Aerobic interval training attenuates remodelling and mitochondrial dysfunction in the post-infarction failing rat heart

Kraljević, Jasenka; Marinović, Jasna; Pravdić, Danijel; Zubin, Petra; Dujić, Željko; Wisløff, Ulrik; Ljubković, Marko

doi:10.1093/cvr/cvt080

Cited by 58 publications

(67 citation statements)

References 44 publications

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“…Several studies have demonstrated that exercise training which induced better aerobic capacity confers sustainable protection against cardiovascular diseases in animal models and humans, improving cardiovascular outcome and quality of life Campos et al, 2012;Erbs et al, 2010;Medeiros et al, 2008;Rognmo et al, 2012). Some of the cellular adaptations induced by exercise include mitochondrial biogenesis, improved efficiency of cardiac mitochondrial oxidative phosphorylation, reduced mitochondria permeability transition, elevated antioxidant capacity and induction of myocardial heat shock proteins (Campos et al, 2012;Kraljevic et al, 2013). However, the molecular mechanisms underlying the beneficial effects of exercise training on cardiovascular diseases are still in debate.…”

Section: Exercise Training and Redox Signalingmentioning

confidence: 99%

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Impact of exercise training on redox signaling in cardiovascular diseases

Campos

Gomes

Ferreira

2013

Food and Chemical Toxicology

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Section: Exercise Training and Redox Signalingmentioning

confidence: 99%

“…Kraljevic and co-workers have recently demonstrated that aerobic interval training restores mitochondrial respiration in a myocardial infarction-induced heart failure animal model (Kraljevic et al, 2013). However, further studies comparing different exercise training protocols are required.…”

Section: Heart Failurementioning

confidence: 99%

Impact of exercise training on redox signaling in cardiovascular diseases

Campos

Gomes

Ferreira

2013

Food and Chemical Toxicology

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“…In stable chronic heart failure, clinical studies have shown that long-term moderate physical training attenuates abnormal cardiac remodeling and improves functional capacity and quality of life [10,11,12,13]. In different cardiac injury models, exercise has been shown to attenuate left ventricular dilation, myocyte hypertrophy, myocardial fibrosis, mitochondrial dysfunction, myocyte calcium handling changes, sympathoexcitation, cardiac dysfunction, and improve inflammatory profile [14,15,16,17,18,19,20,21,22]. …”

Section: Introductionmentioning

confidence: 99%

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

Pagan

Damatto

Cezar

et al. 2015

Cell Physiol Biochem

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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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“…Exercise is an important clinical intervention for the prevention and treatment of MI [19]–[21]. It is well established that exercise decreases sympathetic activity after MI [22]–[24].…”

Section: Introductionmentioning

confidence: 99%

Aerobic Exercise Inhibits Sympathetic Nerve Sprouting and Restores β-Adrenergic Receptor Balance in Rats with Myocardial Infarction

Cui

Cai

et al. 2014

PLoS ONE

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BackgroundCardiac sympathetic nerve sprouting and the dysregulation of β-adrenergic receptor (β-AR) play a critical role in the deterioration of cardiac function after myocardial infarction (MI). Growing evidence indicates that exercise provides protection against MI. The aims of this study were to investigate whether aerobic exercise following MI could inhibit sympathetic nerve sprouting and restore the balance of β3-AR/β1-AR.MethodsMale Sprague-Dawley rats were divided into three groups: sham-operated control group (SC), MI group (MI), and MI with aerobic exercise group (ME). The rats in ME group were assigned to 8 weeks of exercise protocol (16 m/min, 50 min/d, 5 d/wk). The expression of nerve growth factor (NGF), the sympathetic nerve marker-tyrosine hydroxylase (TH), the nerve sprouting marker-growth associated protein 43 (GAP43), and β1- and β2-AR expression in the peri-infarct area of the left ventricle (LV) were measured by Western blot and immunohistochemistry, while β3-AR expression was determined by Western blot and immunofluorescence. Endothelial nitric oxide synthase (NOS2), phospho-NOS2 (p-NOS2), and neuronal nitric oxide synthase (NOS1) were measured by Western blot.ResultsMI increased LV end-diastolic pressure (LVEDP), and decreased LV systolic pressure (LVSP). Compared with the MI group, aerobic exercise significantly decreased LVEDP and increased LVSP. The protein expression of TH, GAP43 and NGF was significantly increased after MI, which was normalized by exercise. Compared with the SC group, the ratios of β2-AR/β1-AR and β3-AR/β1-AR were elevated in the MI group, and the protein expression of β3-AR and NOS1 increased after MI. Compared with the MI group, the ratios of β2-AR/β1-AR and β3-AR/β1-AR were normalized in the ME group, while the protein expression of β3-AR and NOS1 significantly increased, and NOS2 was activated by exercise.ConclusionsAerobic exercise inhibits cardiac sympathetic nerve sprouting, restores β3-AR/β1-AR balance and increases β3-AR expression through the activation of NOS2 and NOS1 after myocardial infarction.

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Aerobic interval training attenuates remodelling and mitochondrial dysfunction in the post-infarction failing rat heart

Abstract: Exercise reduces LV contractile deterioration in post-infarction heart failure and alleviates the extent of mitochondrial dysfunction, which is paralleled with preserved complex I activity.

Cited by 58 publications

References 44 publications

Impact of exercise training on redox signaling in cardiovascular diseases

Impact of exercise training on redox signaling in cardiovascular diseases

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

Aerobic Exercise Inhibits Sympathetic Nerve Sprouting and Restores β-Adrenergic Receptor Balance in Rats with Myocardial Infarction

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