Effect of O2 availability on neuroendocrine variables at rest and during exercise: O2 breathing increases plasma prolactin.

Neuroendrocrine and substrate responses were investigated in eight male athletes during inhalation of either 100% O2 (HE), 14% O2 (HO) or normoxio gas (NO) before, during and after 60 min of cycle ergometry at the same absolute work rate. Concentrations of prolactin (PRL), growth hormone (GH), testosterone (T), adrenocorticotropic hormone (ACTH), cortisol (COR), adrenalin (A), noradrenalin (NA), insulin (INS), ammonia (NH3), free fatty acids, serotonin (5-HT), total protein, branched-chain amino acids (BCAA) and free tryptophan (free TRP) were determined in venous blood and lactate concentration [LA-], partial pressure of oxygen (PO2), oxygen saturation (SO2), partial pressure of carbon dioxide and pH in capillary blood. The PO2 and SO2 were augmented in HE and decreased in HO (P < or = 0.01). In HO and NO no significant changes were found for any other parameter during 30 min of rest prior to exercise. In HE, PRL increased by about 400% during this time, while NA declined (P < or = 0.01). Heart rate (HR) and [LA-] were higher during exercise in HO (P < or = 0.01). In all trials, NH3, NA, A, T, GH and ACTH increased during exercise (P < or = 0.01), while BCAA and INS declined. In comparison to NO and HE, increases of NA, A, GH, COR and ACTH were higher in HO (P < or = 0.01). The PRL in NO and COR in NO and HE did not change significantly. In HE, after the initial increase at rest, PRL declined during exercise but remained higher than in HO. Higher values for NA, A, GH, COR and ACTH in HO were likely to have reflected an augmented relative exercise intensity. Our results showed that PRL but no other hormone increased during acute exposure to hyperoxia. This PRL release was independent of exercise stress and greater than PRL augmentation during hypoxia, which was related to a higher relative exercise intensity as indicated by [LA-] and HR. Responses of plasma NH3, BCAA, free TRP and 5-HT could not explain PRL augmentation induced by the increment in blood SO2 during hyperoxia.