madman
Super Moderator
Abstract
Background Anabolic androgens have been reported to be associated with cardiovascular complications. One study revealed that an increase in vascular stiffness in bodybuilders is associated with anabolic androgens and improvement in vascular function may occur following anabolic androgens discontinuation. The aim of this study was to investigate any possible relation between aortic elastic properties and anabolic androgens.
Methods Study population was divided into 3 groups: Group-1 [n=35] consisted of bodybuilders who denied any current or previous use of anabolic androgens. Group-2 [n=18] was bodybuilders with regular use of anabolic androgens for at least 2 years prior to the start of our study. Group-3 was 13 healthy age-matched sedentary men as a control group. Cardiac echocardiography was performed in the bodybuilders and controls and indexes of aortic function were calculated.
Results Aortic stiffness was approximately twofold higher in anabolic androgens user bodybuilders compared with drugfree bodybuilders [P<0.001].
Conclusion The present study demonstrates that chronic anabolic androgens use clearly produces a significant decrease in the elastic properties of the aorta.
Aortopathic effect of androgenic anabolic steroids
The present study demonstrates that AAS abuse produces a significant increase in aortic stiffness.
Four possible mechanisms may contribute to aortic stiffness in chronic AAS users:
1. AAS decreases elastic and increases fibrous proteins in arterial vascular tissue [20].
2. In an experimental animal model, the treatment of rabbits with anabolic steroids has resulted in the impairment of endothelium-dependent and endothelium-independent dilation in aortic rings [12].
3. In human studies, high-dose androgen use was associated with impaired vascular reactivity.
4. AAS reduces nitric oxide-mediated vasorelaxation in the thoracic aorta by inhibition of guanylate cyclase [12].
Aortic elastic properties are an important component of left ventricular afterload and aortic stiffening with AAS use burdens the left ventricular performance. Thus, it is conceivable that in AAS abusers, the left ventricle is forced to perform under conditions of increased stress with a resultant increase in oxygen demand.
We postulate that chronic use of AAS causes increased aortic stiffness in the beginning. If AAS abuse continues for a prolonged duration, it may lead to an increase in LV size and LV hypertrophy because of increased force against LV ejection. In our study, AAS abusers had more aortic stiffness, but in a comparison between the two groups, the echocardiographic parameters of LV were similar. We believe that if AAS is used for an extended period, it might cause more LV thickening compared to athletes not using AAS, as previous animal studies showed that prolong exposure to aortic stiffness is needed to modify cardiac structures [27].
Study limitation
*In the present study, arterial blood pressure was obtained by the non-invasive cuff sphygmomanometery as a noninvasive method of estimating central pressure. Central arterial pressure, measured close to the heart, may be of more pathophysiological importance than conventional non-invasive cuff blood pressure. Unfortunately, catheter measurement of central pressure is a highly invasive procedure and is not applicable to our study population.
Conclusion
The present study revealed that chronic AAS use produces a significant decrease in the elastic properties of the aorta.
Background Anabolic androgens have been reported to be associated with cardiovascular complications. One study revealed that an increase in vascular stiffness in bodybuilders is associated with anabolic androgens and improvement in vascular function may occur following anabolic androgens discontinuation. The aim of this study was to investigate any possible relation between aortic elastic properties and anabolic androgens.
Methods Study population was divided into 3 groups: Group-1 [n=35] consisted of bodybuilders who denied any current or previous use of anabolic androgens. Group-2 [n=18] was bodybuilders with regular use of anabolic androgens for at least 2 years prior to the start of our study. Group-3 was 13 healthy age-matched sedentary men as a control group. Cardiac echocardiography was performed in the bodybuilders and controls and indexes of aortic function were calculated.
Results Aortic stiffness was approximately twofold higher in anabolic androgens user bodybuilders compared with drugfree bodybuilders [P<0.001].
Conclusion The present study demonstrates that chronic anabolic androgens use clearly produces a significant decrease in the elastic properties of the aorta.
Aortopathic effect of androgenic anabolic steroids
The present study demonstrates that AAS abuse produces a significant increase in aortic stiffness.
Four possible mechanisms may contribute to aortic stiffness in chronic AAS users:
1. AAS decreases elastic and increases fibrous proteins in arterial vascular tissue [20].
2. In an experimental animal model, the treatment of rabbits with anabolic steroids has resulted in the impairment of endothelium-dependent and endothelium-independent dilation in aortic rings [12].
3. In human studies, high-dose androgen use was associated with impaired vascular reactivity.
4. AAS reduces nitric oxide-mediated vasorelaxation in the thoracic aorta by inhibition of guanylate cyclase [12].
Aortic elastic properties are an important component of left ventricular afterload and aortic stiffening with AAS use burdens the left ventricular performance. Thus, it is conceivable that in AAS abusers, the left ventricle is forced to perform under conditions of increased stress with a resultant increase in oxygen demand.
We postulate that chronic use of AAS causes increased aortic stiffness in the beginning. If AAS abuse continues for a prolonged duration, it may lead to an increase in LV size and LV hypertrophy because of increased force against LV ejection. In our study, AAS abusers had more aortic stiffness, but in a comparison between the two groups, the echocardiographic parameters of LV were similar. We believe that if AAS is used for an extended period, it might cause more LV thickening compared to athletes not using AAS, as previous animal studies showed that prolong exposure to aortic stiffness is needed to modify cardiac structures [27].
Study limitation
*In the present study, arterial blood pressure was obtained by the non-invasive cuff sphygmomanometery as a noninvasive method of estimating central pressure. Central arterial pressure, measured close to the heart, may be of more pathophysiological importance than conventional non-invasive cuff blood pressure. Unfortunately, catheter measurement of central pressure is a highly invasive procedure and is not applicable to our study population.
Conclusion
The present study revealed that chronic AAS use produces a significant decrease in the elastic properties of the aorta.
