GH improves endothelial function & lipid profile but increases RPP & PIIIP in drug users

Background: In hypertensive subjects without a history of overt cardiovascular disease (CVD), arterial pulse wave velocity (APWV) is a surrogate measure of arterial stiffness, arterial endothelial dysfunction and CVD and independently predicts the occurrence of cardiovascular events (Boutouyrie, et al, 2002). Amino-terminal propeptide of type III procollagen (PIIIP) is increased in plasma and arterial aneurysm tissue compared with healthy arterial tissue (Ihara et al., 2004). Anabolic-androgenic steroid (AAS) drug use combined with strength training independently predisposes to endothelial dysfunction and decreased arterial compliance (Kasikcioglu et al., 2007). Objectives: To establish if recombinant human growth hormone (rhGH) in an AAS group affected endothelial function, rate pressure product, lipid profile and PIIIP, compared with a control group. Methods: Male subjects (n=48) were randomly divided, using a single blind procedure into two groups: (1): control group (C) n=24, mean ± SD, age 32 ± 11 years; height 1.8 ± 0.06 metres; 2): rhGH using group (0.019 mg.kg-1.day-1) (GH) n=24, mean ± SD, age 32 ± 9 years; height 1.8 ± 0.07 metres. Physiological responses, anthropometry, arterial pulse wave velocity (APWV), blood pressure (BP), heart rate (HR), and biochemical indices were investigated. Results: Body mass index, fat-free mass index significantly increased, body fat significantly decreased within GH (all P<0.017). Insulin like growth factor-I and PIIIP significantly increased within GH (P<0.017) and compared with C (P<0.05). Serum sodium significantly increased (P<0.017) and serum homocysteine, and high sensitivity C-reactive protein, significantly decreased within GH (all P<0.017). Arterial pulse wave velocity, significantly decreased within GH (P<0.017) and compared with C (P<0.05). Total cholesterol, triglycerides and low density lipoprotein all significantly decreased within GH (P<0.017). Resting HR and rate pressure product (RPP) significantly increased within GH (P<0.017) and compared with C (P<0.05). Conclusion: The elevation in PIIIP supports previous research in the area (Velloso et al., 2006). RhGH therapy has been shown to improve cardiovascular risk factors in strength training athletes, using AAS (Graham et al, 2007), however the current study suggest that short term use of rhGH although having beneficial effects on endothelial function, lipoprotein profile and specific inflammatory markers of cardiovascular disease in AAS drug users, may controversially also have an adverse effect on the cardiovascular system, as evidenced by the increase in resting RPP and PIIIP and should therefore not be recommended in drug users.