Exercise-induced skeletal muscle deoxygenation in O-2-supplemented COPD patients

This study was designed to assess quadriceps oxygenation during symptom-limited and constant-load exercise in patients with chronic obstructive pulmonary disease (COPD) and healthy age-matched controls. Thirteen male COPD patients [FEV1: 43 +/- 5% predicted (mean +/- SEM)] and seven healthy male controls performed an incremental exercise test at peak work rate (WR) and a constant-load test at 75% peak WR on a cycle ergometer. Quadriceps hemoglobin saturation (StO(2)) was measured by continuous-wave near-infrared spectrophotometry throughout both exercise tests. StO(2) is the ratio of oxygenated hemoglobin to total hemoglobin and reflects the relative contributions of tissue O-2 delivery and tissue O-2 utilization. Oxygen was supplemented to all patients in order to maintain arterial O-2 saturation normal (> 95%). The StO(2) decreased during symptom-limited exercise, reaching the nadir at peak WR. The decrease in StO(2) was greater (P < 0.05) in healthy subjects (from 74 +/- 2% to 38 +/- 6%) compared with that in COPD patients (from 61 +/- 5% to 45 +/- 4%). However, when StO(2) was normalized relative to the WR, the slope of change in StO(2) during exercise was nearly identical between COPD patients and healthy subjects (0.47 +/- 0.10%/W and 0.51 +/- 0.04%/W, respectively). During constant-load exercise, the kinetic time constant of StO(2) desaturation after the onset of exercise (i.e., equivalent to time to reach approximately 63% of StO(2) decrease) was not different between COPD patients and healthy subjects (19.0 +/- 5.2 and 15.6 +/- 2.5 s, respectively). In O-2-supplemented COPD patients, peripheral muscle oxygenation for a given work load is similar to that in healthy subjects, thus suggesting that skeletal muscle O-2 consumption becomes normal for a given O-2 delivery in COPD patients.