The Effects of Nandrolone Decanoate Along with Prolonged Low-Intensity Exercise on Susceptibility to Ventricular Arrhythmias

Binayi, Fateme; Joukar, Siyavash; Najafipour, Hamid; Karimi, Ali; Abdollahi, Farzane; Masumi, Yaser

doi:10.1007/s12012-015-9313-3

Cited by 9 publications

(8 citation statements)

References 60 publications

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“…Because of the high prevalence of AAS use among athletes, toxicological investigations are therefore fundamental in those cases of sudden death in subjects suspected of consuming AASs [83,84]. To date, there are still few studies published in the literature that correlates SCD in athletes with AAS use, highlighting the pathophysiological mechanisms that cause it and that are mostly based on experimental models derived from animal experiments [73,76,82,[85][86][87][88][89][90][91]. It could be important to investigate new research fields to define the exact mechanism of action.…”

Section: Discussionmentioning

confidence: 99%

Sudden Cardiac Death in Anabolic-Androgenic Steroid Users: A Literature Review

et al. 2020

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Background and objectives: Anabolic-androgenic steroids (AASs) are a group of synthetic molecules derived from testosterone and its related precursors. AASs are widely used illicitly by adolescents and athletes, especially by bodybuilders, both for aesthetic uses and as performance enhancers to increase muscle growth and lean body mass. When used illicitly they can damage health and cause disorders affecting several functions. Sudden cardiac death (SCD) is the most common medical cause of death in athletes. SCD in athletes has also been associated with the use of performance-enhancing drugs. This review aimed to focus on deaths related to AAS abuse to investigate the cardiac pathophysiological mechanism that underlies this type of death, which still needs to be fully investigated. Materials and Methods: This review was conducted using PubMed Central and Google Scholar databases, until 21 July 2020, using the following key terms: “((Sudden cardiac death) OR (Sudden death)) AND ((androgenic anabolic steroid) OR (androgenic anabolic steroids) OR (anabolic-androgenic steroids) OR (anabolic-androgenic steroid))”. Thirteen articles met the inclusion and exclusion criteria, for a total of 33 reported cases. Results: Of the 33 cases, 31 (93.9%) were males while only 2 (61%) were females. Mean age was 29.79 and, among sportsmen, the most represented sports activity was bodybuilding. In all cases there was a history of AAS abuse or a physical phenotype suggesting AAS use; the total usage period was unspecified in most cases. In 24 cases the results of the toxicological analysis were reported. The most detected AASs were nandrolone, testosterone, and stanozolol. The most frequently reported macroscopic alterations were cardiomegaly and left ventricular hypertrophy, while the histological alterations were foci of fibrosis and necrosis of the myocardial tissue. Conclusions: Four principal mechanisms responsible for SCD have been proposed in AAS abusers: the atherogenic model, the thrombosis model, the model of vasospasm induced by the release of nitric oxide, and the direct myocardial injury model. Hypertrophy, fibrosis, and necrosis represent a substrate for arrhythmias, especially when combined with exercise. Indeed, AAS use has been shown to change physiological cardiac remodeling of athletes to pathophysiological cardiac hypertrophy with an increased risk of life-threatening arrhythmias.

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Section: Discussionmentioning

confidence: 99%

Sudden Cardiac Death in Anabolic-Androgenic Steroid Users: A Literature Review

et al. 2020

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“…Frozen pieces of lung were weighed and then homogenized in 5 ml of 0.1 M Tris-HCl buffer (pH 7.4) under ice-cold conditions. The hydroxyproline value in the lung tissue was measured using the ELISA method and a hydroxyproline kit (Shanghai Crystal Day Biotech Co., Ltd., Shanghai) according the manufacturer's protocol [ 16 ].…”

Section: Methodsmentioning

confidence: 99%

Coadministration of Atorvastatin and Amiodarone Increases the Risk of Pulmonary Fibrosis in Rats

