Nandrolone and resistance training induce heart remodeling: Role of fetal genes and implications for cardiac pathophysiology

Tanno, Ana Paula; Neves, Vander José das; Rosa, Kaleizu Teodoro; Cunha, Tatiana Sousa; Giordano, Fernanda Cristina Linarello; Calil, Caroline Morini; Guzzoni, Vinícius; Fernandes, Tiago; Oliveira, Edilamar Menezes de; Novaes, Pedro Duarte; Irigoyen, Maria Cláudia; Moura, Maria José Costa Sampaio; Marcondes, Fernanda Klein

doi:10.1016/j.lfs.2011.08.004

Cited by 40 publications

(35 citation statements)

References 50 publications

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“…Consistent with our findings, other studies have shown that chronic administration of nandrolone along with exercise is associated with significant increase in heart hypertrophy index (25,(28)(29)(30). They showed that reninangiotensin system activity has increased, which can justify the hypertrophic induction during exercise conditions with consumption of nandrolone.…”

Section: Discussionsupporting

confidence: 93%

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Joukar¹,

Baravati²,

Fathpour³

et al. 2015

Res Cardiovasc Med

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Background: Until now, no experimental study has directly assessed the arrhythmogenesis of chronic consumption of anabolic androgenic steroids along with moderate-intensity endurance exercise. Objectives: We evaluated the influence of integration of anabolic androgenic steroids along with moderate-intensity endurance exercise on susceptibility to lethal ventricular arrhythmias in rat. Materials and Methods:The animal groups were as follows: control group (CTL); exercise group (EX) which were under 6 weeks of treadmill exercise; nandrolone group (Nan) which received 5 mg/kg of nandrolone decanoate twice a week; vehicle group (Arach) which received Arachis oil (solvent of nandrolone); trained vehicle group (Arach + Ex); and trained nandrolone group (Nan + Ex). One day after ending of the intervention period, arrhythmia was inducted by intravenous infusion of aconitine and ventricular arrhythmias were recorded. Then malondialdehyde (MDA) and glutathione peroxidase (GPX) of heart tissue were measured. Results: Nandrolone, exercise, and their combination were associated with heart hypertrophy. Exercise could prevent the incremental effect of nandrolone on MDA/GPX ratio. Chronic administration of nandrolone with moderate-intensity endurance exercise had no significant effect on blood pressure, heart rate, and basal electrocardiographic parameters. Combination of nandrolone and exercise significantly increased the incidence of ventricular fibrillation (VF) and reduced the VF latency (P < 0.05). Conclusions:The findings suggest that chronic coadministration of nandrolone with moderate-intensity endurance exercise facilitates the VF occurrence in rat. Complementary studies are needed to elucidate the involved mechanisms of this abnormality.

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Section: Discussionsupporting

confidence: 93%

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Joukar¹,

Baravati²,

Fathpour³

et al. 2015

Res Cardiovasc Med

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“…Two groups used only the 18s gene [13,28], five used only Actb gene [29][30][31][32][33]. Other authors used the Cyclophilin gene [15,31] and eight authors used Gapdh as a reference gene in their studies [12,14,[34][35][36][37][38][39][40]. Only three studies used more than one gene as internal control: Gapdh and large ribosomal protein P0 (RPLP0) genes [41]; Gapdh, Actb, Hprt1 and Cyclophilin gene [42]; the other authors used Ubiquitin C gene as reference gene [43].…”

Section: Genorm Analysismentioning

confidence: 99%

“…Furthermore, physiological and psychological benefits of REx are considered important in physical rehabilitation and treatment programs [11]. Therefore, a number of gene expression and molecular biological studies has been conducted in Rex training and steroids models, including ladder exercise models [12][13][14][15]. There is a methodological gap, in which there is a lack of studies that identify the best reference gene in these areas of knowledge.…”

Section: Introductionmentioning

confidence: 99%

Validation of Reference Genes for qPCR Analysis of Resistance Training and Androgenic Anabolic Steroids on Hypothalamus, Adrenal Gland and Fat Tissue

