Pamella de Souza ◽  
Fabiana de Salvi Guimarães ◽  
Luiz Bozi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Cardiac Remodeling ◽  
Leucine Supplementation

Exercise training delays cardiac remodeling in a mouse model of cancer cachexia

Life Sciences ◽  
2020 ◽  
Vol 260 ◽  
pp. 118392
Author(s):  
L.G. Fernandes ◽  
G.C. Tobias ◽  
A.O. Paixão ◽  
P.M. Dourado ◽  
V.A. Voltarelli ◽  
...  
Keyword(s):  
Exercise Training ◽  
Mouse Model ◽  
Cardiac Remodeling ◽  
Cancer Cachexia

Role of cardiac mast cells in exercise training-mediated cardiac remodeling in angiotensin II-infused ovariectomized rats

Life Sciences ◽  
2019 ◽  
Vol 219 ◽  
pp. 209-218 ◽  
Author(s):  
Rerknapat Jitmana ◽  
Sulaksana Raksapharm ◽  
Anusak Kijtawornrat ◽  
Vitoon Saengsirisuwan ◽  
Tepmanas Bupha-Intr
Keyword(s):  
Angiotensin Ii ◽  
Mast Cells ◽  
Exercise Training ◽  
Cardiac Remodeling ◽  
Ovariectomized Rats

scholarly journals Erratum to: Exercise training in adverse cardiac remodeling

2015 ◽  
Vol 468 (2) ◽  
pp. 367-367 ◽  
Author(s):  
Dirk J. Duncker ◽  
Elza D. van Deel ◽  
Monique C. de Waard ◽  
Martine de Boer ◽  
Daphne Merkus ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Remodeling

Exercise Training and Adverse Cardiac Remodeling and Dysfunction in Mice

2012 ◽  
pp. 269-287
Author(s):  
Dirk J. Duncker ◽  
Elza D. van Deel ◽  
Monique C. de Waard ◽  
Jolanda van der Velden
Keyword(s):  
Exercise Training ◽  
Cardiac Remodeling

Exercise training protects against cancer-induced cardiac remodeling in an animal model of urothelial carcinoma

2018 ◽  
Vol 645 ◽  
pp. 12-18 ◽  
Author(s):  
Ana Isabel Padrão ◽  
Rita Nogueira-Ferreira ◽  
Rui Vitorino ◽  
Dulce Carvalho ◽  
Catarina Correia ◽  
...  
Keyword(s):  
Animal Model ◽  
Exercise Training ◽  
Urothelial Carcinoma ◽  
Cardiac Remodeling

scholarly journals Endurance exercise training attenuates natriuretic peptide release during maximal effort exercise: biochemical correlates of the “athlete’s heart”

2018 ◽  
Vol 125 (6) ◽  
pp. 1702-1709 ◽  
Author(s):  
Ankit B. Shah ◽  
Jodi Zilinski ◽  
Marcel Brown ◽  
Jennifer H. Neary ◽  
Rory B. Weiner ◽  
...  
Keyword(s):  
Exercise Training ◽  
Natriuretic Peptide ◽  
Endurance Exercise ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Cardiac Wall ◽  
Endurance Exercise Training ◽  
Exercise Induced ◽  
Maximal Effort

Endurance exercise training (ET) stimulates eccentric left ventricular hypertrophy (LVH) with left atrial dilation. To date, the biochemical correlates of exercise-induced cardiac remodeling (EICR) remain incompletely understood. Collegiate male rowers ( n = 9) were studied with echocardiography and maximal-effort cardiopulmonary exercise testing (MECPET) before and after 90 days of ET intensification. Midregional proatrial natriuretic peptide (MR-proANP), NH2-terminal pro B-type natriuretic peptide (NT-proBNP), and high-sensitivity troponin T were measured at rest, peak MECPET, and 60 min post-MECPET at both study time points. Endurance exercise training resulted in eccentric LVH (LV mass = 102 ± 8 vs. 110 ± 11 g/m2, P = 0.001; relative wall thickness = 0.36 ± 0.04 vs. 0.37 ± 0.04, P = 0.103), left atrial dilation (74 ± 18 vs. 84 ± 15 ml, P < 0.001), and increased exercise capacity (peak V̇o2 = 53.0 ± 5.9 vs. 67.3 ± 8.2 ml·kg−1·min−1, P < 0.001). Left ventricular remodeling was characterized by an ~7% increase in LV wall thickness but only a 3% increase in LV chamber radius. The magnitude of natriuretic peptide release, examined as percent change from rest to peak exercise, was significantly lower for both MR-proANP (115 [95,127]% vs. 78 [59,87]%, P = 0.04) and NT-proBNP (46 [31,70]% vs. 27 [25,37]%, P = 0.02) after ET. Rowing-based ET and corollary EICR appear to result in an attenuated natriuretic peptide response to maximal effort exercise. This may occur as a function of decreased cardiac wall stress after ET as seen by disproportionally higher ventricular wall thickening compared with chamber dilation. NEW & NOTEWORTHY Using longitudinal pre- and postendurance training natriuretic peptide measurements, we demonstrate that the development of exercise-induced cardiac remodeling results in an attenuated natriuretic peptide response to acute bouts of maximal intensity exercise. Exercise-induced cardiac remodeling was associated with a disproportionally higher ventricular wall thickening compared with chamber dilation, a pattern that reduces cardiac wall stress. These observations advance our understanding of both the structural and biochemical adaptations that underlie the cardiovascular response to endurance training.

