A associação de esteroide anabolizante ao treinamento físico aeróbio leva a alterações morfológicas cardíacas e perda de função ventricular em ratos / Association between anabolic steroids and aerobic physical training leads to cardiac morphological alterations and loss of ventricular function in rats

INTRODUÇÃO: O esteroide anabolizante (EA) associado ao treinamento físico induz mudança da hipertrofia cardíaca (HC) fisiológica para patológica. Entretanto, esses trabalhos foram realizados com atletas de força, sendo os efeitos do EA associados ao treinamento aeróbio poucos conhecidos. Com isso, o objetivo do estudo foi avaliar os efeitos do treinamento aeróbio e dos EA sobre a estrutura e função cardíaca. MÉTODOS: Foram utilizados 28 ratos Wistar divididos em quatro grupos: sedentários controle (SC), sedentários anabolizante (SA), treinados controle (TC) e treinado anabolizante (TA). O EA foi administrado duas vezes por semana (10mg/kg/ semana). O treinamento físico de natação foi realizado durante 10 semanas, cinco sessões semanais. Foram avaliadas a pressão arterial e frequência cardíaca por pletismografia de cauda, função ventricular por ecocardiografia, diâmetro dos cardiomiócitos e fração volume de colágeno por métodos histológicos. RESULTADOS: Não foram observadas diferenças na PA. O grupo TC apresentou redução da frequência cardíaca de repouso após o período experimental, o que não ocorreu no grupo TA. Foram observadas HC de 38 por cento no grupo SA, 52 por cento no grupo TC e de 64 por cento no grupo TA em relação ao grupo SC. O grupo TA apresentou diminuição da função diastólica em relação aos outros grupos. Os grupos treinados apresentaram aumentos significantes no diâmetro dos cardiomiócitos. Os grupos SA e TA apresentaram aumento na fração volume de colágeno em relação aos grupos SC e TC. CONCLUSÃO: Os resultados apresentados mostram que o treinamento físico de natação induz a HC, principalmente pelo aumento do colágeno intersticial, o que pode levar a prejuízos da função diastólica.

INTRODUCTION: Anabolic-androgen steroids (AAS) associated with physical training induce changes from physiological cardiac hypertrophy (CH) to pathological hypertrophy. However, these studies were performed with strength athletes, and the AAS effects associated with aerobic training are still poorly understood. Thus, the aim of this study was to evaluate the effects of aerobic training and AAS on the cardiac structure and function. METHODS: 28 Wistars rats divided in 4 groups were used: sedentary control (SC), sedentary anabolic (SA), trained control (TC) and trained anabolic (TA). The AAS was administered twice a week (10mg/Kg/week). The swimming training was conducted 5 sessions per week during 10 weeks. We evaluated blood pressure and heart rate by tail plethysmography, ventricular function by echocardiography, cardiomyocyte diameter and collagen volumetric fraction by histological methods. RESULTS: There were no differences in BP. TC group showed reduction in rest heart rate after the experimental period, which did not occur in TA group. CH of 38 percent in SA group; 52 percent in TC group and 64 percent in TA group compared to SC group was observed. TA group presented decrease in diastolic function in relation to other groups. The trained groups showed significant increases in cardiomyocytes diameter. SA and TA groups showed increase in collagen volumetric fraction in relation to SC and TC groups. CONCLUSION: The results show that AAS treatment associated to swimming training induces CH, mainly by the increase in interstitial collagen, which can lead to loss of diastolic function.

Anabolic steroid associated to physical training induces deleterious cardiac effects.

PURPOSE: Cardiac aldosterone might be involved in the deleterious effects of nandrolone decanoate (ND) on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis. METHODS: Male Wistar rats were randomized into eight groups (n = 14 per group): Control (C), nandrolone decanoate (ND), trained (T), trained ND (TND), ND + losartan (ND + L), trained ND + losartan (TND + L), ND + spironolactone (ND + S), and trained ND + spironolactone (TND + S). ND (10 mg·kg(-1)·wk(-1)) was administered during 10 wk of swimming training (five times per week). Losartan (20 mg·kg(-1)·d(-1)) and spironolactone (10 mg·kg(-1)·d(-1)) were administered in drinking water. RESULTS: Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (P < 0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (P < 0.05). The ND treatment increased left ventricle-angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), and 11-ß hydroxysteroid dehydrogenase 2 (11ß-HSD2) gene expression and inflammatory markers, TGFß and osteopontin. Both losartan and spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in left ventricle-angiotensin-converting enzyme I activity, CYP11B2, 11ß-HSD2, TGFß, and osteopontin induced by the ND treatment. CONCLUSIONS: We believe this is the first study to show the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGFß and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.