Repeated development and regression of exercise-induced cardiac hypertrophy in rats

1983 ◽  
Vol 54 (3) ◽  
pp. 794-797 ◽  
Author(s):  
R. C. Hickson ◽  
T. M. Galassi ◽  
K. A. Dougherty
Keyword(s):  
Cardiac Hypertrophy ◽  
Exercise Induced

scholarly journals Insulin-Like Growth Factor I Receptor Signaling Is Required for Exercise-Induced Cardiac Hypertrophy

2008 ◽  
Vol 22 (11) ◽  
pp. 2531-2543 ◽  
Author(s):  
Jaetaek Kim ◽  
Adam R. Wende ◽  
Sandra Sena ◽  
Heather A. Theobald ◽  
Jamie Soto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Insulin Like Growth Factor ◽  
Receptor Signaling ◽  
Factor I ◽  
Growth Factor I ◽  
Exercise Induced

scholarly journals Effects of Hypertension and Exercise on Cardiac Proteome Remodelling

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Bernardo A. Petriz ◽  
Octavio L. Franco
Keyword(s):  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Molecular Characteristics ◽  
Hypertension Treatment ◽  
Ischemic Insult ◽  
Left Ventricle Hypertrophy ◽  
Exercise Induced ◽  
Ventricle Hypertrophy ◽  
Related Proteins ◽  
Proteomic Research

Left ventricle hypertrophy is a common outcome of pressure overload stimulus closely associated with hypertension. This process is triggered by adverse molecular signalling, gene expression, and proteome alteration. Proteomic research has revealed that several molecular targets are associated with pathologic cardiac hypertrophy, including angiotensin II, endothelin-1 and isoproterenol. Several metabolic, contractile, and stress-related proteins are shown to be altered in cardiac hypertrophy derived by hypertension. On the other hand, exercise is a nonpharmacologic agent used for hypertension treatment, where cardiac hypertrophy induced by exercise training is characterized by improvement in cardiac function and resistance against ischemic insult. Despite the scarcity of proteomic research performed with exercise, healthy and pathologic heart proteomes are shown to be modulated in a completely different way. Hence, the altered proteome induced by exercise is mostly associated with cardioprotective aspects such as contractile and metabolic improvement and physiologic cardiac hypertrophy. The present review, therefore, describes relevant studies involving the molecular characteristics and alterations from hypertensive-induced and exercise-induced hypertrophy, as well as the main proteomic research performed in this field. Furthermore, proteomic research into the effect of hypertension on other target-demerged organs is examined.

Exercise induced cardiac hypertrophy provides protection against pressure overload

2007 ◽  
Vol 42 (6) ◽  
pp. S142-S143
Author(s):  
Julie R. McMullen ◽  
Xiao-Ming Gao ◽  
Helen Kiriazis ◽  
Xiao-Jun Du ◽  
Kimberly A. Hewitt ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Exercise Induced

Androgen and glucocorticoid mechanisms in exercise-induced cardiac hypertrophy

1984 ◽  
Vol 246 (6) ◽  
pp. H761-H767 ◽  
Author(s):  
R. C. Hickson ◽  
T. M. Galassi ◽  
T. T. Kurowski ◽  
D. G. Daniels ◽  
R. T. Chatterton
Keyword(s):  
Cardiac Hypertrophy ◽  
Receptor Binding ◽  
Dissociation Constants ◽  
Binding Capacity ◽  
Rest Period ◽  
Serum Testosterone ◽  
Female Rats ◽  
Total Serum ◽  
Ventricular Tissue ◽  
Exercise Induced

Female rats were trained daily by means of two 2-h-long bouts of swimming separated by a 30- to 40-min rest period. Absolute ventricular weights of the swimmers were increased above sedentary control values by 6% after 2 days, 15% after 7 days, and 30% after 35 days of exercise. Resting levels of total and free serum testosterone and total 5 alpha-dihydrotestosterone were not altered by the training. Total serum corticosterone concentrations at rest were significantly lower in the 7-day (149 +/- 16 ng/ml) and 35-day (169 +/- 24) swimmers compared with the controls (293 +/- 26). However, free corticosterone was not significantly reduced from controls in any of the swimming groups. Ventricular muscle cytosol androgen receptor binding dissociation constants and receptor binding capacities, measured using [3H]methyltrienolone (R1881), were not significantly different from control values in the exercised groups. Glucocorticoid cytosol receptor binding capacity in ventricular tissue, determined using [3H]dexamethasone, was significantly increased as femtomoles per milligram protein (39.3 +/- 3.1 vs. 31.4 +/- 1.4) and femtomoles per milligram DNA (2,683 +/- 226 vs. 1,786 +/- 71). These findings show that glucocorticoids, rather than androgens, undergo adaptive changes in the circulation and in muscle during the development of exercise-induced cardiac hypertrophy.

