Left ventricular function is not impaired in weight-lifters who use anabolic steroids

Thompson, Paul D.; Sadaniantz, Ara; Cullinane, Eileen M.; Bodziony, Kurt S.; Catlin, Don H.; Torek-Both, George; Douglas, Pamela S.

doi:10.1016/0735-1097(92)90478-6

Cited by 71 publications

(28 citation statements)

References 20 publications

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“…17,47 There are many anecdotal reports of adverse myocardial effects of exogenous androgens in humans, 38 although this is not a universal finding. 48 Third, there are implications for androgen regulation of gene expression in heart beyond cardiac hypertrophy. Our findings help to open an avenue of investigation aimed at elucidating the cellular basis for the increased relative propensity of women to QT prolongation and torsade de pointes in various settings.…”

Section: Discussionmentioning

confidence: 99%

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

et al. 1998

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Background-The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain.Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response. Methods and Results-We used reverse transcription-polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [ 3 H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion. Conclusions-Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.(Circulation. 1998;98:256-261.)

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Section: Discussionmentioning

confidence: 99%

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

et al. 1998

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“…In contrast to these definite findings, studies comparing echocardiographic variables between anabolicandrogenic steroids using and nonusing strength athletes have not yielded unequivocal results (Ahlgrim and Guglin 2009). Some studies have not demonstrated any structural difference with abuse (Thompson et al 1992) or showed that the myocardial remodeling is independent from anabolic-androgenic steroid use in power athletes (Dickerman et al 1998). Considering the high prevalence of anabolic-androgenic steroids abuse in population, the number of cases featuring associated cardiac illness reported in current literature appears rather small.…”

mentioning

confidence: 42%

Drug-Induced Cardiomyopathies

Klimas¹

2012

Cardiomyopathies - From Basic Research to Clinical Management

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“…Several studies demonstrated an increase in left ventricular end diastolic volume, left ventricular mass and/or worsening diastolic function [11][12][13], while other studies demonstrated no cardiovascular changes with anabolic steroid use [14][15][16]. However, in bodybuilding, the doses used are often 10-100 times the therapeutic dose; in one report involving 24 weight lifters, the lowest dose was 350% of the usual therapeutic dose [17].…”

Section: Discussionmentioning

confidence: 99%

Effect of Testosterone and Resistance Training on Cardiac Mass and Contractility in Men with COPD

Budoff¹,

Mao²,

Rambod³

et al. 2011

J Allergy Ther

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Introduction: Testosterone therapy and resistance training have been demonstrated to improve muscle mass and strength in patients with testosterone deficiency. However the effects on cardiac mass and contractility of these interventions have not been identified in prospective placebo-controlled trials. The hypothesis of this trial was that resistance training and testosterone replacement would improve cardiac mass and contractility in male COPD patients with low testosterone levels. Methods:We conducted a 10 week trial in a 2 by 2 factorial design, randomizing 53 patients to replacement doses of testosterone enanthate (100 mg weekly) or placebo, as well as to a program of lower extremity resistance training or no exercise. We performed rest and exercise cardiac computed tomography (CCT) studies before and after 10 weeks of therapy to evaluate right and left heart function. Patients were injected with 40-50 ml of non-ionic, iodinated contrast and cine CCT images were obtained at rest. Patients were exercised to 60% of their maximal work rate on a semi-supine ergometer, then re-injected with another bolus of 40-50 ml of contrast and re-imaged. We evaluated cardiac output and left ventricular (LV) and right ventricular (RV) mass, LV and RV stroke volume, ejection fractions and end-diastolic volumes at rest and exercise, before and after therapy.Results: 42 men with COPD (mean FEV 1 =40%pred. pre-bronchodilator) and low testosterone levels (mean=320ng/dl) completed the 10 week protocol. Factorial analysis demonstrated that testosterone, but not resistance training increased LV and RV mass (by 4.9% and 8.3%, respectively). Resistance training, but not testosterone, was associated with increased LV ejection fraction at rest and during exercise (by 5.5% and 4.4%, respectively). In the entire study group, increases in both left and right ventricular mass were correlated with increases in lean body mass (assessed by DEXA) (r=0.49 and r=0.65, respectively). Conclusions:In men with COPD, testosterone replacement and strength training are associated with distinct alterations in cardiac structure and function. Specifically, resistance training improved ejection fraction, while testosterone increased lean body mass and LV mass.

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Left ventricular function is not impaired in weight-lifters who use anabolic steroids

Cited by 71 publications

References 20 publications

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

Drug-Induced Cardiomyopathies

Effect of Testosterone and Resistance Training on Cardiac Mass and Contractility in Men with COPD

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