Patients with chronic obstructive pulmonary disease (COPD) usually stop exe
rcise before reaching physiological limits in terms of O-2 delivery and ext
raction. A plateau in lower limb O-2 uptake (<V)over dot>o(2),) and blood f
low occurs despite progression of the imposed workload during cycling in so
me patients with COPD, suggesting that maximal capacity to transport O-2 ha
d been reached and that it had been extracted in the peripheral exercising
muscles. This study addresses this observation. Symptom-limited incremental
cycle exercise was performed by 14 men [62 +/- 11 (SD) yr] with severe COP
D (forced expiratory volume in 1 s = 35 +/- 7% of predicted value). Leg blo
od flow was measured at each exercise step with a thermodilution catheter i
nserted in the femoral vein. This value was multiplied by two to account fo
r both working legs (<(Q)over dot)(LEGS)). Arterial and femoral venous bloo
d was sampled at each exercise step to measure blood gases. Leg O-2 consump
tion (<(V)over dot>(2LEGS)) was calculated according to the Fick equation.
Total body <(V)over dot>o(2) (<(V)over dot>o(2TOT)) was measured from expir
ed gas analysis, and tidal volume (<(V)over dot>T) and minute ventilation (
<(V)over dot>E) were derived from the flow signal. In eight patients, work
rate was increasing. In six subjects, a plateau in <(V)over dot>o(2LEGS) an
d <(Q)over dot>(LEGS) occurred during exercise (increment of <3% between 2
consecutive increasing workloads) despite the increase in workload and <(V)
over dot>o(2TOT) [corresponding mean was 110 +/- 38 ml (11 +/- 4%)]. These
six patients also exhibited a plateau in O-2 extraction during exercise. Pe
ak exercise work rate was higher in the eight patients without a plateau th
an in the six with a plateau (51 +/- 10 vs. 40 +/- 13 W, P = 0.043). <(V)ov
er dot>T, <(V)over dot>E, and dyspnea were significantly greater at submaxi
mal exercise in patients of the plateau group compared with those of the no
nplateau group. These results show that, in some patients with COPD, blood
flow directed to peripheral muscles and O-2 extraction during exercise may
be limited. We speculate that redistribution of cardiac output and O-2 from
the lower limb exercising muscles to the ventilatory muscles is a possible
mechanism.