It has been argued that the lactate threshold (LT) serves as an index to reflect circulatory insufficiency in transporting oxygen during submaximal exercise in patients with chronic heart failure (CHF). We examined whether or not the LT was related to an insufficient oxygen supply in patients with CHF. Sixty-nine patients were divided by NYHA classification. All underwent invasive cardiopulmonary exercise testing. The rate of increase in oxygen delivery (O2D) versus VO2 (delta O2D/delta VO2) was significantly lowered when work rate exceeded LT, that is, 1.32 +/- 0.35 to 1.05 +/- 0.37 (p < 0.01), 1.22 +/- 0.40 to 0.98 +/- 0.40 (p < 0.05), and 1.04 +/- 0.26 to 0.78 +/- 0.39 (p < 0.05) in NYHA classes I, II, and III, respectively. However, the rate of increase in leg O2D versus leg VO2 (delta LO2D/delta LVO2) did not change, that is, 1.25 +/- 0.20 to 1.29 +/- 0.20 (NS), 1.27 +/- 0.23 to 1.21 +/- 0.28 (NS), and 1.19 +/- 0.24 to 1.15 +/- 0.17 (NS) in classes I, II, and III, respectively. Leg venous PO2 was significantly different among three groups, that is, 23.7 +/- 3.4 mmHg, 23.2 +/- 2.8 mmHg, and 20.1 +/- 2.3 mmHg (p < 0.001), respectively. Thus, the oxygen supply to the working muscle did not become insufficient when work rate exceeded LT, and the LT occurred at different levels of leg PO2. It was concluded that the LT was not a result of anaerobiosis in patients with CHF.