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The Response of Molecular Isoforms of Growth Hormone to Acute Exercise in Trained Adult Males¹

Metabolic Research Unit, Department of Medicine, and Statistics Section, Department of Social and Preventative Medicine, University of Queensland, Princess Alexandra Hospital (J.D.W., R.C.C., J.H.), 4102 Brisbane, Australia; Neuroendocrine Unit, Department of Medicine, Innenstadt University Hospital (M.B., C.J.S.), 80336 Munich, Germany; SEMPR, Serviço do Endocrinologia e Metabologia do Hospital de Clínicas da Universidade Federal do Paraná (C.L.B.), 80060-240 Curitiba, Brazil; Research Center for Endocrinology and Metabolism, Sahlgrenska Hospital (P.A.L., L.C., T.R.), S-413 45 Gothenberg, Sweden; Department of Endocrinology, St. Thomas’s Hospital (M.-L.H.), London, United Kingdom SE1 7EH; Department of Internal Medicine and Cardiovascular Sciences, Frederico II University (R.N.), 80131 Naples, Italy; and Department of Medicine M (Endocrinology and Diabetes), Aarhus University Hospital (R.D.), 8000 Aarhus, Denmark

Address all correspondence and requests for reprints to: Dr. Jennifer D. Wallace, Metabolic Research Unit, University of Queensland, Department of Medicine, Princess Alexandra Hospital, 4102 Brisbane, Australia. E-mail: jwallace{at}medicine.pa.uq.edu.au

Circulating GH consists of multiple molecular isoforms, all derived from the one gene in nonpregnant humans. To assess the effect of a potent stimulus to pituitary secretion on GH isoforms, we studied 17 aerobically trained males (age, 26.9 ± 1.5 yr) in a randomized, repeat measures study of rest vs. exercise. Exercise consisted of continuous cycle ergometry at approximately 80% of predetermined maximal oxygen uptake for 20 min. Serum was assayed for total, pituitary, 22-kDa, recombinant, non-22-kDa, 20-kDa, and immunofunctional GH. All isoforms increased during, peaked at the end, and declined after exercise. At peak exercise, 22-kDa GH was the predominant isoform. After exercise, the ratios of non-22 kDa/total GH and 20-kDa GH/total GH increased and those of recombinant/pituitary GH decreased. The disappearance half-times for pituitary GH and 20-kDa GH were significantly longer than those for all other isoforms. We conclude that 1) all molecular isoforms of GH measured increased with and peaked at the end of acute exercise, with 22-kDa GH constituting the major isoform in serum during exercise; and 2) the proportion of non-22-kDa isoforms increased after exercise due in part to slower disappearance rates of 20-kDa and perhaps other non-22-kDa GH isoforms. It remains to be determined whether the various biological actions of different GH isoforms impact on postexercise homeostasis.

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