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J Appl Physiol 104: 1341-1350, 2008. First published March 20, 2008; doi:10.1152/japplphysiol.01364.2007
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Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics

Gaspar R. Chiappa,1 Audrey Borghi-Silva,1,2 Leonardo F. Ferreira,1,3 Claúdia Carrascosa,1 Cristino Carneiro Oliveira,1 Joyce Maia,1 Ana Cristina Gimenes,1 Fernando Queiroga, Jr,1 Danilo Berton,1 Eloara M. V. Ferreira,1 Luis Eduardo Nery,1 and J. Alberto Neder1

1Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo, São Paulo; and 2Cardiopulmonary Laboratory, Nucleus of Research in Physical Exercise, Federal University of São Carlos, São Carlos, Brazil; and 3Department 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 O2 uptake (VO2p) kinetics during exercise, which may stem from inadequate muscle O2 delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O2 delivery to uptake during exercise. We tested the hypothesis that, along with slowed VO2p kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (QT) following the onset of heavy-intensity exercise. We measured VO2p, QT (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 VO2p (r = –0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of VO2p (42 ± 13 vs. 73 ± 24 s) and QT (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 O2 uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O2 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 O2 delivery and utilization and may contribute to the slower VO2p 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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