Some obese patients with sleep-related breathing disorders develop sleep hypoventilation, others do not. We tried to differentiate between peripheral (obstructive and restrictive) and central (respiratory drives) causes of hypercapnia and examined the lung function, blood gases, sleep-related breathing and hypercapnic ventilatory responses (HCVR) in 23 obese patients (22 men, 41–64 yr, body mass index 38.15.9 kg/m2). Patients with a PCO2 above 45 Torr during NREM-sleep (n=13) significantly differed from those with lower PCO2 in the HCVR (1.160.70 vs. 2.792.05 L/min/Torr, p<0.04), the total airway resistance Rt (0.370.15 vs. 0.230.09 kPa/l/s, p<0.02), and the forced vital capacity (91.312.8 vs. 110.930.0%, p<0.05), whereas the differences in the hypercapnic P0.1 response (11.8 vs. 28.2 Pa/Torr, p>0.11) and the apnea-hypopnea index (58.0 vs. 41.2 h-1, p>0.15) did not reach the level of significance. We conclude that both, central and peripheral factors contribute to the etiology of sleep-related hypoventilation in obese patients.