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

I. Vogiatzis, D. Athanasopoulos, G. Stratakos, C. Garagouni, A. Koutsoukou, R. Boushel, C. Roussos, S. Zakynthinos

Research output: Contribution to journalArticle

Abstract

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.
Original languageEnglish
Pages (from-to)364-372
Number of pages9
JournalScandinavian Journal of Medicine & Science in Sports
Volume19
Issue number3
DOIs
Publication statusPublished - 19 May 2009
Externally publishedYes

Keywords

  • COPD
  • Exercise
  • Tissue oxygenation
  • NIRS

Cite this

Vogiatzis, I., Athanasopoulos, D., Stratakos, G., Garagouni, C., Koutsoukou, A., Boushel, R., ... Zakynthinos, S. (2009). Exercise-induced skeletal muscle deoxygenation in O-2-supplemented COPD patients. Scandinavian Journal of Medicine & Science in Sports, 19(3), 364-372. https://doi.org/10.1111/j.1600-0838.2008.00808.x
Vogiatzis, I. ; Athanasopoulos, D. ; Stratakos, G. ; Garagouni, C. ; Koutsoukou, A. ; Boushel, R. ; Roussos, C. ; Zakynthinos, S. / Exercise-induced skeletal muscle deoxygenation in O-2-supplemented COPD patients. In: Scandinavian Journal of Medicine & Science in Sports. 2009 ; Vol. 19, No. 3. pp. 364-372.
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Vogiatzis, I, Athanasopoulos, D, Stratakos, G, Garagouni, C, Koutsoukou, A, Boushel, R, Roussos, C & Zakynthinos, S 2009, 'Exercise-induced skeletal muscle deoxygenation in O-2-supplemented COPD patients', Scandinavian Journal of Medicine & Science in Sports, vol. 19, no. 3, pp. 364-372. https://doi.org/10.1111/j.1600-0838.2008.00808.x

Exercise-induced skeletal muscle deoxygenation in O-2-supplemented COPD patients. / Vogiatzis, I.; Athanasopoulos, D.; Stratakos, G.; Garagouni, C.; Koutsoukou, A.; Boushel, R.; Roussos, C.; Zakynthinos, S.

In: Scandinavian Journal of Medicine & Science in Sports, Vol. 19, No. 3, 19.05.2009, p. 364-372.

Research output: Contribution to journalArticle

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T1 - Exercise-induced skeletal muscle deoxygenation in O-2-supplemented COPD patients

AU - Vogiatzis, I.

AU - Athanasopoulos, D.

AU - Stratakos, G.

AU - Garagouni, C.

AU - Koutsoukou, A.

AU - Boushel, R.

AU - Roussos, C.

AU - Zakynthinos, S.

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N2 - 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.

AB - 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.

KW - COPD

KW - Exercise

KW - Tissue oxygenation

KW - NIRS

U2 - 10.1111/j.1600-0838.2008.00808.x

DO - 10.1111/j.1600-0838.2008.00808.x

M3 - Article

VL - 19

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JO - Scandinavian Journal of Medicine & Science in Sports

JF - Scandinavian Journal of Medicine & Science in Sports

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