OPIOID MODULATION OF THE GAMMA-AMINOBUTYRIC ACID-CONTROLLED INHIBITION OF EXERCISE-STIMULATED GROWTH-HORMONE AND PROLACTIN SECRETION IN NORMAL MEN

Citation
V. Coiro et al., OPIOID MODULATION OF THE GAMMA-AMINOBUTYRIC ACID-CONTROLLED INHIBITION OF EXERCISE-STIMULATED GROWTH-HORMONE AND PROLACTIN SECRETION IN NORMAL MEN, European journal of endocrinology, 131(1), 1994, pp. 50-55
Citations number
26
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
08044643
Volume
131
Issue
1
Year of publication
1994
Pages
50 - 55
Database
ISI
SICI code
0804-4643(1994)131:1<50:OMOTGA>2.0.ZU;2-2
Abstract
The possible involvement of endogenous opioids in the gamma-aminobutyr ic acid-controlled (GABAergic) inhibition of growth hormone (GH) and p rolactin (PRL) during physical exercise was evaluated in normal men. A fter fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. Th e workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (1O mg as a n iv bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. Duri ng exercise, plasma GH and PRL levels rose 5.5- and 1.9-fold, respecti vely. The administration of naloxone did not modify, whereas sodium va lproate significantly reduced the plasma GH and PRL rise during exerci se. In the presence of sodium valproate, GH and PRL levels rose 3- and 1.5-fold, respectively, in response to exercise. When naloxone was gi ven together with sodium valproate, both GH and PRL responses to exerc ise were abolished completely. These data suggest the involvement of a GABAergic mechanism in the regulation of GH and PRL responses to phys ical exercise in men. Furthermore, the data argue against a role of na loxone-sensitive endogenous opioids in the control of these hormonal r esponses to exercise, whereas they suggest a modulation by opioids of the GABAergic inhibitory action.