Sleep hypoventilation is common in hypercapnic COPD and may contribute to daytime hypercapnia. The contributions of respiratory drive and respiratory mechanics to alterations in minute ventilation (VI) in sleep in this group have not been assessed. We assessed VI, breathing pattern, upper airway and total respiratory resistance (UAR, RRS) intra-oesohageal diaphragmatic EMG (EMGoes), intrinsic PEEP (PEEPi), dynamic compliance (Cdyn), pressure-time product of oesophageal pressure (PTPoes), Tension-Time Index of the diaphragm (TTIdi), end-expiratory lung volume (EELV) and respiratory drive (assessed as the slope of Poes vs time in the isovolumetric interval before PEEPi is overcome). Meausurements were made in wakefulness and NREM sleep on 76% N₂/ 24% O₂ and on 76% He/ 24% O₂ (heliox). Satisfactory data for analysis were obtained in 10 patients. 5 had measurements on heliox. VI fell (mean (SEM)) (8.84(0.46) to 6.64(0.91) l min^-1, p=0.011) between wake and Stage II sleep, due to a fall in tidal volume. No changes were seen in PEEPi, Cdyn, EELV, PTPoes, TTIdi, EMGoes or respiratory drive. UAR increased (3.11(0.8) to 10.24(2.96) cmH₂O l^-1 sec (p=0.013) but RRS was unchanged. UAR was reduced on heliox (5.20(1.67) to 3.45(1.35) cmH₂O l^-1 sec, p=0.049) but VI during sleep did not increase. PTPoes (350.2(51.0) to 259.4(46.3) cmH₂O sec min^-1, p=0.016), TTIdi (0.13(0.02) to 0.10(0.02) p=0.04), and respiratory drive (20.48(4.69) to 15.02(4.57) cmH₂O sec^-1, p=0.01) were all reduced. This suggests respiratory drive alters to maintain a preset VI in sleep, irrespective of load, at least while the fatigue threshold of respiratory muscles is not exceeded.