The objective of the study was investigate the pulmonary gas exchange response to exercise in 16 male patients with chronic heart failure (CHF) due to previous myocardial infarction and left ventricular dysfunction (ejection fraction < 45%). All patients underwent a symptom-limited exercise test during which cardiac frequency (fC), tidal volume (VT), respiratory frequency (fR), minute ventilation (V'E), oxygen consumption (V'O2) and carbon dioxide production (V'CO2) were measured on a breath-by-breath basis. Ventilatory equivalent for carbon dioxide (V'E/V'CO2) and lactate threshold (LT) were calculated. Arterial blood gas levels were measured at rest and at peak exercise. The dead space (VD) to tidal volume ratio (VD/VT) and alveolar-arterial oxygen gradient (PA-a,O2) were computed. Two subgroups of patients were identified according to peak V'O2 (V'O2,peak), group A (n = 7), V'O2,peak > 14 mL.kg-1.min-1 (17.2 +/- 2.5 SEM, range 14.5-20.8), and group B (n = 9), V'O2,peak < 14 mL.kg-1.min-1 (11.9 +/- 1.8, range 9.2-13.6). Arterial oxygen tension (Pa,O2) increased from rest to peak exercise in both groups (group A: 12.2 +/- 0.94 to 13.4 +/- 0.82 kPa (91.4 +/- 7.1 to 100.4 +/- 6.2 mmHg), p < 0.05; group B: 11.7 +/- 1.0 to 13.4 +/- 1.1 kPa (88.0 +/- 7.8 to 100.9 +/- 8.2 mmHg), p < 0.01), while a significant reduction in arterial carbon dioxide tension (Pa,CO2), from rest to peak exercise, was observed in group B only (4.64 +/- 0.39 to 4.08 +/- 0.36 kPa (34.9 +/- 2.8 to 30.7 +/- 2.7 mmHg), p < 0.005). Maximal V'E and maximal power (Powermax) were significantly lower in group B compared to group A (V'E 37.6 +/- 8.4 versus 52.1 +/- 13.8 L.min-1, p < 0.05; Powermax 64.4 +/- 12 versus 82.8 +/- 14.1 W, p < 0.01). fC was not significantly different at peak exercise, although the work load was significantly higher in group A. VD/VT failed to decrease significantly at maximal exercise in both groups. In group B, V'E/V'CO2 tended to be higher than in group A. In chronic heart failure patients, measurements of arterial blood gas levels during exercise might help to identify those subjects with a more pronounced depression of left ventricular function. At peak exercise, high ventilatory demand and respiratory alkalosis were observed in group B patients, suggesting an increased responsiveness of the respiratory centre that might be one major factor contributing to this excessive ventilatory response to exercise; vice versa, a combination of ventilation-perfusion mismatch, wasted ventilation and unpaired peripheral blood circulation seem to play only a minor role.