CLINICAL STUDY: ANABOLIC STEROIDS
Androgenic anabolic steroids and arterial structure and function in male bodybuilders
Mark A. Sader, MBBS, FRACP* ,
Kaye A. Griffiths, DMU*,
Robyn J. McCredie, BSc*,
David J. Handelsman, MBBS, PhD, FRACP and
David S. Celermajer, MBBS, PhD, FRACP* ||
* Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia
The Heart Research Institute, The University of Sydney, Sydney, Australia
Department of Andrology, Concord Hospital, Sydney, Australia
The ANZAC Research Institute, The University of Sydney, Sydney, Australia
|| Department of Medicine, The University of Sydney, Sydney, Australia
Manuscript received December 29, 1999;
revised manuscript received August 17, 2000,
accepted September 28, 2000.
Reprint requests and correspondence: Dr. David Celermajer, Department of Cardiology, Royal Prince Alfred Hospital, Missenden Road, Camperdown 2050, NSW, Australia davidc{at}card.rpa.cs.nsw.gov.au
OBJECTIVES
The study examined arterial and cardiac structure and function in bodybuilders using androgenic anabolic steroids (AAS), compared to non-steroid-using bodybuilder controls.
BACKGROUND
Adverse cardiovascular events have been reported in bodybuilders taking anabolic steroids. The cardiovascular effects of AAS, however, have not been investigated in detail.
METHODS
We recruited 20 male bodybuilders (aged 35 ± 3 years), 10 actively using AAS and 10 who denied ever using steroids. Serum lipid and hormone levels, carotid intima-media thickness (IMT), arterial reactivity, and left ventricular (LV) dimensions were measured. Vessel diameter was measured by ultrasound at rest, during reactive hyperemia (an endothelium-dependent response, leading to flow-mediated dilation, FMD), and after sublingual nitroglycerin (GTN, an endothelium-independent dilator). Arterial reactivity was also measured in 10 age-matched non-bodybuilding sedentary controls.
RESULTS
Use of AAS was associated with significant decreases in high density lipoprotein cholesterol, sex hormone binding globulin, testosterone and gonadotrophin levels, and significant increases in LV mass and self-reported physical strength (p < 0.05). Carotid IMT (0.60 ± 0.04 mm vs. 0.63 ± 0.07 mm), arterial FMD (4.7 ± 1.4% vs. 4.1 ± 0.7%) and GTN responses (11.0 ± 1.9% vs. 14.4 ± 1.7%) were similar in both bodybuilding groups (p > 0.2). The GTN responses were significantly lower and carotid IMT significantly higher in both bodybuilding groups, however, compared with the non-bodybuilding sedentary controls (p = 0.01).
CONCLUSIONS
Although high-level bodybuilding is associated with impaired vascular reactivity and increased arterial thickening, the use of AAS per se is not associated with significant abnormalities of arterial structure or function.
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Abbreviations and Acronyms
| | AAS | = androgenic anabolic steroids | | BP | = blood pressure | | FMD | = flow-mediated dilation | | FSH | = follicle-stimulating hormone | | GTN | = sublingual nitroglycerin | | HDL | = high density lipoprotein | | IMT | = intima-media thickness | | LH | = luteinizing hormone | | LV | = left ventricle/left ventricular | | SHBG | = sex hormone binding globulin |
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