TY - JOUR
T1 - Impaired vasoreactivity in bodybuilders using androgenic anabolic steroids
AU - Lane, H. A.
AU - Grace, F.
AU - Smith, J. C.
AU - Morris, K.
AU - Cockcroft, J.
AU - Scanlon, M. F.
AU - Davies, J. S.
PY - 2006/6/6
Y1 - 2006/6/6
N2 - Background: Anabolic androgenic steroids are used by some bodybuilders to enhance performance. While the cardiovascular implications of supraphysiological androgen levels requires further clarification, use is associated with sudden death, left ventricular hypertrophy, thrombo-embolism and cerebro-vascular events. Materials and methods: To further understand the effect of androgenic anabolic steroid abuse on vascular function, this study assessed vascular stiffness (pulse-wave analysis) and cardiovascular risk factors in 28 male, bodybuilding subjects, of whom ten were actively receiving anabolic agents (group A; 26.4 ± 7.2 years) and eight had undergone a 3-month 'wash-out' period (group B; 32.1 ± 7.1 years). The remaining ten bodybuilding subjects (group C; 24.4 ± 4.4 years) denied any past use of anabolic steroids or other performance enhancing drugs. Comparisons were made with ten sedentary male controls (group D, 29.3 ± 4.7 years). Results: Endothelial independent dilatation in response to glycerol trinitrate was significantly impaired in the group currently using anabolic steroids (group A) compared with the other three groups [A (5.63 ± 3.24%) versus; B (11.10 ± 4.91%), C (17.88 ± 9.2%) and D (14.46 ± 3.9%), P < 0.0005, respectively], whereas no significant differences in endothelial-dependant dilatation were detected between the groups [A (5.0 ± 3.0%), B (7.4 ± 3.4%), C (9.6 ± 4.5%) and D (8.2 ± 3.3%), P < 0.059, respectively]. Conclusions: Previous studies described a decline in vascular reactivity occurring in bodybuilding subjects which is independent of anabolic steroid use and may result from smooth muscle hypertrophy with increased vascular stiffness. This study revealed impaired vascular reactivity associated with anabolic agents and that improvement in vascular function may occur following their discontinuation.
AB - Background: Anabolic androgenic steroids are used by some bodybuilders to enhance performance. While the cardiovascular implications of supraphysiological androgen levels requires further clarification, use is associated with sudden death, left ventricular hypertrophy, thrombo-embolism and cerebro-vascular events. Materials and methods: To further understand the effect of androgenic anabolic steroid abuse on vascular function, this study assessed vascular stiffness (pulse-wave analysis) and cardiovascular risk factors in 28 male, bodybuilding subjects, of whom ten were actively receiving anabolic agents (group A; 26.4 ± 7.2 years) and eight had undergone a 3-month 'wash-out' period (group B; 32.1 ± 7.1 years). The remaining ten bodybuilding subjects (group C; 24.4 ± 4.4 years) denied any past use of anabolic steroids or other performance enhancing drugs. Comparisons were made with ten sedentary male controls (group D, 29.3 ± 4.7 years). Results: Endothelial independent dilatation in response to glycerol trinitrate was significantly impaired in the group currently using anabolic steroids (group A) compared with the other three groups [A (5.63 ± 3.24%) versus; B (11.10 ± 4.91%), C (17.88 ± 9.2%) and D (14.46 ± 3.9%), P < 0.0005, respectively], whereas no significant differences in endothelial-dependant dilatation were detected between the groups [A (5.0 ± 3.0%), B (7.4 ± 3.4%), C (9.6 ± 4.5%) and D (8.2 ± 3.3%), P < 0.059, respectively]. Conclusions: Previous studies described a decline in vascular reactivity occurring in bodybuilding subjects which is independent of anabolic steroid use and may result from smooth muscle hypertrophy with increased vascular stiffness. This study revealed impaired vascular reactivity associated with anabolic agents and that improvement in vascular function may occur following their discontinuation.
KW - Anabolic steroids
KW - Bodybuilders
KW - Endothelium
KW - Vascular function
UR - http://www.scopus.com/inward/record.url?scp=33745035189&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2362.2006.01667.x
DO - 10.1111/j.1365-2362.2006.01667.x
M3 - Article
C2 - 16796605
AN - SCOPUS:33745035189
SN - 0014-2972
VL - 36
SP - 483
EP - 488
JO - European Journal of Clinical Investigation
JF - European Journal of Clinical Investigation
IS - 7
ER -