Pozzi¹,

Le²,

Fern³

et al. 2016

J Steroids Horm Sci

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Background: Real-time quantitative Polymerase Chain Reaction (qPCR) is a technique used for quantification of gene expression and the use of reference genes is very important to normalize the quantification results. Aim:To validate the most suitable reference genes for resistance exercise training (REx) and use of nandrolone decanoate (DECA) in three different rat tissues. Methods:A total of 40 adult male Wistar rats were distributed into four groups: exposed to vehicle three times per week (wk) (CT); eight wk of REx exposed to vehicle three times per wk (T); exposed to DECA three times per wk (D); eight wk of REx exposed to DECA three times per wk (TD). Stability of the following genes was evaluated: beta actin (Actb), alpha Tubulin (Tubulin), Glyceraldehyde-3-phosphate dehydrogenase (Gapdh), Hypoxanthine phosphoribosyltransferase-1 (Hprt1) and 18s Ribossomal RNA (18s) in hypothalamus, adrenal gland and mesenteric fat tissue using GeNorm, NormFinder and BestKeeper software. Results:In hypothalamus and adrenal, all genes were suitable and none was rejected by statistical analysis; however, in fat tissue, Actb, Gapdh and Hprt1 genes were rejected by geNorm but not the others two software. Conclusion:In hypothalamus and adrenal all selected genes analized were stable and can be used for qPCR gene expression analysis. However, in fat tissue we suggest the Tubulin gene as most stable gene.

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“…Fetal gene expression in pathological cardiac hypertrophy has been extensively investigated for many years (Park et al, 2011; Sheehy et al, 2009; Tanno et al, 2011; Zhao et al, 2004). The most studied and well-characterized fetal genes whose expression is significantly up-regulated in myocardial pathogenesis include atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and α-skeletal actin (Holtwick et al, 2003; McKie et al, 2010; Stilli et al, 2006).…”

Section: Distinct Features Of Pathological Cardiac Hypertrophymentioning

confidence: 99%

Regression of pathological cardiac hypertrophy: Signaling pathways and therapeutic targets

Hou

Kang

2012

Pharmacology & Therapeutics

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Pathological cardiac hypertrophy is a key risk factor for heart failure. It is associated with increased interstitial fibrosis, cell death and cardiac dysfunction. The progression of pathological cardiac hypertrophy has long been considered as irreversible. However, recent clinical observations and experimental studies have produced evidence showing the reversal of pathological cardiac hypertrophy. Left ventricle assist devices used in heart failure patients for bridging to transplantation not only improve peripheral circulation but also often cause reverse remodeling of the geometry and recovery of the function of the heart. Dietary supplementation with physiologically relevant levels of copper can reverse pathological cardiac hypertrophy in mice. Angiogenesis is essential and vascular endothelial growth factor (VEGF) is a constitutive factor for the regression. The action of VEGF is mediated by VEGF receptor-1, whose activation is linked to cyclic GMP-dependent protein kinase-1 (PKG-1) signaling pathways, and inhibition of cyclic GMP degradation leads to regression of pathological cardiac hypertrophy. Most of these pathways are regulated by hypoxia-inducible factor. Potential therapeutic targets for promoting the regression include: promotion of angiogenesis, selective enhancement of VEGF receptor-1 signaling pathways, stimulation of PKG-1 pathways, and sustention of hypoxia-inducible factor transcriptional activity. More exciting insights into the regression of pathological cardiac hypertrophy are emerging. The time of translating the concept of regression of pathological cardiac hypertrophy to clinical practice is coming.

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Nandrolone and resistance training induce heart remodeling: Role of fetal genes and implications for cardiac pathophysiology

Abstract: This study indicated that nandrolone, whether associated with resistance training or not, induces cardiac hypertrophy, which is associated with enhanced collagen content, re-expression of fetal genes the in left ventricle, and impaired diastolic and systolic function.

Cited by 40 publications

References 50 publications

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Validation of Reference Genes for qPCR Analysis of Resistance Training and Androgenic Anabolic Steroids on Hypothalamus, Adrenal Gland and Fat Tissue

Regression of pathological cardiac hypertrophy: Signaling pathways and therapeutic targets

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