We appreciate the comments made by Kasikcioglu and Dickerman concerning our published study.  The assumption of “hypertrophic cardiomyopathy”-like myocardial changes and the difficulty of assessment of these changes is also supported by our recent findings pointing to a reduced diastolic function in bodybuilders with anabolic steroid abuse by using cardiac tissue doppler imaging, while conventional echocardiographic methods (M-Mode, blood doppler) showed no significant changes in comparison to anabolic-free controls or endurance-athletes .
Concerning the points raised by Dickerman, we are well aware of the intrinsic limitations of such a study as already mentioned in the discussion of our results. However, our left ventricular dimensions correspond to the results found by other authors in anabolic-free strength athletes [3-5] and we do not share the opinion that differences in measurements of wall thicknesses of approximately 1 mm between authors are significant. The echocardiographic measurements in our cross-sectional study were made by the same experienced investigator. Nonetheless we certainly do not exclude wall thicknesses of approximately 13 mm in anabolic-free athletes, especially in athletes with higher body dimensions or from strength-endurance disciplines. 
Also, we did not state that the training regimen would be the same in bodybuilders as in weightlifters, but indeed we discussed that these differences would lead to the opposite changes than the one observed by inducing a more eccentric type of left ventricular hypertrophy in the bodybuilders. Finally we do not share the opinion of Dickerman that our data show a lower cardiovascular performance in the weightlifters because of the different level of exhaustion and the similar indicator of submaximal ergometric performance in comparison with the group of bodybuilders.
The claimed concentrations of testosterone were not described in this publication but reported elsewhere.  As already suggested by the normal concentrations of luteinizing hormone and follicle-stimulating hormone no abnormally increased testosterone concentrations were found in the ex- users, but 2 ex-users showed testosterone levels below the normal range.
We agree with Dickerman that this publication as well as the current comments are fruitful by stimulating a more critical approach for future studies.
(1). Urhausen A, Albers T, Kindermann W. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart 2004;90:496- 501
(2). Urhausen A, Krieg A, Scharhag J, Kindermann W. Tissue velocity imaging in the assessment of left ventricular function in endurance athletes vs. strength athletes abusing anabolic steroids. Med Sci Sports Exerc 2003;35(Suppl):S318
(3). Snoeckx LHEH, Abeling HFM, Lambregts JAC, Schmitz JJF, Verstappen FTJ, Renemann RS: Echocardiographic dimensions in athletes in relation to their training program. Med Sci Sports Exerc 1982;14:428-434
(4). George KP, Wolfe LA, Burggraf GW: The athletic heart syndrome: a critical review. Sports Med 1991;11;300-331
(5). Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P: The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med 1991;324:295-301
(6). Urhausen A, Monz T, Kindermann W. Echocardiographic criteria of physiological left ventricular hypertrophy in combined strength- and endurance-trained athletes. Int J Card Imaging 1997;13:43-52
(7). Urhausen A, Albers T, Kindermann W. Reversibility of the effects on blood cells, lipids, liver function and hormones in former anabolic- androgenic steroid abusers. J Steroid Biochem Mol Biol 2003;84:369-375
Cardiac Maladaptation in athletes using anabolic steroides
I read with great interest the published study by Urhausen et al.  It is known that anabolic steroid use in athletes has become a major medical issue. Although Urhausen et al. found that left ventricular wall thickness related to fat-free body mass did not differ between users and ex-users, Sachtleben et al.  previously reported that the parameters of left ventricular thickness showed significant differences between nonusers and users. Apart from this, Sachtleben et al. also demonstrated that maximal oxygen consumption in the anabolic steroid user group was lower than that of nonuser group. In other words, a decrease in shortening fraction of left ventricle was also observed between users off and user on groups. This may indicate non-adaptive changes within the myocardium, and thus cause the heart to become a less effective pump. Furthermore, Pearson et al.  found that left ventricular diastolic functions were reduced in a group of anabolic steroid user. It strikes me that myocardium is over stimulated to irregular grow by anabolic steroids, and they may lead to cell disarray in the myocardium, like as hypertrophic cardiomyopathy. Completely recovery to pre-training ventricular morphology is not obtained even though anabolic steroids are discontinued for a long time period.
