title: Effect of exercise-induced acidosis on aldosterone secretion in men.
abstract: The present study was carried out to elucidate whether an exercise-induced increase in plasma hydrogen ion concentration influences aldosterone secretion. Six healthy men (aged 22-25 years) performed two intermittent exercise tests with and without drug administration. The intensities of these exercise tests were 40% maximal oxygen uptake (VO2max) and 90% VO2max, respectively. Administration of 2-mg Dexamethasone and 50-mg Captopril caused an almost complete suppression of adrenocorticotropic hormone (ACTH) and an enhancement of the elevation in renin concentration during exercise, indicating successful inhibition of ACTH release and angiotensin II production during exercise. While the magnitude of the increase in aldosterone in the drug experiment was depressed compared with the control experiment, a significant increase in aldosterone concentration was observed at the end of the 90% VO2max exercise. Whilst the change in aldosterone concentration did not correlate with the change in plasma potassium concentration, there was a significant correlation between aldosterone and plasma hydrogen ion concentrations in the drug experiment. Since the correlation coefficient was low (r = 0.455), the biological meaning of this correlation should be further investigated. These results would suggest that an elevation of plasma hydrogen ion concentration induced by exercise per se appears to be related, at least in part, with increased aldosterone secretion, independent of the pituitary-adrenal axis, and the renin-angiotensin system.
authors.affiliation: Division of Basic Science, School of Science and Engineering, Ishinomaki Senshu University, Miyagi, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yamauchi
authors.forename: T
authors.initials: T
authors.lastname: Harada
authors.forename: M
authors.initials: M
authors.lastname: Kurono
authors.forename: N
authors.initials: N
authors.lastname: Matsui
mesh_terms: D000138:Acidosis / Q000097:blood / Q000209:etiology* / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006863:Hydrogen-Ion Concentration; D008297:Male; D010101:Oxygen Consumption; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000097:blood; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D005938:Glucocorticoids; D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D002216:Captopril; D012083:Renin; D011188:Potassium; D006854:Hydrocortisone