title: Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise.
abstract: 1. Physical effort involves, along with an increase in the plasma concentration of beta-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.
authors.affiliation: Department of Pathophysiology, University of Leuven, Belgium.
authors.forename: J
authors.initials: J
authors.lastname: Staessen
authors.forename: R
authors.initials: R
authors.lastname: Fiocchi
authors.forename: R
authors.initials: R
authors.lastname: Bouillon
authors.forename: R
authors.initials: R
authors.lastname: Fagard
authors.forename: P
authors.initials: P
authors.lastname: Hespel
authors.forename: P
authors.initials: P
authors.lastname: Lijnen
authors.forename: E
authors.initials: E
authors.lastname: Moerman
authors.forename: A
authors.initials: A
authors.lastname: Amery
mesh_terms: D000305:Adrenal Cortex Hormones / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D000450:Aldosterone / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D004311:Double-Blind Method; D004837:Epinephrine / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009638:Norepinephrine / Q000378:metabolism; D005082:Physical Exertion; D011897:Random Allocation; D012083:Renin / Q000097:blood
chemical_list: D000305:Adrenal Cortex Hormones; D009270:Naloxone; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012083:Renin; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine