Exercise training early after acute myocardial infarction reduces stress-induced hypoperfusion and improves left ventricular function

Giallauria, Francesco; Acampa, Wanda; Ricci, Francesca; Vitelli, Alessandra; Torella, Giorgio; Lucci, Rosa; Prete, Giuseppina Del; Zampella, Emilia; Assante, Roberta; Rengo, Giuseppe; Leosco, Dario; Cuocolo, Alberto; Vigorito, Carlo

doi:10.1007/s00259-012-2302-x

Cited by 59 publications

(42 citation statements)

References 38 publications

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“…Thus, the beneficial effects seen in trained post-TAC GRK5 overexpressing mice must be due to a non-GRK5 event, much like the overall swimming phenotype presented in present study. Further, these findings agree with recent clinical findings which suggest moderate exercise shortly after cardiac insult can improve cardiac function and ultimately lifespan in humans 36 . The mechanism by which cardiac function is preserved in trained TAC TgGRK5 mice remains to be elucidated.…”

Section: Discussionsupporting

confidence: 92%

Differential Role of G Protein–Coupled Receptor Kinase 5 in Physiological Versus Pathological Cardiac Hypertrophy

Traynham

Cannavò

Zhou

et al. 2015

Circulation Research

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Rationale G protein-coupled receptor (GPCR) kinases (GRKs) are dynamic regulators of cellular signaling. GRK5 is highly expressed within myocardium and is up-regulated in heart failure (HF). Although GRK5 is a critical regulator of cardiac GPCR signaling, recent data has uncovered non-canonical activity of GRK5 within nuclei that plays a key role in pathological hypertrophy. Targeted cardiac elevation of GRK5 in mice leads to exaggerated hypertrophy and early HF after transverse aortic constriction (TAC) due to GRK5 nuclear accumulation. Objective In this study we investigated the role of GRK5 in physiological, swimming induced hypertrophy (SIH). Methods and Results Cardiac-specific GRK5 transgenic mice (TgGRK5) and non-transgenic littermate control (NLC) mice were subjected to a 21-day high intensity swim protocol (or no swim sham controls). SIH and specific molecular and genetic indices of physiological hypertrophy were assessed including nuclear localization of GRK5 and compared to TAC. Unlike after TAC, swim-trained TgGRK5 and NLC mice exhibited similar increases in cardiac growth. Mechanistically, SIH did not lead to GRK5 nuclear accumulation, which was confirmed in vitro as insulin-like growth factor-1, a known mediator of physiological hypertrophy, was unable to induce GRK5 nuclear translocation in myocytes. We found specific patterns of altered gene expression between TAC and SIH with GRK5 overexpression. Further, SIH in post-TAC TgGRK5 mice was able to preserve cardiac function. Conclusions These data suggest that while nuclear-localized GRK5 is a pathological mediator after stress, this non-canonical nuclear activity of GRK5 is not induced during physiological hypertrophy.

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Section: Discussionsupporting

confidence: 92%

Differential Role of G Protein–Coupled Receptor Kinase 5 in Physiological Versus Pathological Cardiac Hypertrophy

Traynham

Cannavò

Zhou

et al. 2015

Circulation Research

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“…It is generally accepted that moderate exercise has beneficial effects on the cardiovascular system [21,22]. Previous studies have proposed that cardiovascular diseases such as HF and hypertension are often associated with SNS overactivity [23–25].…”

Section: Discussionmentioning

confidence: 99%

Aerobic exercise protects against pressure overload-induced cardiac dysfunction and hypertrophy via β3-AR-nNOS-NO activation

Wang

et al. 2017

PLoS ONE

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Aerobic exercise confers sustainable protection against cardiac hypertrophy and heart failure (HF). Nitric oxide synthase (NOS) and nitric oxide (NO) are known to play an important role in exercise-mediated cardioprotection, but the mechanism of NOS/NO stimulation during exercise remains unclear. The aim of this study is to determine the role of β3-adrenergic receptors (β3-ARs), NOS activation, and NO metabolites (nitrite and nitrosothiols) in the sustained cardioprotective effects of aerobic exercise. An HF model was constructed by transverse aortic constriction (TAC). Animals were treated with either moderate aerobic exercise by swimming for 9 weeks and/or the β3-AR-specific inhibitor SR59230A at 0.1 mg/kg/hour one day after TAC operation. Myocardial fibrosis, myocyte size, plasma catecholamine (CA) level, cardiac function and geometry were assessed using Masson’s trichrome staining, FITC-labeled wheat germ agglutinin staining, enzyme-linked immuno sorbent assay (ELISA) and echocardiography, respectively. Western blot analysis was performed to elucidate the expression of target proteins. The concentration of myocardial NO production was evaluated using the nitrate reductase method. Myocardial oxidative stress was assessed by detecting the concentration of myocardial super oxidative dismutase (SOD), malonyldialdehyde (MDA), and reactive oxygen species (ROS). Aerobic exercise training improved dilated left ventricular function and partially attenuated the degree of cardiac hypertrophy and fibrosis in TAC mice. Moreover, the increased expression of β3-AR, activation of neuronal NOS (nNOS), and production of NO were detected after aerobic exercise training in TAC mice. However, selective inhibition of β3-AR by SR59230A abolished the upregulation and activation of nNOS induced NO production. Furthermore, aerobic exercise training decreased the myocardial ROS and MDA contents and increased myocardial levels of SOD; both effects were partially attenuated by SR59230A. Our study suggested that aerobic exercise training could improve cardiac systolic function and alleviate LV chamber dilation, cardiac fibrosis and hypertrophy in HF mice. The mechanism responsible for the protective effects of aerobic exercise is associated with the activation of the β3-AR-nNOS-NO pathway.

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“…Mounting evidence suggests that exercise training alone or as core component of cardiac rehabilitation (CR) programs has several beneficial effects reducing mortality [1], preventing cardiac remodeling [2,3], and improving cardiovascular functional capacity and myocardial perfusion [4][5][6][7]. The improvement of endothelial function [8], the anti-inflammatory properties [9,10], the improvement of neurohormonal and autonomic balance [11][12][13][14][15], and the reduction of oxidative stress [16] might be some of the putative mechanisms by which exercise training exerts its beneficial effects.…”

Section: Introductionmentioning

confidence: 99%

Clinical characteristics and course of patients with diabetes entering cardiac rehabilitation

Giallauria

Fattirolli

Tramarin

et al. 2015

Diabetes Research and Clinical Practice

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Exercise training early after acute myocardial infarction reduces stress-induced hypoperfusion and improves left ventricular function

Cited by 59 publications

References 38 publications

Differential Role of G Protein–Coupled Receptor Kinase 5 in Physiological Versus Pathological Cardiac Hypertrophy

Differential Role of G Protein–Coupled Receptor Kinase 5 in Physiological Versus Pathological Cardiac Hypertrophy

Aerobic exercise protects against pressure overload-induced cardiac dysfunction and hypertrophy via β3-AR-nNOS-NO activation

Clinical characteristics and course of patients with diabetes entering cardiac rehabilitation

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