However, the prevalence of this phenomenon is difficult to evaluate, and it is commonly believed that, because of ventilatory limitation, the vast majority of patients with COPD are unable to exercise sufficiently to activate their skeletal muscles and, thereby, produce a significant amount of lactic acid . Even if the peak lactate concentration achieved during exercise is lower in COPD than in normal subjects, abnormal lactate kinetics may be important. Increased lactic acidosis for a given exercise work rate places particular stress on the respiratory system. By numerous mechanisms, it results in a greater nonaerobic carbon dioxide production , enhancing the ventilatory needs while the acidemia may act directly as a breathing stimulus. Abnormal lactate kinetics in patients with COPD might also indicate that the peripheral muscle energy metabolism during exercise is altered in these individuals, with early activation of anaerobic glycolysis .
This study sought to examine whether lactate kinetics during exercise are commonly abnormal in patients with COPD and to evaluate the possible relationship of lactate kinetics with functional status. Serial arterial lactate concentration measurements were obtained during exercise in 54 COPD patients of varying functional status and in 10 age-matched normal subjects.