EXERCISE CAPACITY AND HORMONAL RESPONSE IN ADULTS WITH CHILDHOOD-ONSET GROWTH-HORMONE DEFICIENCY DURING LONG-TERM SOMATROPIN TREATMENT

Growth hormone (GH) deficiency in adults in associated with reduced mu scular strength and peak oxygen uptake (peak Vo(2)). How these variabl es are influenced by long-term somatropin therapy in adults with child hood onset GH-deficiency has not been precisely defined. The effect of somatropin treatment in 20 childhood onset GH-deficient adults on mus cular strength, maximal exercise capacity, and hormonal response to ex ercise were therefore examined in a double-blind placebo-controlled st udy with recombinant human GH (rhGH, 12 mu g/kg/day) for 6 months, fol lowed by 36 months of open-labeled uninterrupted therapy, after which treatment was stopped for 9 months. After 6 months of treatment, exerc ise capacity increased significantly, as assessed by time to exhaustio n [mean change (95% CI) 0.8 (0.2, 1.4) min, P < 0.05], total (accumula ted) work [11.6 (0.8, 22.4) kJ, P < 0.05] and peak Vo(2) [2.6 (0.3, 4. 9) ml/kg/min, P < 0.01], whereas no significant changes were observed during placebo. This effect on exercise capacity remained unchanged du ring long-term somatropin treatment, mainly due to increased capacity among patients with isolated GH deficiency. Nine months after stopping treatment, peak Vo(2) decreased by 11% from 32.8 +/- 2.5 to 29.1 +/- 2.1 ml/kg/min (P < 0.05). Maximal muscular handgrip strength was not a ffected by treatment. Long-term GH therapy resulted in decreased respi ratory exchange value (R value) at rest and during exercise (P < 0.001 ), suggesting a metabolic role with increased fat combustion. Resting and submaximal noradrenaline levels decreased during somatropin treatm ent (P < 0.05), while no effect was observed for other exercise-induce d hormonal responses, including adrenaline, insulin, prolactin, renin, and ACTH. We conclude that somatropin therapy to childhood onset GH d eficient adults has a favourable effect on exercise capacity and may h ave a potentially beneficial effect on plasma catecholamines. (C) 1998 Churchill Livingstone.