Long-Term Low Intensity Physical Exercise Attenuates Heart Failure Development in Aging Spontaneously Hypertensive Rats

Background: Physical exercise is a strategy to control hypertension and attenuate pressure overload-induced cardiac remodeling. The influence of exercise on cardiac remodeling during uncontrolled hypertension is not established. We evaluated the effects of a long-term low intensity aerobic exercise protocol on heart failure (HF) development and cardiac remodeling in aging spontaneously hypertensive rats (SHR). Methods: Sixteen month old SHR (n=50) and normotensive Wistar-Kyoto (WKY, n=35) rats were divided into sedentary (SED) and exercised (EX) groups. Rats exercised in treadmill at 12 m/min, 30 min/day, 5 days/week, for four months. The frequency of HF features was evaluated at euthanasia. Statistical analyses: ANOVA and Tukey or Mann-Whitney, and Goodman test. Results: Despite slightly higher systolic blood pressure, SHR-EX had better functional capacity and lower HF frequency than SHR-SED. Echocardiography and tissue Doppler imaging showed no differences between SHR groups. In SHR-EX, however, left ventricular (LV) systolic diameter, larger in SHR-SED than WKY-SED, and endocardial fractional shortening, lower in SHR-SED than WKY-SED, had values between those in WKY-EX and SHR-SED not differing from either group. Myocardial function, assessed in LV papillary muscles, showed improvement in SHR-EX over SHR-SED and WKY-EX. LV myocardial collagen fraction and type I and III collagen gene expression were increased in SHR groups. Myocardial hydroxyproline concentration was lower in SHR-EX than SHR-SED. Lysyl oxidase gene expression was higher in SHR-SED than WKY-SED. Conclusion: Exercise improves functional capacity and reduces decompensated HF in aging SHR independent of elevated arterial pressure. Improvement in functional status is combined with attenuation of LV and myocardial dysfunction and fibrosis.

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Moderate intensity exercise does not modulate myostatin and follistatin gene expression in the gastrocnemius muscle of spontaneously hypertensive rats with heart failure

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.lb484 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Ricardo Luiz Damatto ◽

Luana Pagan ◽

Aline Lima ◽

Marcelo Cezar ◽

Paula Martinez ◽

...

Keyword(s):

Gene Expression ◽

Heart Failure ◽

Spontaneously Hypertensive Rats ◽

Gastrocnemius Muscle ◽

Moderate Intensity ◽

Hypertensive Rats ◽

Moderate Intensity Exercise ◽

Spontaneously Hypertensive

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Voluntary physical exercise-induced vascular effects in spontaneously hypertensive rats

Clinical Science ◽

10.1042/cs20040171 ◽

2004 ◽

Vol 107 (6) ◽

pp. 571-581 ◽

Cited By ~ 31

Author(s):

Ulrika HÄGG ◽

Irene ANDERSSON ◽

Andrew S. NAYLOR ◽

Julia GRÖNROS ◽

Ingibjörg H. JONSDOTTIR ◽

...

Keyword(s):

Gene Expression ◽

Physical Exercise ◽

Vascular Function ◽

Spontaneously Hypertensive Rats ◽

Aortic Wall ◽

Hypertensive Rats ◽

Vascular Effects ◽

Spontaneously Hypertensive ◽

Wall Stiffness ◽

Vascular Beds

Forced training has been shown to have beneficial vascular effects in various animal exercise models. In the present study, we explored possible physiological and molecular effects of voluntary physical exercise on various vascular beds. SHR (spontaneously hypertensive rats) performed voluntary exercise for 5 weeks in a computerized wheel cage facility. Ex vivo myograph studies revealed an increased sensitivity of the ACh (acetylcholine)-mediated vasodilation in resistance arteries of the exercised animals (ED50=15.0±3.5 nmol/l) compared with the controls (ED50=37.0±8.8 nmol/l; P=0.05). The exercise/control difference was abolished after scavenging reactive oxygen radicals. In conduit arteries, ACh induced a similar vasodilatory response in both groups. The in vivo aortic wall stiffness, assessed by means of Doppler tissue echography, was significantly lower in the exercising animals than in controls. This was demonstrated by significantly increased peak systolic aortic wall velocity (P=0.03) and the velocity time integral (P=0.01) in exercising animals compared with controls. The relative gene expression of eNOS (endothelial nitric oxide synthase) was similar in both groups of animals, whereas Cu/ZnSOD (copper/zinc superoxide dismutase) gene expression was significantly increased (+111%; P=0.0007) in the exercising animal compared with controls. In conclusion, voluntary physical exercise differentially improves vascular function in various vascular beds. Increased vascular compliance and antioxidative capacity may contribute to the atheroprotective effects associated with physical exercise in conduit vessels.

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Transcriptome of the NTS in exercise-trained spontaneously hypertensive rats: implications for NTS function and plasticity in regulating blood pressure

Physiological Genomics ◽

10.1152/physiolgenomics.00074.2012 ◽

2013 ◽

Vol 45 (1) ◽

pp. 58-67 ◽

Cited By ~ 10

Author(s):

Hidefumi Waki ◽

Sabine S. Gouraud ◽

Mohammad E. R. Bhuiyan ◽

Miwa Takagishi ◽

Toshiya Yamazaki ◽

...

Keyword(s):

Gene Expression ◽

Blood Pressure ◽

Spontaneously Hypertensive Rats ◽

Expression Profiles ◽

Potential Contribution ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Daily Exercise ◽

Receptor Interactions

The nucleus tractus solitarii (NTS) controls the cardiovascular system during exercise, and alteration of its function may underlie exercise-induced cardiovascular adaptation. To understand the molecular basis of the NTS's plasticity in regulating blood pressure (BP) and its potential contribution to the antihypertensive effects, we characterized the gene expression profiles at the level of the NTS after long-term daily wheel running in spontaneously hypertensive rats (SHRs). Genome-wide microarray analysis was performed to screen for differentially expressed genes in the NTS between exercise-trained (12 wk) and control SHRs. Pathway analysis using the Kyoto Encyclopedia of Genes and Genomes database revealed that daily exercise altered the expression levels of NTS genes that are functionally associated with metabolic pathways (5 genes), neuroactive ligand-receptor interactions (4 genes), cell adhesion molecules (3 genes), and cytokine-cytokine receptor interactions (3 genes). One of the genes that belonged to the neuroactive ligand-receptor interactions category was histamine receptor H1. Since we confirmed that the pressor response induced by activation of this receptor is increased after long-term daily exercise, it is suggested that functional plasticity in the histaminergic system may mediate the facilitation of blood pressure control in response to exercise but may not be involved in the lowered basal BP level found in exercise-trained SHRs. Since abnormal inflammatory states in the NTS are known to be prohypertensive in SHRs, altered gene expression of the inflammatory molecules identified in this study may be related to the antihypertensive effects in exercise-trained SHRs, although such speculation awaits functional validation.

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