Exercise-induced skeletal muscle deoxygenation in O2-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 [FEV 1 : 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.