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Responses of the Growth Hormone (GH) and Insulin-Like Growth Factor Axis to Exercise, GH Administration, and GH Withdrawal in Trained Adult Males: A Potential Test for GH Abuse in Sport¹

Metabolic Research Unit, Department of Medicine, University of Queensland, Princess Alexandra Hospital (J.D.W., R.C.C.), Brisbane 4102, Australia; Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney (R.B.), Sydney 2065, Australia; the Department of Endocrinology, Aarhus Community Hospital (H.Ø., R.D., J.O.J., J.S.C.), Aarhus, Denmark; the Department of Endocrinology, St. Thomas’s Hospital (N.K., C.P., P.H.S.), London, United Kingdom SE1 7EH; the Research Center for Endocrinology and Metabolism, Sahlgrenska Hospital (T.R., B.-Å.B.), S-41345 Göteborg, Sweden; and the Department of Endocrinology, Frederico II Hospital (A.C., L.S.), 80131 Napoli, Italy

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 abuse by elite athletes is currently undetectable. To define suitable markers of GH doping, we assessed the effects of acute exercise, GH administration, and GH withdrawal on the GH/insulin-like growth factor (IGF) axis in athletic adult males. Acute endurance-type exercise increased serum GH, GH-binding protein (GHBP), total IGF-I, IGF-binding protein (IGFBP)-3, and acid-labile subunit (ALS), each peaking at the end of exercise. IGFBP-1 increased after exercise was completed. Free IGF-I did not change with exercise. Recombinant human GH treatment (0.15 IU/kg·day) for 1 week increased serum total IGF-I, IGFBP-3, and ALS, exaggerating the responses to exercise. IGFBP-2 and IGFBP-1 were trivially suppressed. After GH withdrawal, the GH response to identical exercise was suppressed. Total IGF-I, IGFBP-3, and ALS returned to baseline over 3–4 days. In summary, 1) acute exercise transiently increased all components of the IGF-I ternary complex, possibly due to mobilization of preformed intact complexes; 2) GH pretreatment augmented the exercise-induced changes in ternary complexes; 3) postexercise IGFBP-1 increments may protect against delayed onset hypoglycemia; 4) serum total IGF-I, IGFBP-3, and ALS may be suitable markers of GH abuse; and 5) differences in disappearance times altered the sensitivity of each marker for detecting GH abuse.

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