Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics
1 Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo, São Paulo; and 2 Cardiopulmonary Laboratory, Nucleus of Research in Physical Exercise, Federal University of São Carlos, São Carlos, Brazil; and 3 De...
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Published in: | Journal of applied physiology (1985) Vol. 104; no. 5; pp. 1341 - 1350 |
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Main Authors: | , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Bethesda, MD
Am Physiological Soc
01-05-2008
American Physiological Society |
Subjects: | |
Online Access: | Get full text |
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Summary: | 1 Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo, São Paulo; and 2 Cardiopulmonary Laboratory, Nucleus of Research in Physical Exercise, Federal University of São Carlos, São Carlos, Brazil; and 3 Department of Physiology, University of Kentucky, Lexington, Kentucky
Submitted 21 December 2007
; accepted in final form 13 March 2008
Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O 2 uptake ( O 2 p ) kinetics during exercise, which may stem from inadequate muscle O 2 delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O 2 delivery to uptake during exercise. We tested the hypothesis that, along with slowed O 2 p kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output ( T ) following the onset of heavy-intensity exercise. We measured O 2 p , T (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly ( P < 0.05) lower in patients and related to the kinetics of O 2 p ( r = –0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of O 2 p (42 ± 13 vs. 73 ± 24 s) and T (67 ± 11 vs. 96 ± 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 ± 2.4 vs. 16.5 ± 3.4 s). Consequently, the time constant ratio of O 2 uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O 2 delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O 2 delivery and utilization and may contribute to the slower O 2 p kinetics compared with age-matched controls.
blood flow; chronic obstructive pulmonary disease; hemodynamics; near-infrared spectroscopy; oxygen consumption; kinetics
Address for reprint requests and other correspondence: J. A. Neder, Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Respiratory Division, Dept. of Medicine, Federal Univ. of São Paulo - Paulista School of Medicine (UNIFESP-EPM), Rua Professor Francisco de Castro 54, Vila Clementino, CEP: 04020-050, São Paulo, Brazil (e-mail: albneder{at}pneumo.epm.br ) |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/japplphysiol.01364.2007 |