Effect of sleep apnea syndrome on the circadian profile of cortisol in obese men

It has been hypothesized that sleep apnea syndrome (SAS) increases hypothalamicpituitary-adrenal axis activity and, through increased cortisol levels, participates in the pathophysiology of metabolic and cardiovascular complications. We compared the circadian profiles of cortisol in obese men with [obSAS+; apnea-hypopnea index (AHI) [greater than or equal to] 20/h] and without SAS (obSAS-; AHI [less than or equal to] 5/h). 1) Salivary cortisol (5 samples: before/30 min after dinner, 2100, upon/30 rain after awakening) was measured in 15 obSAS+, 19 obSAS-, and 19 normal-weight controls (NWC). 2) Plasma cortisol (every 30 rain for 24 h under highly controlled conditions and portable EEG device) was measured in 9 obSAS+, 8 obSAS-, and 10 NWC men. Visceral adipose tissue surface was measured by CT scan. In both studies, obSAS+ and obSAS- men were comparable for age, BMI, waist circumference, and waist-to-hip ratio. First, no difference was found, using ANOVA for repeated measures, between obSAS+ and obSAS- subjects for any salivary cortisol measurement. No correlation was found between salivary cortisol and AHI or nocturnal Sa[O.sub.2]. Similarly, obSAS+ and obSAS- men showed no difference in plasma cortisol rhythmicity: 24-h minimum, maximum, and mean, ANOVA for repeated measures, mathematical modeling of cortisol rhythm (COSINOR), and morning secretory peak. Conversely, ANOVA for repeated measures showed decreased cortisol levels in obese vs. NWC men during both the trough (2200-0130) and the peak (0600-0900) independently of SAS status. We show that SAS per se is not associated with any change of the level or of the features of salivary and plasma cortisol rhythmicity and confirm that men with visceral obesity display lower plasma cortisol levels than NWC men. cortisol; circadian rhythm; obesity; sleep-disordered breathing