Context: Previous studies on the association between the hypothalamic-pituitary-adrenal (HPA) axis activity and sleep apnea (SA) and obesity are inconsistent and/or limited.

Objective: In this study, we evaluated the activity of the HPA axis in non-psychologically distressed obese subjects with and without SA and examined the impact of continuous positive airway pressure (CPAP) in SA patients.

Design-Participants: In Study I, 4-night sleep laboratory recordings and serial 24h plasma measures of cortisol were obtained in 45 obese men with and without apnea and non-obese controls. Sleep apneic patients were re-assessed after 3 months of CPAP use. In Study II, 38 obese men with and without sleep apnea and non-obese controls were challenged with ovine CRH administration after 4 nights in the sleep laboratory.

Results: The sleep patterns were similar between obese and non-obese controls. Twenty-four hour plasma cortisol levels were highest in non-obese controls, intermediate in obese apneic patients, and lowest in obese controls (8.8 ± 0.4 vs. 8.1 ± 0.3 vs. 7.5 ± 0.3 µg/dl, P <0.05). CPAP tended to reduce cortisol levels in the apneic patients (diff: -0.7 ± .4 µg/dl, P = 0.1). CRH administration resulted in a higher ACTH response in both obese groups compared to non-obese controls; the three groups were not different in cortisol response.

Conclusions: Non-psychologically distressed, normally-sleeping, obese men had low cortisol secretion. The cortisol secretion was slightly activated by SA and returned to low by CPAP use. The low cortisol secretion in obesity through its inferred hyposecretion of hypothalamic CRH might predispose the obese to sleep apnea.