scholarly journals Structural and functional alterations in heart and skeletal muscle following severe TAC in mice: impact of moderate exercise training

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Julia Böttner ◽  
Sarah Werner ◽  
Volker Adams ◽  
Sarah Knauth ◽  
Angela Kricke ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Remodeling ◽  
Exercise Program ◽  
Pressure Overload ◽  
Exercise Group ◽  
Moderate Exercise ◽  
Cross Sectional ◽  
Reduced Ejection Fraction ◽  
Musculus Soleus

Abstract Background Heart failure (HF) is the leading cause of death in western countries. Cardiac dysfunction is accompanied by skeletal alterations resulting in muscle weakness and fatigue. Exercise is an accepted interventional approach correcting cardiac and skeletal dysfunction, thereby improving mortality, re-hospitalization and quality of life. Animal models are used to characterize underpinning mechanisms. Transverse aortic constriction (TAC) results in cardiac pressure overload and finally HF. Whether exercise training improves cardiac remodeling and peripheral cachexia in the TAC mouse model was not analyzed yet. In this study, 2 weeks post TAC animals were randomized into two groups either performing a moderate exercise program (five times per week at 60% VO2 max for 40 min for a total of 8 weeks) or staying sedentary. Results In both TAC groups HF characteristics reduced ejection fraction (− 15% compared to sham, p < 0.001), cardiac remodeling (+ 22.5% cardiomyocyte cross sectional area compared to sham; p < 0.001) and coronary artery congestion (+ 34% diameter compared to sham; p = 0.008) were observed. Unexpectedly, peripheral cachexia was not detected. Furthermore, compared to sedentary group animals from the exercise group showed aggravated HF symptoms [heart area + 9% (p = 0.026), heart circumference + 7% (p = 0.002), right ventricular wall thickness − 30% (p = 0.003)] while muscle parameters were unchanged [Musculus soleus fiber diameter (p = 0.55), Musculus extensor digitorum longus contraction force (p = 0.90)]. Conclusion The severe TAC model is inappropriate to study moderate exercise effects in HF with respect to cardiac and skeletal muscle improvements. Further, the phenotype induced by different TAC procedures should be well documented and taken into account when planning experiments.

scholarly journals Aerobic Exercise Inhibited P2X7 Purinergic Receptors to Improve Cardiac Remodeling in Mice with Type 2 Diabetes

2021 ◽  
Author(s):  
Ting Wang ◽  
Jianmin Li ◽  
Hui Li ◽  
Xin Zhong ◽  
Luya Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Cardiac Remodeling ◽  
Purinergic Receptors ◽  
Cardiac Fibrosis ◽  
Ventricular Remodeling ◽  
Control Group ◽  
Collagen Deposition

Abstract Background Diabetic cardiomyopathy (DCM), the main complication of diabetes mellitus, presents as cardiac dysfunction by ventricular remodeling. In addition, the inhibition of P2X7 purinergic receptors (P2X7R) alleviates cardiac fibrosis and apoptosis in Type 1 diatebes. However, whether exercise training improves cardiac remodeling by regulating P2X7R remains unknown. Methods Db/db mice spontaneously induced with type 2 diabetes and high-fat diet (HFD) and mice with streptozotin (STZ)-induced type 2 diabetes mice were treated by 12-week treadmill training. Cardiac functions were observed by two-dimensional echocardiography. Hematoxylin-eosin staining, Sirius red staining and transmission electron microscopy were respectively used to detect cardiac morphology, fibrosis and mitochondria. In addidion, real-time polymerase chain reaction and Western Blot were used to detect mRNA and protein levels. Results Studying the hearts of db/db mice and STZ-induced mice, we found that collagen deposition and the number of disordered cells signiଁcantly increased compared with the control group. However, exercise markedly reversed these changes, and the same tendency was observed in the expression of MMP9, COL-I, and TGF-β, which indicated cardiac fibrotic and hypertrophic markers, including ANP and MyHC expression. In addition, the increased Caspase-3 level and the ratio of Bax/Bcl2 were reduced by exercise training, and similar results were observed in the TUNEL test. Notably, the expression of P2X7R was greatly upregulated in the hearts of db/db mice and HFD+STZ-induced DM mice and downregulated by aerobic exercise. Moreover, we indicated that P2X7R knock out signiଁcantly reduced the collagen deposition and disordered cells in the DM group. Furthermore, the apoptosis levels and TUNEL analysis were greatly inhibited by exercise or in the P2X7R−/− group in DM. We found significant differences between the P2X7R−/−+DM+EX group and DM+EX group in myocardial tissue apoptosis and fibrosis, in which the former is significantly milder. Moreover, compared with the P2X7R−/−+DM group, the P2X7R−/−+DM+EX group represented a lower level of cardiac fibrosis. The expression levels of TGF-β at the protein level and TGF-β and ANP at the genetic level were evidently decreased in the P2X7R−/−+DM+EX group. Conclusion Aerobic exercise reversed cardiac remodeling in diabetic mice at least partly through inhibiting P2X7R expression in cardiomyocytes.

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