Exercise-induced increases in plasma catecholamines and growth hormone are augmented by selective α₂-adrenoceptor blockade in man

A specific alpha₂-adrenoceptor antagonist (idazoxan) was used in man to examine the neuroregulation of growth hormone (GH) release and the effect of alpha₂-adrenoceptors on noradrenaline release. In the first study, GH-releasing factor (GRF)-induced GH release was unaffected in 6 normal volunteers by the prior administration of idazoxan, suggesting that the alpha₂-receptors involved in GH release are not operative at pituitary level. In the second study, 6 normal volunteers performed a bicycle exercise test with and without prior treatment with idazoxan. The exercise-induced GH response (to 13 ± 5 mU/l) was significantly augmented by idazoxan (to 20 ± 7 mU/l) which contrasts with the current view of GH release being regulated by stimulatory hypothalamic alpha₂-adrenoceptors and suggests that these alpha₂-adrenoceptors are capable of exerting a dual effect on GH release. The exercise-induced increase in plasma noradrenaline (to 1.45 + 0.19 micrograms/l) and in heart rate (to 142 + 5 beats/min) were also augmented by idazoxan (to 2.24 ± 0.23 micrograms/l and 152 ± 6 beats/min). A similar augmentation of the plasma adrenaline response to exercise was also found, whereas the blood glucose, plasma insulin and potassium response to exercise was unaffected by idazoxan. These results suggest that during exercise in man, alpha₂-adrenoceptors exert a tonic inhibitory influence on noradrenaline release which also serves to limit the exercise-induced tachycardia.