Obstructive sleep apnoea (OSA) is a relatively common condition producing disabling somnolence and profound physiological responses to hypoxaemic episodes during sleep. Sleep apnea was found to be two to three times more prevalent in middle-aged men than in women. Obesity is a major risk factor for OSA. Metabolic and hormonal changes associated with obesity could increase airway collapsibility via several mechanisms.  Mild to moderate weight loss can substantially improve sleep apnea. We investigated the interaction between OSA and endocrine axes by determing the nocturnal serum levels of LH, testosterone, GH, leptin and cortisol with simultaneous sleep recordings in middle-aged obese men with obstructive sleep apnea and in healthy controls of similar body weight and age. Hormone measurements were conducted at base line and following nine months of nasal continuous positive airway pressure (nCPAP treatment). OSA patients had significantly lower LH and testosterone secreted at night compared with controls, independent of age and degree of obesity. Patients had also suppressed GH secretion at night and increased leptin levels, which were positively correlated with BMI but not with severity of OSA. Although patients and controls had similar amounts of cortisol secreted during sleep, the nocturnal cortisol rise was delayed in OSA. Cortisol onset time and onset level were negatively correlated with deep sleep.

After nine months of nCPAP treatment parameters of OSA severity were normalized, BMI, leptin and LH values remained unchanged whereas testosterone and GH concentrations increased, yet to subnormal values. Cortisol onset during nCPAP treatment was partially corrected during nCPAP treatment.

We conclude that obese middle-aged men with OSA have hyperleptinemia, decreased androgen and GH secretion, delayed cortisol onset during sleep and leptin resistance. These changes in hormones secretion are partially corrected during chronic nCPAP treatment. Our findings support the hypothesis that obstructive sleep apnea is a manifestation of the metabolic syndrome, syndrome X, promoting atherosclerosis and cardiovascular disease in patients with OSA.