Limitation of lower limb Vo2 during cycling exercise in COPD patients

Patients with chronic obstructive pulmonary disease (COPD) usually stop exercise before reaching physiological limits in terms of O-2 delivery and extraction. A plateau in lower limb O-2 uptake (<V)over dot>o(2),) and blood flow occurs despite progression of the imposed workload during cycling in some patients with COPD, suggesting that maximal capacity to transport O-2 had 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 COPD (forced expiratory volume in 1 s = 35 +/- 7% of predicted value). Leg blood flow was measured at each exercise step with a thermodilution catheter inserted in the femoral vein. This value was multiplied by two to account for both working legs (<(Q)over dot)(LEGS)). Arterial and femoral venous blood was sampled at each exercise step to measure blood gases. Leg O-2 consumption (<(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 expired 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) and <(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. Peak exercise work rate was higher in the eight patients without a plateau than in the six with a plateau (51 +/- 10 vs. 40 +/- 13 W, P = 0.043). <(V)over dot>T, <(V)over dot>E, and dyspnea were significantly greater at submaximal exercise in patients of the plateau group compared with those of the nonplateau 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.