In endurance-trained athletes, displaying a moderate but sustained endogenous cortisol increase: (1) ACTH responses following pituitary stimulation are not blunted, (2) cortisol responses following maximal adrenal stimulation are not blunted. Our results favour the hypothesis of a decreased pituitary sensitivity to cortisol negative feedback whereas the hypothesis of a major decreased adrenal sensitivity to ACTH was discarded. The greater ability of saliva assays to detect a cortisol increase strongly supports its use in the study of HPA physiology, whether under basal or dynamic conditions.

In normal subjects with low body fat, a strenuous exercise-and-rest lowers leptin levels by a mean of 30%. A role of lipolysis possibly via increased plasma free fatty acids and glycerol levels is suggested. Cortisol does not seem to be involved.

Objective: Muscular exercise induces hypothalamo-pituitary-adrenal (HPA) axis activation and when regularly repeated, as in endurance training, leads to HPA axis adaptation. To assess whether nonprofessional endurance-trained (ET) men with a substantial training load and no clinical or biological features of HPA axis overactivity can present subtle alterations of HPA axis sensitivity to glucocorticoid negative feedback, nine ET men were subjected to HPA axis testing using the dexamethasone±corticotrophin-releasing hormone (CRH) test. Design: Nine endurance-trained men and eight healthy age-matched sedentary men were studied. Morning plasma cortisol and 24 h urinary free cortisol (UFC) were determined and a low dose dexamethasone suppression test (LDDST) was performed followed by CRH stimulation (dexamethasone±CRH test). Results: After a day without physical exercise, at 0800 h, plasma ACTH and cortisol concentrations, and the 24 h UFC and UFC/urinary creatinine (UC) ratio were similar in ET and sedentary men. By contrast, clear differences between the groups were seen in cortisol and ACTH responses to the dexamethasone±CRH test. In eight ET subjects, after LDDST, basal ACTH and cortisol levels were similar to those of sedentary men, whereas one ET subject displayed a poor suppression of cortisol level (131 nmol/l). After injection of CRH, however, three of nine ET men's cortisol levels were not suppressed by dexamethasone but instead displayed significant CRH-induced increase (peak cortisol: 88, 125 and 362 nmol/l). No sedentary subject exhibited any increase in cortisol levels. Conclusion: Three of nine ET men with a mean maximum rate of O 2 uptake (V O2, max ) of 61 ml/kg per min, running 50±70 km per week, were resistant to glucocorticoid suppression during the combined dexamethasone±CRH test.

In men, the hypothalamic-pituitary-testicular axis controls the secretion of testosterone which, in this sex, is a major anabolic hormone. Physical exercise modulates testosterone concentration, affecting the whole axis by poorly understood mechanisms. We have reported in this preliminary study the short and long-term effects of exercise on the function of the gonadotropic axis in trained compared to untrained subjects. Environmental factors known to interfere with pituitary function were minimized. Four marathon and four sedentary men, were studied during 5 days successively using different combinations of two factors: duration and intensity of running tests. Day 0 (D0) was a rest day, and the exercises were: D1 and D2 brief (20 min), light (50% maximal heart rate, HRmax, D1) or intense (80% HRmax, D2), D3 and D4 prolonged (120 min) and light (50% HRmax, D3) or intense (80% HRmax, D4). Testosterone (free and total) and luteinizing hormone (LH) concentrations were measured before, during and after exercise. The baseline concentrations of plasma testosterone were lower in the long distance runners than in the sedentary group [41.8 (SEM 5.5) vs 64.5 (SEM 7.9) pmol.l-1, respectively; P < 0.05]. This phenomenon was centrally mediated as LH concentration was apparently inappropriately low [3.4 (SEM 0.4) vs 4.3 (SEM 1.0) UI.l-1; P > 0.05]. Light to moderate exercise did not modify testosterone and LH concentrations. Conversely, intense and prolonged exercise increased testosterone concentration [73.2 (SEM 9.0) vs 92 (SEM 11.0) pmol.l-1 in the long distance runners and sedentary group, respectively; P < 0.05] and lowered LH concentrations [2.1 (SEM 0.3) vs 3.4 (SEM 0.3) UI.l-1 in the long distance runners and sedentary group, respectively; P < 0.05 compared to D0, at the same time]. In our conditions of exercise, negative feedback of testosterone upon LH persisted, as positive feedback of low testosterone concentrations was apparently lacking (inappropriately low LH concentration with regard to low basal testosterone concentration).