The ability of the 13C aminopyrine breath test (APBT) to reflect hepatocellular metabolic capacity and therefore to predict lactate removal following incremental exercise in male COPD patients was evaluated. Two previous patients with COPD who had histories of heavy alcohol intake but no overt liver disease showed prolonged lactate elevation following exercise. The possibility of subclinical hepatic disease affecting lactate removal was considered. No patient in the present study had clinical evidence of liver disease. Four of 9 patients had an abnormal APBT (mean 5.0% cumulative dose 13CO2 excreted over 2 h). Patients with a normal APBT (group 1) and with an abnormal APBT (group 2) were compared. The groups did not differ in age or severity of lung disease. An incremental exercise test was performed and lactate samples were collected before, during, and for 90 min following exercise. Exercise parameters (work rate, duration, VO2max, VEmax, and peak lactate) did not differ between groups. Comparing group 1 with group 2 mean values, the time to recover to resting lactate values (Trecov 45 vs 76 min, respectively, p less than 0.005) and the time required for lactate level to return to the normal range (Tnorm 35 vs 65 min, respectively, p less than 0.005) were statistically different. Furthermore, the 2-h excretion of 13CO2 was inversely correlated with both Trecov (r = -0.76, p less than 0.05) and Tnorm (r = -0.79, p less than 0.05). We conclude that subclinical derangement of hepatocellular capacity, as determined by APBT, may adversely affect lactate removal following exercise.