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Pharmacodynamics of Growth Hormone Abuse Biomarkers and the Influence of Gender and Testosterone: A Randomized Double-Blind Placebo-Controlled Study in Young Recreational Athletes

Garvan Institute of Medical Research and St. Vincent’s Hospital (A.E.N., U.M., J.L.H., I.H.W., K.-c.L., K.K.H.), Sydney, New South Wales 2010, Australia; Commonwealth Scientific and Industrial Research Organization Mathematical and Information Sciences (G.S.), North Ryde, New South Wales 2113, Australia; Australian Sports Drug Testing Laboratory (C.J.H., R.K.), National Measurement Institute, Sydney, New South Wales 2073, Australia; ANZAC Research Institute (M.J.S., D.J.H.), University of Sydney, Concord Hospital, Concord, New South Wales 2139, Australia; and Kolling Institute of Medical Research (R.C.B.), University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales 2065, Australia

Address all correspondence and requests for reprints to: Professor Ken K. Y. Ho, Pituitary Research Unit, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst 2010, Australia. E-mail: K.Ho{at}garvan.org.au.

Context: IGF axis proteins and collagen peptides are promising markers of GH abuse.

Objective: Our objective was to investigate whether responses of serum IGF axis and collagen markers to GH differ between men and women, and are influenced by testosterone (T).

Design: This was a randomized, double-blind, placebo-controlled study of 8-wk treatment followed by 6-wk washout.

Setting: The study was performed at a clinical research facility.

Participants: A total of 96 recreationally trained healthy athletes (63 men, 33 women), aged 18–40 yr, were studied.

Intervention: All subjects received GH (2 mg/d sc) or placebo for 8 wk; men also received T (250 mg/wk im) or placebo for 5 wk.

Main Outcome Measures: Serum IGF axis proteins (IGF-I, IGF binding protein-3, and acid labile subunit) and collagen peptides (N-terminal propeptide of type I procollagen, C-terminal telopeptide of type I collagen, and N-terminal propeptide of type III procollagen) were measured.

Results: GH induced significant increases in IGF axis and collagen markers that were greater in men than women (P < 0.001). Of the IGF axis markers, IGF-I showed the greatest increase. The relative incremental responses of the collagen markers in general were greater than the IGF markers, especially for PIIINP. The collagen markers increased and decreased more slowly with most remaining elevated (P < 0.01) after 6 wk, in comparison to IGF markers, which returned to baseline within 1 wk. Addition of T to GH amplified the response of PIIINP by more than 1.5-fold but did not affect any other marker. T alone did not affect IGF axis markers but modestly increased collagen markers.

Conclusions: These markers of GH abuse are less responsive in women. The increases in collagen markers have a different time course to the IGF markers and extend the window of detection in both sexes. The response of PIIINP is increased by coadministration of T.