Cardiac alterations induced of anabolic steroid in sedentary and trained rats

Author(s)

Ana Paula Tanno

• Document type: Doctoral Thesis
• Press: Campinas, SP.
• Institution: Universidade Estadual de Campinas (UNICAMP). Instituto de Biologia
• Defense date: 2007-02-14

Examining board members

Fernanda Klein Marcondes; Iraides Nunes dos Santos; Maria Cecília Ferraz de Arruda Veiga; Maria Claudia Costa Irigoyen; Oduvaldo Camara Marques Pereira

• Advisor: Fernanda Klein Marcondes

Abstract

High doses of anabolic androgenic steroids (AAS) are used without therapeutic indication in order to increase the muscle power or improve the physical appearance. However the beneficial effects of AAS on the athletic performance are still questionable and it is well established that AAS abuse is associated with many detrimental side-effects. Since the sideeffects of AAS on the cardiovascular system are not well understood, the aim of this study was to evaluate the influence of nandrolone and resistance physical training on the cardiac function in male Wistar rats divided into 4 groups: sedentary + vehicle (SV), trained + vehicle (TV), sedentary + AAS (SAAS) and trained + AAS (TAAS). The animals were treated for 6 weeks with vehicle (propyleneglycol, 0.2 mL/Kg) or nandrolone decanoate (Deca-Durabolin, 5 mg/Kg), i.m., 2x/ week. Training was performed by jumping into water (4 sets, 10 repetitions, 30 seconds rest), 50-70% body weight-load, 5 days/week, 6 weeks). At the end of experimental period, the rats were sacrificed, right atria was isolated to obtained in vitro concentration-effect curves (CEC) to catecholamines and left ventricle (LV) was analyzed for collagen quantification (n=5-10/group). Other rats, submitted to the same treatments were anesthetized and submitted to echodopplercardiography (n=7- 10/group). Data were compared by two-way ANOVA and Tukey test (p<0.05). AAS and physical training induced supersensitivity to catecholamines and reduced the density of adrenoceptors in right atria. Physical training and AAS induced left ventricular concentric hypertrophy, and this effect was more pronounced in TAAS group, as demonstrated by the increase in left ventricle mass/body weight ratio (SV:1.78±0.06 < TV:1.98±0.06 = SAAS:2.07±0.05 < TAAS:2.27±0.05 g/Kg) and relative wall thickness index (SV:0.38±0.01 < TV:0.46±0.01 = SAAS:0.51±0.02 < TAAS:0.56±0.02). AAS decreased cardiac output index (SV:213±11 = TV:204±19 > SAAS:184±18 = TAAS:151±14 mL/min/g) and increased cardiac collagen content (SV:2.93±0.22 = TV:6.48±1.01 (AU)