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.