If chronic hypercapnia in patients with severe COPD occurs as a consequence of respiratory muscle (RM) weakness or fatigue, we would expect that ventilatory muscle recruitment (VMR) and exercise performance in stable hypercapnic patients would differ from those in eucapnic patients. We evaluated exercise performance and RM function at rest and during exercise in 19 eucapnic (PCO2 40 +/- 3 mm Hg), and 13 hypercapnic (PCO2 52 +/- 10 mm Hg) patients with severe COPD. A metabolic cart was used to determine (V) over dot (E), (V) over dot O-2, (V) over dot CO2, and HR. Gastric (Pg) and esophageal (Ppl) balloons were used to measure Pg, Ppl, and Pdi, Ventilatory muscle recruitment pattern (VMR) was partitioned using end-inspiratory and end-expiratory Pg and Ppl, Hypercapnic patients had lower FEV1 (0.60 +/- 0.24 versus 0.95 +/- 0.31 L, p < 0.001), MVV (28 +/- 11 versus 41 +/- 13 L, p < 0.001), resting PO2 (61 +/- 11 Versus 70 +/- 11 mm Hg, p < 0.001), peak PO2 (60 +/- 20 versus 75 +/- 22 mm Hg, p < 0.005), and (V) over dot (max) (24 +/- 10 versus 32 +/- 12 L/min, p < 0.001). Patients in both groups had similar FRC (5.7 +/- 1.6 versus 5.0 +/- 1.5 L), (V) over dot O-2max (0.58 +/- 0.30 versus 0.76 +/- 0.32 L/min), Watts (45 +/- 48 versus 71 +/- 59), (V) over dot (E)/MVV (88 +/- 33 versus 79 +/- 14), and HRmax (117 +/- 17 versus 128 +/- 18 beats/min). Pi(max) (67 +/- 28 versus 65 +/- 32 cm H2O) and PEmax (98 +/- 34 versus 96 +/- 40 cm H2O) were also similar in both groups. VMR (Delta Pg/Delta Ppl) at: rest (-0.28 +/- 0.51 versus 0 +/- 0.35) and during exercise (0.4 +/- 0.2 versus 0.39 +/- 0.15) was equally affected In both groups. We conclude that exercise capacity and ventilatory muscle recruitment are similarly impaired in eucapnic and hypercapnic patients with severe COPD. these findings make inability of the lung to increase ventilation and not respiratory muscle dysfunction a more attractive explanation for CO2 retention in stable hypercapnic patients.