AAS abuse produces a significant increase in aortic stiffness

madman

Member
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 produce 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 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 two groups, echocardiographic parameters of LV were similar. We believe that if AAS is used for an extended period, it might cause in 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 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 in our study population.








Conclusion


The present study revealed that chronic AAS use produces significant decrease in the elastic properties of the aorta.
 

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sh1973

Active Member
No. They are talking about anabolic androgenic steroids (AAS).
That’s a grey area Vince, because many body builders do only use the same exact testosterone we’re taking just in larger doses. Testosterone and deca are by far the most abused anabolics in the bodybuilding world. It would be nice if the article clarified dose, levels etc...
 

madman

Member
Hello Madman,


Would a TRT user like myself get this at 40 mg test cypionate eod? 500 ius hcg twice weekly? Also, what is your trt protocol sir?

With trt we are replacing physiological levels of the primary sex hormone and anabolic steroid in males which is responsible for the beneficial effects (mood, energy, libido, erectile function, muscle, strength, recovery, cardiovascular, brain, bone, immune system).

Having healthy T levels would be cardiovascular protective.

My protocol was 150 mg/week (75 mg every 3.5 days).

Currently 120 mg/week (60 mg every 3.5 days).

I have always run my TT/FT levels on the higher-end physiological range.







Conclusion

Using the reductio ad absurdum logic, we contradicted the initial assumption of an overall harmful effect of T on the CV system. Although T has been demonstrated to have overall favorable effects on vasomotion, arterial stiffness, atherosclerosis, cardiac electrophysiology, oxygen delivery, cardiac contractility, and remodeling, it possesses a prothrombotic effect due to its action on platelet function and blood viscosity. In summary, based on the current evidence, CV disease does not appear to be increased in patients undergoing TRT.178,179 Most physicians against TRT will argue that TRT is “neutral” in terms of CV safety. While the latter is possible, the indication for TRT has never been to address CV dysfunction but rather to improve various signs and symptoms in LOH that correlate well with low testosterone levels. Nonetheless, in older patients with a known CV risk factor, a tailored approach is suggested.14,25 Symptoms, comorbidities, baseline and target levels of T, formulation, and therapy timing25,180,181 should be considered to improve sexual function, mood, depressive symptoms, and the mobility of patients with low testosterone levels.13,33,182,183






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Table 1. Summary of the effects of testosterone on the vessel and endothelial function: small, medium, large vessels. Coronary arteries vasomotion. Testosterone exerts a vasodilating action through a rapid, non-genomic, and endothelial-independent action on K and Ca channels. Moreover, it has also an endothelial-dependent vasodilating effect mediated by NO. Peripheral arterial stiffness. Testosterone reduces arterial stiffness through, an androgen receptor-dependent modulation of apoptosis and senescence of vascular smooth muscle cells. Testosterone vasodilating action and anti-inflammatory effects may also have a role. Large vessel atherosclerosis. Testosterone exerts several anti-atherogenic actions, including an anti-inflammatory effect which may hinder the initial development of atheroma. The effect on VSMSs is complex and may be reliant on the stage of plaque development. VSMCs migration and proliferation could be considered protective against plaque destabilization, while VSMCs apoptosis could be responsible for plaque vulnerability.






Figure legend: Fig. 1 Summary of testosterone cardiovascular (CV) effects. Created with images adapted from SMART - Servier Medical Art (SMART - Servier Medical ART), licensed under a Creative Common Attribution 3.0 License (Creative Commons — Attribution 3.0 Unported — CC BY 3.0)

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Nelson Vergel

Founder, ExcelMale.com

 

Joe Sixpack

Active Member
That’s a grey area Vince, because many body builders do only use the same exact testosterone we’re taking just in larger doses. Testosterone and deca are by far the most abused anabolics in the bodybuilding world. It would be nice if the article clarified dose, levels etc...
Yes. It always annoys me when the medical community talks about "steroids" and their impact on various human properties. As if taking 70mg/week of testosterone is equivalent to taking 1gram/week testosterone + whatever other mega dose cocktail of other AAS might be used/abused. It's sloppy science.
 
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