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
Main Authors: Chiappa, Gaspar R, Borghi-Silva, Audrey, Ferreira, Leonardo F, Carrascosa, Claudia, Oliveira, Cristino Carneiro, Maia, Joyce, Gimenes, Ana Cristina, Queiroga, Fernando, Jr, Berton, Danilo, Ferreira, Eloara M. V, Nery, Luis Eduardo, Neder, J. Alberto
Format: Journal Article
Language:English
Published: Bethesda, MD Am Physiological Soc 01-05-2008
American Physiological Society
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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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ISSN:8750-7587
1522-1601
DOI:10.1152/japplphysiol.01364.2007