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Original Studies |
Metabolic Research Unit (J.D.W., R.C.C., J.H.), Department of Medicine, and Statistics Section, Department of Social and Preventative Medicine, University of Queensland, Princess Alexandra Hospital, Brisbane 4102, Australia; Neuroendocrine Unit (M.B., C.J.S.), Department of Medicine, Innenstadt University Hospital, 80336 Munich, Germany; Serviço do Endocrinologia e Metabologia do Hospital de Clínicas da Universidade Federal do Paraná (C.L.B.), 80060-240 Curitiba, Brasil; Research Centre for Endocrinology and Metabolism (P.A.L., L.C., T.R.), Sahlgrenska Hospital, Gothenberg, S-413 45 Sweden; Department of Endocrinology (M.B.), St. Thomass Hospital, London SE1 7EH, United Kingdom; Department of Internal Medicine and Cardiovascular Sciences (A.C.), Frederico II University, 80131 Naples, Italy; and Department of Medicine M (Endocrinology and Diabetes) (R.D.), Aarhus University Hospital, Aarhus, 8000 Denmark
Address all correspondence and requests for reprints to: Jennifer D. Wallace, Metabolic Research Unit, University of Queensland, Department of Medicine, Princess Alexandra Hospital, Brisbane 4102, Australia. E-mail: jwallace{at}medicine.pa.uq.edu.au
GH is being used by elite athletes to enhance sporting performance. To examine the hypothesis that exogenous 22-kDa recombinant human GH (rhGH) administration could be detected through suppression of non-22-kDa isoforms of GH, we studied seventeen aerobically trained males (age, 26.9 ± 1.5 yr) randomized to rhGH or placebo treatment (0.15 IU/kg/day for 1 week). Subjects were studied at rest and in response to exercise (cycle-ergometry at 65% of maximal work capacity for 20 min). Serum was assayed for total GH (Pharmacia IRMA and pituitary GH), 22-kDa GH (2 different 2-site monoclonal immunoassays), non-22-kDa GH (22-kDa GH-exclusion assay), 20-kDa GH, and immunofunctional GH. In the study, 3 h after the last dose of rhGH, total and 22-kDa GH concentrations were elevated, reflecting exogenous 22-kDa GH. Non-22-kDa and 20-kDa GH levels were suppressed. Regression of non-22-kDa or 20-kDa GH against total or 22-kDa GH produced clear separation of treatment groups. In identical exercise studies repeated between 24 and 96 h after cessation of treatment, the magnitude of the responses of all GH isoforms was suppressed (P < 0.01), but the relative proportions were similar to those before treatment. We conclude: 1) supraphysiological doses of rhGH in trained adult males suppressed exercise-stimulated endogenous circulating isoforms of GH for up to 4 days; 2) the clearest separation of treatment groups required the simultaneous presence of high exogenous 22-kDa GH and suppressed 20-kDa or non-22-kDa GH concentrations; and 3) these methods may prove useful in detecting rhGH abuse in athletes.
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