Treadmill exercise training prevents myocardial mechanical dysfunction induced by androgenic-anabolic steroid treatment in rats.

Danilo S Bocalini,Cássia T Bergamaschi,Ruy R Campos,Abram Beutel,Paulo J Tucci

doi:10.1371/journal.pone.0087106

Danilo S Bocalini, Cássia T Bergamaschi + Show 3 more

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https://doi.org/10.1371/journal.pone.0087106

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Abstract

Elevated concentrations of testosterone and its synthetic analogs may induce changes in cardiovascular function. However, the effects of the combination of anabolic/androgenic steroid (AAS) treatment and exercise training on systolic and diastolic cardiac function are poorly understood. In the present study, we aimed to investigate the effects of low-dose steroid treatment (stanozolol) on cardiac contractile parameters when this steroid treatment was combined with exercise training in rats and the effects of chronic steroid treatment on the Frank-Starling (length-tension curves) relationship. Male Wistar rats were randomly assigned to one of four groups: U (untrained), US (untrained and treated with stanozolol 5 mg/kg/week), T (trained, 16 m/min/1 h) and TS (trained and treated with stanozolol 5 mg/kg/week). Continuous exercise training was conducted 5 days/week for 8 consecutive weeks. The speed of the treadmill was gradually increased to a final setting of 16 m/min/1 h. Experiments were divided into two independent series: 1) central hemodynamic analysis for mean arterial blood pressure (MAP) and cardiac output (CO) measurements and 2) isolated papillary muscle preparation in Krebs solution. Stanozolol treatment significantly increased the MAP and the heart size in untrained and trained rats (U 113±2; T 106±2; US 138±8 and TS 130±7 mmHg). Furthermore, stanozolol significantly decreased developed tension and dT/dt (maximal and minimal) in U rats. However, the developed tension was completely restored by training. The Frank/Starling relationship was impaired in rats treated with stanozolol; however, again, training completely restored diastolic function. Taken together, the present data suggest that AAS treatment is able to decrease cardiac performance (systolic and diastolic functions). The combination of stanozolol and physical training improved cardiac performance, including diastolic and systolic functions, independent of changes in central hemodynamic parameters. Therefore, changes in ventricular myocyte calcium transients may play a cardioprotective role.

Highlights

Testosterone and its synthetic analogs have been used to increase skeletal muscle mass and enhance physical performance
It is well described that anabolic/androgenic steroids (AAS) have cardiovascular actions and that the heart is a target tissue of AAS, and testosterone is the main physiological hormone in this class [1,2]
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]

Summary

Introduction

Testosterone and its synthetic analogs have been used to increase skeletal muscle mass and enhance physical performance. It is well described that anabolic/androgenic steroids (AAS) have cardiovascular actions and that the heart is a target tissue of AAS, and testosterone is the main physiological hormone in this class [1,2]. Administered AAS induce cardiac hypertrophy in vitro and in vivo [4,5]. 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]. The adaptations of cardiac muscle to chronic low-dose AAS exposure and their association with physical exercise are still poorly understood and were the major focus of the present study

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