FUNCTION OF THE GH IGF-1 AXIS IN HEALTHY MIDDLE-AGED MALE RUNNERS/

Citation
Mr. Ambrosio et al., FUNCTION OF THE GH IGF-1 AXIS IN HEALTHY MIDDLE-AGED MALE RUNNERS/, Neuroendocrinology, 63(6), 1996, pp. 498-503
Citations number
44
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
Journal title
ISSN journal
00283835
Volume
63
Issue
6
Year of publication
1996
Pages
498 - 503
Database
ISI
SICI code
0028-3835(1996)63:6<498:FOTGIA>2.0.ZU;2-8
Abstract
In an attempt to examine the effect of prolonged physical activity on the function of the GH/IGF-1 axis during the aging process in man, we have evaluated basal and GHRH (GHRH-29: 1 mu g/kg i.v. as a bolus) sti mulated GH secretion as well as basal plasma IGF-1 levels in a group o f 25 healthy runners (50-60 years, mean age 55.5 +/- 0.6) and 24 age-m atched relatively sedentary normal controls (mean age 55.8 +/- 0.7). T he runners had a minimum distance in kilometers of 26 km/week for at l east 15 years, and competed in distances ranging from 16 km to the mar athon. In runners, GHRH induced an increase of GH which was significan tly higher (p < 0.001) than that observed in the age-matched controls. Baseline IGF-1 levels were significantly higher (p < 0.001) in traine d runners (171 +/- 8.4 mu g/l) compared to the controls (91.1 +/- 5.5 mu g/l). These data show that in middle-age prolonged physical activit y increases the function of the GH/IGF-1 axis. To clarify the possible mechanisms underlying the GH/IGF-1 secretory pattern in the runners, the GH responses to both single and combined administration of GHRH an d arginine (ARG: 30 g infused over 30 min), a GH secretagogue likely a cting via inhibition of hypothalamic somatostatin release, were invest igated in 6 runners (mean age 55 +/- 1.9 years) and 6 controls (mean a ge 55 +/- 0.9 years). ARG clearly increased the GH response to GHRH in the controls, whereas it was unable to further potentiate the GH-rele asing effect of GHRH in runners, thus suggesting that the increased GH responsiveness to GHRH might be due to an exercise-related decrease i n endogenous hypothalamic somatostatinergic activity.