Effects of nandrolone and resistance training on the blood pressure, cardiac electrophysiology, and expression of atrial β-adrenergic receptors

Neves, Vander José das; Tanno, Ana Paula; Cunha, Tatiana Sousa; Fernandes, Tiago; Guzzoni, Vinícius; Silva, Carlos Alberto da; Oliveira, Edilamar Menezes de; Moura, Maria José Costa Sampaio; Marcondes, Fernanda Klein

doi:10.1016/j.lfs.2013.04.002

Cited by 18 publications

(9 citation statements)

References 45 publications

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“…Our findings related to the influence of supraphysiological AAS administration on noninvasively measured systolic blood pressure support those of several other animal studies ( 16 , 17 ). In humans, increased blood pressure, or even hypertension has been linked to high levels of circulating androgens, induced either by various endocrinological diseases [polycystic ovary syndrome (PCOS), adrenogenital syndrome, virilizing gonadal tumors, enzyme defects, medication induced hyperandrogenism] ( 18 , 19 ), or by AAS abuse in athletes or amateur bodybuilders ( 1 , 2 ).…”

Section: Discussionsupporting

confidence: 92%

Impact of chronic administration of anabolic androgenic steroids and taurine on blood pressure in rats

Roşca

Stoian

Badiu

et al. 2016

Braz J Med Biol Res

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Supraphysiological administration of anabolic androgenic steroids has been linked to increased blood pressure. The widely distributed amino acid taurine seems to be an effective depressor agent in drug-induced hypertension. The purpose of this study was to assess the impact of chronic high dose administration of nandrolone decanoate (DECA) and taurine on blood pressure in rats and to verify the potentially involved mechanisms. The study was conducted in 4 groups of 8 adult male Wistar rats, aged 14 weeks, treated for 12 weeks with: DECA (A group); vehicle (C group); taurine (T group), or with both drugs (AT group). Systolic blood pressure (SBP) was measured at the beginning of the study (SBP1), 2 (SBP2) and 3 months (SBP3) later. Plasma angiotensin-converting enzyme (ACE) activity and plasma end products of nitric oxide metabolism (NOx) were also determined. SBP3 and SBP2 were significantly increased compared to SBP1 only in the A group (P<0.002 for both). SBP2, SBP3 and ACE activity showed a statistically significant increase in the A vs C (P<0.005), andvs AT groups (P<0.05), while NOx was significantly decreased in the A and AT groups vs controls (P=0.01). ACE activity was strongly correlated with SBP3 in the A group (r=0.71, P=0.04). These findings suggest that oral supplementation of taurine may prevent the increase in SBP induced by DECA, an effect potentially mediated by angiotensin-converting enzyme.

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Section: Discussionsupporting

confidence: 92%

Impact of chronic administration of anabolic androgenic steroids and taurine on blood pressure in rats

Roşca

Stoian

Badiu

et al. 2016

Braz J Med Biol Res

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“…In a clinical study, administration of 600 mg testosterone per week has been found to bring up the circulating level of four to six times higher than natural production in male (Bhasin et al 1996). In animal studies, cardiovascular adverse effects were also detected after 10-25 mg/kg/week treatment of testosterone for 4-10 weeks (Rocha et al 2007, Barbosa Dos Santos et al 2013, das Neves et al 2013, Hassan & Kamal 2013. The transition in a time-dependent manner of testosterone-induced cardiac hypertrophy toward pathological direction reported in this study provides an important caution for those who need long-term use of the hormone and also begs for information of the underlying mechanistic induction of hypertrophy.…”

Section: Discussionmentioning

confidence: 96%

Supra-physiological dose of testosterone induces pathological cardiac hypertrophy

