Nandrolone combined with strenuous resistance training reduces vascular nitric oxide bioavailability and impairs endothelium-dependent vasodilation.

Anabolic Androgenic Steroids (AASs) misuse has increased among adolescents and recreational athletes due to their potential effects on muscle hypertrophy. On the other hand, AAS might induce alterations on cardiovascular system, although some controversies regarding AAS on vascular properties remain unknown. To address this question, we aimed to investigate the effects of high doses of nandrolone combined with strenuous resistance training (RT) on function and structure of thoracic aorta. Rats were randomized into four groups: non-trained vehicle (NTV), trained vehicle (TV), non-trained nandrolone (NTN), and trained nandrolone (TN), and submitted to 6 weeks of treatment with nandrolone (5 mg/kg, twice a week) and/or resistance training. In vitro response of thoracic aorta to acetylcholine (ACh) was analyzed. Vascular nitric oxide (NO) and reactive oxygen species (ROS) synthesis were evaluated using 4,5-diaminofluorescein diacetate (DAF-2) and hydroethidine fluorescent techniques, respectively. Thoracic aorta was processed for microscopy analyses and tunica media thickness was measured. ACh-mediated relaxation response was impaired in endothelium intact aortic rings isolated from trained rats (TV and TN) as compared with their matched non-trained groups. TN rats showed reduced ACh-mediated vasodilatation than NTN rats. NO production and bioavailability decreased in thoracic aorta of nandrolone-treated rats in relation to their matched non-trained group (NTN vs. NTV; TN vs. TV). ROS production and tunica media thickness were increased in TN rats when compared with TV rats. These findings indicate that high doses of nandrolone combined with strenuous RT affect NO bioavailability and might induce endothelial dysfunction and arterial morphological alterations.

Effect of a puzzle on the process of students' learning about cardiac physiology.

The aim of the present study was to evaluate the effects of using a puzzle to learn about cardiac physiology. Students were divided into control and game groups. In class 1, the control group had a 2-h theoretical class about cardiac physiology, including a detailed description of the phases of the cardiac cycle, whereas the game group had a 50-min theoretical class without the description of the cardiac cycle. In class 2, the control group did an assessment exercise before an activity with the cardiac puzzle and the game group answered questions after the above-mentioned activity. While solving the puzzle, the students had to describe the cardiac cycle by relating the concepts of heart morphology and physiology. To evaluate short-term learning, the number of wrong answers and grades in the assessment exercise were compared between the control and game groups. To evaluate medium-term learning, we compared the grades obtained by students of the control and game groups in questions about cardiac physiology that formed part of the academic exam. In the assessment exercise, the game group presented a lower number of errors and higher score compared with the control group. In the academic exam, applied after both groups had used the puzzle, there was no difference in the scores obtained by the control and game groups in questions about cardiac physiology. These results showed a positive effect of the puzzle on students' learning about cardiac physiology compared with those not using the puzzle.

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

AIMS: This study was performed to assess isolated and combined effects of nandrolone and resistance training on the blood pressure, cardiac electrophysiology, and expression of the ß1- and ß2-adrenergic receptors in the heart of rats. MAIN METHODS: Wistar rats were randomly divided into four groups and submitted to a 6-week treatment with nandrolone and/or resistance training. Cardiac hypertrophy was accessed by the ratio of heart weight to the final body weight. Blood pressure was determined by a computerized tail-cuff system. Electrocardiography analyses were performed. Western blotting was used to access the protein levels of the ß1- and ß2-adrenergic receptors in the right atrium and left ventricle. KEY FINDINGS: Both resistance training and nandrolone induced cardiac hypertrophy. Nandrolone increased systolic blood pressure depending on the treatment time. Resistance training decreased systolic, diastolic and mean arterial blood pressure, as well as induced resting bradycardia. Nandrolone prolonged the QTc interval for both trained and non-trained groups when they were compared to their respective vehicle-treated one. Nandrolone increased the expression of ß1- and ß2-adrenergic receptors in the right atrium for both trained and non-trained groups when they were compared to their respective vehicle-treated one. SIGNIFICANCE: This study indicated that nandrolone, associated or not with resistance training increases blood pressure depending on the treatment time, induces prolongation of the QTc interval, and increases the expression of ß1- and ß2-adrenergic receptors in the cardiac right atrium, but not in the left ventricle.

