• I Vogiatzis, D Athanasopoulos, G Stratakos, C Garagouni, A Koutsoukou, R Boushel, C Roussos, and S Zakynthinos.
• "G. P. Livanos and M. Simou Laboratories", Evangelismos Hospital, Department of Critical Care Medicine and Pulmonary Services, National and Kapodistrian University of Athens, Athens, Greece. gianvog@phed.uoa.gr
• Scand J Med Sci Sports. 2009 Jun 1;19(3):364-72.

AbstractThis 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 (StO2) was measured by continuous-wave near-infrared spectrophotometry throughout both exercise tests. StO2 is the ratio of oxygenated hemoglobin to total hemoglobin and reflects the relative contributions of tissue O2 delivery and tissue O2 utilization. Oxygen was supplemented to all patients in order to maintain arterial O2 saturation normal (> 95%). The StO2 decreased during symptom-limited exercise, reaching the nadir at peak WR. The decrease in StO2 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 StO2 was normalized relative to the WR, the slope of change in StO2 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 StO2 desaturation after the onset of exercise (i.e., equivalent to time to reach approximately 63% of StO2 decrease) was not different between COPD patients and healthy subjects (19.0 +/- 5.2 and 15.6 +/- 2.5 s, respectively). In O2-supplemented COPD patients, peripheral muscle oxygenation for a given work load is similar to that in healthy subjects, thus suggesting that skeletal muscle O2 consumption becomes normal for a given O2 delivery in COPD patients

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