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis

2013 ◽  
Vol 305 (1) ◽  
pp. H124-H134 ◽  
Author(s):  
Tamás Radovits ◽  
Attila Oláh ◽  
Árpád Lux ◽  
Balázs Tamás Németh ◽  
László Hidi ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Rat Model ◽  
Left Ventricular ◽  
Heart Weight ◽  
Stroke Work ◽  
Functional Changes ◽  
Exercise Induced

Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressure-conductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 ± 0.09 vs. 2.03 ± 0.08 g/kg, P < 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV end-diastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 ± 0.8 vs. 64.1 ± 1.5%, P < 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 ± 6.8 vs. 54.3 ± 4.8 mmHg, P = 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 ± 0.02 vs. 0.65 ± 0.08, P < 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 ± 0.007 vs. 0.040 ± 0.006 mmHg/μl) and improved LV active relaxation (τ: 10.1 ± 0.6 vs. 11.9 ± 0.2 ms, P < 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.

Effect of nandrolone decanoate on exercise-induced cardiac hypertrophy in rats

2002 ◽  
Vol 34 (6) ◽  
pp. A86
Author(s):  
Jan Kyselovic ◽  
Karol Michalak ◽  
Jan Klimas ◽  
Peter Krenek ◽  
Peter Martinka
Keyword(s):  
Cardiac Hypertrophy ◽  
Nandrolone Decanoate ◽  
Exercise Induced

Exercise-Induced Cardiac Hypertrophy

1994 ◽  
Vol 17 (5) ◽  
pp. 288-308 ◽  
Author(s):  
Hélène Perrault ◽  
René A. Turcotte
Keyword(s):  
Cardiac Hypertrophy ◽  
Exercise Induced

scholarly journals Serum Natriuretic Peptides as Differential Biomarkers Allowing for the Distinction between Physiologic and Pathologic Left Ventricular Hypertrophy

2016 ◽  
Vol 45 (2) ◽  
pp. 344-352 ◽  
Author(s):  
Michael E. Dunn ◽  
Thomas G. Manfredi ◽  
Kevin Agostinucci ◽  
Steven K. Engle ◽  
Josh Powe ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Left Ventricular ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
Drug Induced ◽  
Peroxisome Proliferator Activated Receptor ◽  
Sprague Dawley Rats ◽  
Exercise Induced

Given the proven utility of natriuretic peptides as serum biomarkers of cardiovascular maladaptation and dysfunction in humans and the high cross-species sequence conservation of atrial natriuretic peptides, natriuretic peptides have the potential to serve as translational biomarkers for the identification of cardiotoxic compounds during multiple phases of drug development. This work evaluated and compared the response of N-terminal proatrial natriuretic peptide (NT-proANP) and N-terminal probrain natriuretic peptide (NT-proBNP) in rats during exercise-induced and drug-induced increases in cardiac mass after chronic swimming or daily oral dosing with a peroxisome proliferator-activated receptor γ agonist. Male Sprague-Dawley rats aged 8 to 10 weeks were assigned to control, active control, swimming, or drug-induced cardiac hypertrophy groups. While the relative heart weights from both the swimming and drug-induced cardiac hypertrophy groups were increased 15% after 28 days of dosing, the serum NT-proANP and NT-proBNP values were only increased in association with cardiac hypertrophy caused by compound administration. Serum natriuretic peptide concentrations did not change in response to adaptive physiologic cardiac hypertrophy induced by a 28-day swimming protocol. These data support the use of natriuretic peptides as fluid biomarkers for the distinction between physiological and drug-induced cardiac hypertrophy.

Comparison of Nigella sativa- and Exercise-Induced Models of Cardiac Hypertrophy: Structural and Electrophysiological Features

2014 ◽  
Vol 14 (3) ◽  
pp. 208-213 ◽  
Author(s):  
Lubna Ibrahim Al-Asoom ◽  
Basil Abdulrahman Al-Shaikh ◽  
Abdullah Omar Bamosa ◽  
Mohammad Nabil El-Bahai
Keyword(s):  
Cardiac Hypertrophy ◽  
Nigella Sativa ◽  
Exercise Induced
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