CONTRIBUTION OF THE RESPIRATORY MUSCLES TO THE LACTIC-ACIDOSIS OF HEAVY EXERCISE IN COPD

Patients with COPD usually are limited in their exercise tolerance by a limited ventilatory capacity, Lactic acidosis induced by exercise in creases the stress on the ventilatory system due to CO2 generated by b icarbonate buffering and hydrogen ion stimulation. Patients with COPD are often observed to increase blood lactate levels at low levels of e xercise. We wished to determine whether patients with COPD who experie nce lactic acidosis do so because of respiratory muscle production of lactate. Eight patients with moderate to severe COPD (FEV(1)=43.5+/-11 .6% predicted) and 5 healthy subjects performed 10 min of moderate con stant work rate exercise either breathing spontaneously or volitionall y increasing their ventilation for 5 min to approximate the peak minut e ventilation seen during incremental exercise, During volitional incr eased ventilation, 3% CO2 was added to the inspirate to prevent alkalo sis and hypocapnia. In neither the healthy subjects nor the COPD group was the end-exercise lactate level significantly higher during voliti onal ventilation increase than during spontaneous ventilation. Further , in the COPD patients, the blood lactate levels during volitional ven tilation increase were much lower than during maximal exercise (averag ing 2.4 vs 5.3 mmol/L) despite similar ventilation levels (averaging 5 0 and 53 L/min). We conclude that it is unlikely that the respiratory muscles have an important influence on the blood lactate level elevati on seen during maximal exercise in COPD patients.