Take a look at the Recent articlesAnabolic steroid abuse in athletes has been associated with a wide range of adverse conditions, including hypogonadism, testicular atrophy, anabolic steroids hypertrophic cardiomyopathy spermatogenesis, gynaecomastia, and psychiatric disturbance. But what effect does steroid abuse have on the cardiovascular system? Left ventricular hypertrophy LVH independently predicts cardiovascular mortality and morbidity across diverse disease states. The nature of these underlying mechanisms remains poorly understood. In this regard, escalating attention has focused on anaboic potential role of steroid hormones on LV growth anabolic steroids hypertrophic cardiomyopathy.
Cardiac effects of anabolic steroids
Anabolic steroid abuse in athletes has been associated with a wide range of adverse conditions, including hypogonadism, testicular atrophy, impaired spermatogenesis, gynaecomastia, and psychiatric disturbance. But what effect does steroid abuse have on the cardiovascular system? Left ventricular hypertrophy LVH independently predicts cardiovascular mortality and morbidity across diverse disease states.
The nature of these underlying mechanisms remains poorly understood. In this regard, escalating attention has focused on the potential role of steroid hormones on LV growth responses. Whether of local or systemic origin, endogenous steroid hormones appear to drive LV growth.
Systemic glucocorticoid excess is associated with significant hypertrophy. This action is more likely to be direct, rather than mediated through an elevated pressor burden, 2 with aldosterone having similar effects. Given these putative effects of steroid hormones and AAS in particular on LV growth, we might expect exposure to exogenously administered steroid hormones to be associated with an exaggerated LV hypertrophic response to any other hypertrophic stimulus.
Exercise is just such a potent cardiac hypertrophic stimulus. These are known to increase skeletal muscle mass and strength 7 —effects which form the basis for their administration to enhance athletic performance. The largest group to make such use of AAS are the very group whose LVH response to exercise is likely to be the greatest—the strength or resistance training RT athletes.
In this issue of Heart , Urhausen and colleagues report the results of a cross sectional study of cardiac morphology in relation to AAS use. Left ventricular wall thickness and cavity dimensions were assessed using echocardiography, and muscle mass LVMM calculated using the Devereux equation.
These results suggest that AAS use increases the LV hypertrophic response to exercise, an effect which might last for well over a year. Such data must nonetheless be treated with caution.
We know, for example, that the magnitude and pattern of hypertrophy is dependent on the nature, duration, and intensity of exercise undertaken. In the study under discussion, training patterns will have varied.
One might suspect that subjects taking AAS were also the most motivated to train whether by initial predisposition, or psychological impact of the steroid use itself. However, this does not seem to be the case as the authors report that the magnitude of training did not differ between U, ExU, and WL groups. Even so, more subtle differences in training pattern may have existed between bodybuilders, powerlifters, and weightlifters.
Although all groups lift exceptionally heavy weights, the total load and training pattern are likely to differ. Other factors may also have been of influence. Diet including the use of supplements may have differed between groups, as might the use of other agents. Abusers of AAS frequently also self administer other drugs including stimulants, antioestrogens, human chorionic gonadotrophin hCG , and human growth hormone hGH.
Neither can mechanistic inferences be drawn from the data: Certainly, resting systolic blood pressure is higher in the U v ExU group, a difference which persists as a trend for exercising blood pressure.
The use of such drugs as well as differences in patterns of training may also have influenced fat-free mass and body surface area. The adjustment for such anthropometric measures may have contributed to the significance of the comparison between ExU and WL. Finally, it is noticeable that the ExU group were younger than the U group, and it may be that LV growth responses differ with subject age.
Nonetheless, these data are consistent with existing data. Over a decade ago, De Piccoli demonstrated that LV mass among bodybuilders who used AAS was greater than that in non-users, and did not regress over a nine week period of abstinence.
If AAS use is associated with an exaggerated LV hypertrophic response to training, what are the likely health implications?
They may be profound. In terms of non-cardiac morbidity, AAS use is associated with hypogonadism, testicular atrophy, impaired spermatogenesis, baldness, acne, gynaecomastia, and psychiatric disturbance. Such drugs also have toxic effects on metabolic profile and hepatic structure and function, 10 as well as potentially promoting neoplastic growth.
LVH is an independent risk factor for cardiovascular mortality and through whatever mechanism one might anticipate an excess cardiovascular mortality among AAS users in whom LVH occurs. In addition, the recognised association of AAS use with hypertension and dislipidaemia raised low density lipoprotein and reduced high density lipoprotein cholesterol, and raised triglycerides , 10 as well as influences on coagulation and platelet aggregation, 10 might increase such risk.
In some cases, infarction has occurred without evident coronary thrombosis or atherosclerosis, leading to the hypothesis that ASS may induce coronary vasospasm in susceptible individuals.
Findings included hypertrophy 7 cases , myocardial or endocardial fibrosis 5 , cardiac steatosis 1 , myocardial coagulation necrosis 2 , and coronary atheroma 4.
Cardiac changes were adjudged to have contributed to death by poisoning in two cases. The influence of steroid hormones on the heart thus warrants further study. Evidently, the potential impact of steroid abuse on public health is a matter of concern. Perhaps more importantly, however, such studies might lead to a greater understanding of the shared mechanisms through which cardiac growth and cardiovascular disease are mediated.
Such issues are increasingly exciting as the identification of local myocardial steroid synthesis and its potential pathogenicity 19 is paralleled by the demonstrated efficacy of steroid antagonists in cardiac disease.
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