Cholinergic but not serotonergic mediation of exercise-induced growth hormone secretion.

In order to clarify the roles of cholinergic and serotonergic neurotransmission in the mediation of exercise-induced growth hormone (GH) release, normal young volunteers of both sexes were studied. Exercise was for 20 minutes at 800 kpm for the men and 500 kpm for the women. Pretreatment with 0.4 mg atropine 1 hour prior to exercise, or with methysergide 2 mg po q 6 h for 48 hours prior to exercise, were used to evaluate the influence of cholinergic and serotonergic blockade, respectively. Five of the ten men studied failed to raise GH values with exercise, perhaps because the exercise was not vigorous enough for their high degree of fitness. Of three non-responders restudied, at the same workload, one responded on the second occasion. The mean peak GH with exercise 13.4 +/- 3.27 ng/ml, was reduced to 2.4 +/- 1.28 ng/ml (p less than 0.01) after atropine, but was unaffected by methysergide (15.2 +/- 6.58 ng/ml, p greater than 0.5). Prolactin did not rise with exercise, and was not affected by atropine, but lowered by methysergide as expected. Cholinergic neurotransmission therefore represents a key link in exercise-induced GH secretion, but serotonergic influences are probably not involved.