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

AIMS: This study was conducted to assess the isolated and combined effects of nandrolone and resistance training on cardiac morphology, function, and mRNA expression of pathological cardiac hypertrophy markers. MAIN METHODS: Wistar rats were randomly divided into four groups and submitted to 6 weeks of treatment with nandrolone and/or resistance training. Cardiac parameters were determined by echocardiography. Heart was analyzed for collagen infiltration. Real-time RT-PCR was used to assess the pathological cardiac hypertrophy markers. KEY FINDINGS: Both resistance training and nandrolone induced cardiac hypertrophy. Nandrolone increased the cardiac collagen content, and reduced the cardiac index in non-trained and trained groups, when compared with the respective vehicle-treated groups. Nandrolone reduced the ratio of maximum early to late transmitral flow velocity in non-trained and trained groups, when compared with the respective vehicle-treated groups. Nandrolone reduced the alpha-myosin heavy chain gene expression in both non-trained and trained groups, when compared with the respective vehicle-treated groups. Training reduced the beta-myosin heavy chain gene expression in the groups treated with vehicle and nandrolone. Only the association between training and nandrolone increased the expression of the skeletal alpha-actin gene and atrial natriuretic peptide in the left ventricle. SIGNIFICANCE: 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.

Vascular sensitivity to phenylephrine in rats submitted to anaerobic training and nandrolone treatment.

The effect of anaerobic physical training and nandrolone treatment on the sensitivity to phenylephrine in thoracic aorta and lipoprotein plasma levels of rats was studied. Sedentary and trained male Wistar rats were treated with vehicle or nandrolone (5 mg/kg IM; twice per week) for 6 weeks. Training was performed by jumping into water (4 sets, 10 repetitions, 30-second rest, 50% to 70% body weight load, 5 days/week, 6 weeks). Two days after the last training session, the animals were killed and blood samples for lipoprotein dosage were obtained. Thoracic aorta was isolated and concentration-effect curves of phenylephrine were performed in intact endothelium and endothelium-denuded aortic rings in the absence or presence of NG-L-arginine-methyl ester. No changes were observed in endothelium-denuded aortic rings. However, in endothelium-intact thoracic aorta, anaerobic physical training induced subsensitivity to phenylephrine (pD2=7.11+/-0.07) compared with sedentary group (7.55+/-1.74), and this effect was canceled by the inhibition of nitric oxide synthesis. No difference was observed between trained (7.22+/-0.07) and sedentary (7.28+/-0.09) groups treated with nandrolone. Anaerobic training induced an increase in high-density lipoprotein levels in vehicle-treated rats, but there were no changes in nandrolone-treated groups. Training associated with nandrolone induced an increase in low-density lipoprotein levels but no change in the other groups. If altering endothelium-dependent vasodilatation is considered to be a beneficial adaptation to anaerobic physical training, it is concluded that nandrolone treatment worsens animals' endothelial function, and this effect may be related to lipoprotein blood levels.

Esteróides anabólicos androgênicos e sua relação com a prática desportiva / Anabolic androgenic steroids and the relation to the sportive practice

Os esteróides anabólicos androgênicos (EAA) são um grupo de compostos naturais e sintéticos formados a partir da testosterona ou um de seus derivados, cuja indicação terapêutica clássica está associada a situações de hipogonadismo e quadros de deficiência do metabolismo protéico. Atuando sobre os receptores androgênicos, modulam de forma indissociável tanto os efeitos androgênicos como os anabólicos. Tais substâncias variam na relação entre a atividade anabólica: androgênica, mas nenhum fármaco atualmente disponível é capaz de desencadear somente efeitos anabólicos. O primeiro relato da utilização dos EAA com o objetivo de melhorar o desempenho atlético ocorreu em 1954, na Áustria, e, desde então, esta prática tornou-se amplamente difundida. Obviamente, o uso de EAA está fora dos limites competitivos e foi declarado ilegal pelos setores governamentais desportivos nacionais e internacionais...