Pirompol

Teekabut

Weerachatyanukul

et al. 2016

Journal of Endocrinology

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Testosterone and androgenic anabolic steroids have been misused for enhancement of physical performance despite many reports on cardiac sudden death. Although physiological level of testosterone provided many regulatory benefits to human health, including the cardiovascular function, supra-physiological levels of the hormone induce hypertrophy of the heart with unclear contractile activation. In this study, dose- and time-dependent effects of high-testosterone treatment on cardiac structure and function were evaluated. Adult male rats were divided into four groups of testosterone treatment for 0, 5, 10, and 20 mg/kg BW for 4, 8, or 12 weeks. Increases in both percentage heart:body weight ratio and cardiomyocyte cross-sectional area in representing hypertrophy of the heart were significantly shown in all testosterone-treated groups to the same degree. In 4-week-treated rats, physiological cardiac hypertrophy was apparent with an upregulation of α-MHC without any change in myofilament contractile activation. In contrast, pathological cardiac hypertrophy was observed in 8- and 12-week testosterone-treated groups, as indicated by suppression of myofilament activation and myocardial collagen deposition without transition of MHC isoforms. Only in 12-week testosterone-treated group, eccentric cardiac hypertrophy was demonstrated with unaltered myocardial stiffness, but significant reductions in the phosphorylation signals of ERK1/2 and mTOR. Results of our study suggest that the outcome of testosterone-induced cardiac hypertrophy is not dose dependent but is rather relied on the factor of exposure to duration in inducing maladaptive responses of the heart.

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“…Upregulation of adrenergic system may also be involved in cardiac hypertrophy according to the finding of Penna et al [20] and increased expression of β-adrenergic receptors in steroid-treated heart confirms the role of adrenergic system in cardiac hypertrophy [21,50,51]. It was also suggested that upregulation of renin-angiotensin system and associated cardiac remodeling is responsible for the steroidinduced hypertrophy in trained animals [34].…”

Section: Discussionmentioning

confidence: 81%

Ischemic Preconditioning Efficacy Following Anabolic Steroid Usage: A Clear Difference Between Sedentary and Exercise-Trained Rat Hearts

et al. 2018

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Previous studies show that anabolic steroids impair innate cardioprotective mechanisms. Here, we investigated the effect of supraphysiological doses of nandrolone on ischemic preconditioning (IPC) as a potent cardioprotective tool against ischemia reperfusion (IR) injury in rat hearts. Male Wistar rats in two experimental settings of sedentary and exercise-trained (60 min/ day swimming, 5 days/week, for 8 weeks) were either pretreated with intramuscular injections of arachis oil (Arach, n = 16) as vehicle or nandrolone decanoate (ND, n = 8), 10 mg/kg/week, for 8 weeks. At the end, the hearts were excised and perfused in a Langendorff system. Then, the vehicle-treated hearts subdivided into the IR (30 min of LAD coronary artery occlusion and 120 min reperfusion, n = 8) and IPC (three cycles of 3-min ischemia and 3-min reperfusion before test ischemia, n = 8) groups and nandrolone-treated hearts served as ND + IPC (nandrolone pretreatment before IR and IPC protocols, n = 8) group. Post-ischemic cardiac function and infarct size were assessed. Reperfusion arrhythmias were analyzed using a standard scoring system. In sedentary hearts, ND slightly increased heart-to-body weight ratio and increased baseline cardiac contractile function. In trained hearts, ND markedly increased heart-to-body weight ratio which was also associated with enhanced baseline cardiac function. ND pretreatment enhanced protective effects of IPC in sedentary group; however, abolished these effects in exercise-trained group. The arrhythmia score was not significantly different between nandrolone-treated groups vs. respective preconditioned groups. Our findings show that ND impairs IPC-induced cardioprotection in exercise-trained rat hearts. Cardiac hypertrophy seems to play a crucial role in this response.

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Effects of nandrolone and resistance training on the blood pressure, cardiac electrophysiology, and expression of atrial β-adrenergic receptors

Cited by 18 publications

References 45 publications

Impact of chronic administration of anabolic androgenic steroids and taurine on blood pressure in rats

Impact of chronic administration of anabolic androgenic steroids and taurine on blood pressure in rats

Supra-physiological dose of testosterone induces pathological cardiac hypertrophy

Ischemic Preconditioning Efficacy Following Anabolic Steroid Usage: A Clear Difference Between Sedentary and Exercise-Trained Rat Hearts

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