Anabolic Steroid - and Exercise - Induced Cardio-Depressant Cytokines and Myocardial β1 Receptor Expression in CD1 Mice

Abstract

Few animal model studies have been conducted in order to evaluate the impact of androgenic anabolic steroids (AAS) supraphysiological doses on the cardiovascular system and myocardial injury. Twenty-five male CD1 mice (8-10 weeks old; 35g initial body weight) were randomized into three AAS treated groups and two control groups. The AAS mice received intramuscular Nandrolone Decanoate (DECA-DURABOLIN), vehicled in arachidis oil, for 42 days, twice per week, with different dosages, studying plasma lipid analysis, cardiac histopathological features, cardiac β (1) adrenergic receptor expression, and the effects of the myocardial expression of inflammatory mediators (IL-1β, TNF-α) on the induction of cardiomyocytes apoptosis (HSP 70, TUNEL), using proteomic and immunohistochemical analysis. The mice had free movements in their animal rooms (two groups) or exercised by running on a motor-driven treadmill the others three groups. Recurring high dose AAS administration and physical training in mice produce significant increase in body weight and for total cholesterol. A moderate increase of the heart weight, cardiac hypertrophy and wide colliquative myocytolysis, were observed in high dose AAS administration and physical training group. The expression of HSP70 and inflammatory cytokine IL-1β, increased in the three AAS-treated groups. TNF- α showed a more extensive expression in the AAS-high dose group. A significant apoptotic process randomly sparse in the myocardium was described. Our data support the hypothesis that the combined effects of vigorous training, anabolic steroid abuse and stimulation of the sympathetic nervous system, may predispose to myocardial injury.

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

“…Although the association between AAS and exercise may change exercise-induced physiological cardiac hypertrophy into pathophysiological hypertrophy, the physiological mechanisms of this change are still poorly understood (Riezzo et al, 2011a). Riezzo et al (2011a) reported increased heart weight, and cardiac hypertrophy in trained mice treated with high doses of nandrolone, and attributed this effect to an enhanced protein synthesis in response to the nandrolone administration.…”

“…Although the association between AAS and exercise may change exercise-induced physiological cardiac hypertrophy into pathophysiological hypertrophy, the physiological mechanisms of this change are still poorly understood (Riezzo et al, 2011a). Riezzo et al (2011a) reported increased heart weight, and cardiac hypertrophy in trained mice treated with high doses of nandrolone, and attributed this effect to an enhanced protein synthesis in response to the nandrolone administration. It has been also suggested that β-adrenoceptor-mediated mechanisms are involved in the development of cardiac hypertrophy (Hannan et al, 2003;Sethi et al, 2007;Riezzo et al, 2011b), depending on the type and stage of hypertrophy (Sethi et al, 2007).…”

Treadmill Exercise Training Prevents Myocardial Mechanical Dysfunction Induced by Androgenic-Anabolic Steroid Treatment in Rats

“…Exogenously administered AAS induce cardiac hypertrophy in vitro and in vivo [4], [5]. Furthermore, high doses of AAS administered in conjunction with vigorous exercise training in mice leads to cardiac hypertrophy, increased inflammatory cytokine levels and significant stimulation of the sympathetic nervous system [6]. Therefore, the combination of such factors may predispose subjects to myocardial injury.…”

Acceleration of neutrophil precursors’ maturation and immunostimulation of CD3+, CD4+ lymphocytes by stanozolol in mice

“…Chronic AAS abuse results in different patterns of pathologic alterations which depend on dose, frequency and mode of use. The latency of sub-acute or chronic effect (multiple-dose treatments) can be the result of either drug accumulation or the sum of sub-toxic effects which, over time, may become evident in clear clinical symptoms unrelated to the kinetics of the substance in question [40]. Increases in total cholesterol occur with anabolic steroids and this has been shown to augment coronary artery response to catecholamines.…”

“…Recently, it has also been reported that the combined effects of vigorous training, anabolic steroid abuse and stimulation of the sympathetic nervous system, may dispose to myocardial injury [40].…”