1. Urhausen A, Albers T, Kindermann W. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart 2004;90:496-501.
2. Sachtleben TR, Berg KE, Elias BA, Cheatham JP, Felix GL, Hofschire PJ. The effects of anabolic steroids on myocardialstructure and cardiovascular fitness. Med Sci Sports Exer 1993;25:1240-1245.
3. Pearson AC, Schiff M, Mrosek D, Labovitz AJ, Williams GA. Left ventricular diastolic function in weight lifters. Am J Cardiol 1986;58:1254-1259.
Re: Are the cardiac effects of anabolic steroid abuse in strength athletes reversible?
I read the article by Urhausen et al. “Are the cardiac effects of anabolic steroid abuse in strength athletes reversible?” with great interest, however there are several factors that should be discussed.
First, the only subjects with left ventricular posterior wall measurements beyond normal limits were the users, which were only slightly enlarged >11.4 mm. We previously reported on the occurrence of left ventricular posterior wall thickening up to 13 mm in elite drug-free bodybuilders. In addition, several of the ex-users had a history of growth hormone use which is known to directly stimulate myocardial growth. One must question the ex-users left ventricular dimensions upon cessation of anabolic steroids. Is it possible that myocardium and skeletal muscle mass are not linearly related in the rate of atrophy? In addition, the ex-users are still training and could be utilizing the same intensity, as when on anabolic steroids, thus creating enough of a pressor response to blunt myocardial atrophy. As physicians we must also understand that not all anabolic agents have the same physiological effects. Specifically, anabolic steroids are a class of compounds that are thought to each bind to the androgen receptor, however, the molecular structure of each compound varies and even small alterations can induce different physiological and biochemical responses. For example, when looking at three of the injectable oil-based testosterones; enanthate, propionate and cypionate, we found that polycythemia was induced consistently in subjects abusing enanthate versus propionate or cypionate, despite almost having near identical molecular structures. While we understand and accept the inability to control for self-reported abuse of unknown quality and quantity of medications, we must also not assume that the subjects are taking the same medications. Serum testosterone levels would have been beneficial to have measured on each subject. Could some of the ex-users have still been using or could there levels still be elevated? Lastly, we disagree with the comment that training regimens do not differ among the groups, it is obvious from the performance data that the weightlifters had significantly (p <_0.001 worse="worse" performance="performance" in="in" cardiovascular="cardiovascular" exercise="exercise" and="and" the="the" anthropomorphic="anthropomorphic" data="data" shows="shows" much="much" higher="higher" average="average" of="of" bodyfat="bodyfat" weightlifters.="weightlifters." this="this" study="study" offered="offered" useful="useful" information="information" for="for" future="future" studies="studies" such="such" as="as" longitudinal="longitudinal" on="on" individual="individual" athletes="athletes" off="off" anabolic="anabolic" steroids="steroids" however="however" we="we" feel="feel" did="did" not="not" clearly="clearly" implicate="implicate" a="a" cause="cause" concentric="concentric" left="left" ventricular="ventricular" hypertrophy="hypertrophy" ex-="ex-" users="users" when="when" considering="considering" multiple="multiple" aforementioned="aforementioned" uncontrolled="uncontrolled" variables.="variables." p="p">References
1. Urhausen A, Albers T, Kindermann W. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart 2004;90:496- 501.
2. Dickerman RD, Schaller F, McConathy WJ. Left ventricular wall thickening does occur in elite power athletes with or without anabolic steroid Use. Cardiology 1998;90:145-148.
3. Saca L. Growth hormone: a new therapy for heart failure? Baillieres Clin Endocrinol Metab. 1998;12:217-31.
4. McDougall JD, Tuxen D, Sale DG, Moroz JR, Sutton JR. Arterial pressure response to heavy resistance exercise. J Appl Physiol 1985;58:785 -789.
5. Dickerman RD, Pertusi R, Miller J, Zachariah NY.Androgen-induced erythrocytosis: is it erythropoietin? Am J Hematol 1999;61:154-155.
Departments of Surgery and Medicine, University of North Texas Health Science Center, Fort Worth, TX, USA, 76107-2699
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