Nasri

Joukar²,

Kheradmand³

et al. 2015

Med Princ Pract

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Objective: The purpose of this study was to evaluate the effect of atorvastatin administration on amiodarone-induced pulmonary fibrosis in rats. Materials and Methods: Thirty-six male Wistar rats were randomly divided into 4 groups. The control group (CTL) received distilled water (0.3 ml intratracheally on days 0 and 2 and 0.5 ml orally from day 0 for 3 weeks). The atorvastatin group (AT), in addition to intratracheal distilled water, received 1 mg/kg of atorvastatin orally from day 0 for 3 weeks. The amiodarone group (AMI) received 2 intratracheal instillations of amiodarone (6.25 mg/kg in 0.3 ml of water) on days 0 and 2 and 0.5 ml of distilled water (like the CTL). The amiodarone plus atorvastatin group (AMI + AT) received both these drugs (same doses and methods as for the AMI and AT). After 28 days, the rate of lung fibrosis was estimated according to pathological criteria of lung sections and measurements of hydroxyproline in pieces of left lung tissue. Results: The lung hydroxyproline content was higher in the treated groups (CTL: 0.35 ± 0.017, AT: 0.38 ± 0.012, AMI: 0.375 ± 0.018 and AMI + AT: 0.38 ± 0.012 unit/mg protein), but did not reach significance when compared with the CTL (p = 0.56). Amiodarone administration significantly increased the score of pulmonary fibrosis (0.5) in comparison with the AT (0.125) and CTL (0) (p < 0.5). The combination of amiodarone and atorvastatin exacerbated the pulmonary fibrosis (1.5; p < 0.01) compared to the AMI (0.5; p < 0.001), AT (0.125) and CTL (0). Conclusion: In this study, the concomitant administration of amiodarone and atorvastatin increased pulmonary fibrosis in rats.

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“…While ND associated with resistance exercise has been shown to improve physical performance and muscle mass gains, its abuse can lead to side effects as well as somatic consequences, including effects in cardiac and skeletal muscles such as an increase in extracellular collagen production, interstitial fibrosis, also changing the vascularization which impairs the angiogenesis, and hypertrophic myopathy [6,9,25,26]. Also, the toxic effect of ND on the NMJ has already been demonstrated, with a reduction in the safety margin of synaptic transmission in sedentary rats [27].…”

Section: Introductionmentioning

confidence: 99%

Effects of Nandrolone Decanoate on Skeletal Muscle and Neuromuscular Junction of Sedentary and Exercised Rats

Tibúrcio,

Leite,

Muller

et al. 2023

Medicina

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Background and Objectives: Nandrolone decanoate (ND) is the most widely used among the anabolic androgenic steroids (AAS), synthetic substances derived from testosterone, to improve muscular and health gains associated with exercises. The AAS leads to physical performance enhancement and presents anti-aging properties, but its abuse is associated with several adverse effects. Supraphysiological doses of AAS with or without physical exercise can cause morphological and functional alterations in neuromuscular interactions. This study aims to investigate the effects of ND supraphysiological doses in neuromuscular interactions, focusing on the soleus muscle and its neuromuscular junctions (NMJs) in rats, associated or not with physical exercise. Materials and Methods: Forty male Sprague Dawley rats were divided into four groups: sedentary and exercised groups, with or without ND at the dose of 10 mg/kg/week. The animals were treated for eight weeks, with intramuscular injections, and the soleus muscle was collected for morphological analyses. Results: The supraphysiological doses of ND in the sedentary group caused muscle degeneration, evidenced by splitting fibers, clusters of small fibers, irregular myofibrils, altered sarcomeres, an increase in collagen deposition and in the number of type I muscle fibers (slow-twitch) and central nuclei, as well as a decrease in fibers with peripheral nuclei. On the other hand, in the ND exercise group, there was an increase in the NMJs diameter with scattering of its acetylcholine receptors, although no major morphological changes were found in the skeletal muscle. Thus, the alterations caused by ND in sedentary rats were partially reversed by physical exercise. Conclusions: The supraphysiological ND exposure in the sedentary rats promoted an increase in muscle oxidative pattern and adverse morphological alterations in skeletal muscle, resulting from damage or post-injury regeneration. In the ND-exercised rats, no major morphological changes were found. Thus, the physical exercise partially reversed the alterations caused by ND in sedentary rats.

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The Effects of Nandrolone Decanoate Along with Prolonged Low-Intensity Exercise on Susceptibility to Ventricular Arrhythmias

Cited by 9 publications

References 60 publications

Sudden Cardiac Death in Anabolic-Androgenic Steroid Users: A Literature Review

Sudden Cardiac Death in Anabolic-Androgenic Steroid Users: A Literature Review

Coadministration of Atorvastatin and Amiodarone Increases the Risk of Pulmonary Fibrosis in Rats

Effects of Nandrolone Decanoate on Skeletal Muscle and Neuromuscular Junction of Sedentary and Exercised Rats

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