The pathophysiologic mechanism for exertional dyspnea, the main symptom of patients with heart failure, has not been fully clarified. To determine the relationship between exercise hyperpnea and the lactic acidosis in patients with heart failure, we evaluated ventilation during incremental exercise both below and above the lactic acidosis threshold in 16 normal subjects and in 48 patients with cardiovascular disease while expired gas was analyzed continuously. The peak oxygen uptake and oxygen uptake at the lactic acidosis threshold decreased significantly as the New York Heart Association (NYHA) functional class severity increased. the slope of the increase in ventilation to the increase in oxygen uptake (delta VE/delta VO2) at work rates below the lactic acidosis threshold did not differ between normal subjects and patients with heart failure. Above the lactic acidosis threshold, however, the slope of delta VE/delta VO2, which was higher than that below the lactic acidosis threshold in each of four groups, was steeper in patients in NYHA Class II (60.8 +/- 17.9) and Class III (66.5 +/- 21.2) when compared with that in the normal subjects (46.6 +/- 13.5) or the patients in NYHA Class I (46.1 +/- 10.3). The lactic acidosis caused by decreased oxygen transport to working muscles accounts for the higher ventilation during exercise in cardiac patients. These data suggest that the increased ventilation during exercise, which must be related to exertional dyspnea, in patients with cardiovascular disease is primarily the consequence of a stimulus to regulate arterial pH.