In this study, the relationship between the arterial lactate concentration and VO2 during exercise was obtained in a large group of COPD patients with a wide range of functional status and compared with that of normal subjects of similar age. We found that the increase in lactate was abnormally high in the majority (70%) of COPD patients, despite evidence of limitations in ventilation and gas exchange during exercise. In addition, the deterioration in functional status was accompanied by a progressively steeper slope of the La/ VO2 relationship. This may reflect gradual worsening in skeletal muscle oxidative capacity as the functional status and, presumably, the level of daily activity decreased.
The increase in blood lactate concentration during exercise depends on the balance between lactate production and degradation. Although lack of oxygen is not a prerequisite for lactic acid production , modifying oxygen delivery to the working muscles influences the increase in blood lactate during exercise. Decreasing the oxygen supply by exposing subjects to a hypoxic environment will increase blood lactic acid level . By contrast, increasing oxygen supply by improving cardiac output during exercise will reduce blood lactic acid level . Skeletal muscle metabolic activity also markedly influences lactate production . It is now suggested that lactate production reflects a balance between glycogen phosphorylase activation and the activity of pyruvate dehydrogenase and oxidative enzymes .