Submitted on December 21, 2007
Accepted on March 13, 2008
Kinetics of Muscle Deoxygenation are Accelerated at the Onset of Heavy Intensity Exercise in Patients with COPD: Relationship to Central Cardiovascular Dynamics
Gaspar R. Chiappa1, Audrey Borghi-Silva2, Leonardo F. Ferreira3, Claudia Carrascosa4, Cristino Carneiro Oliveira4, Joyce Maia4, Ana Cristina Gimenes5, Fernando Queiroga4, Danilo Berton4, Eloara MV Ferreira4, Luis Eduardo Nery4, and J. Alberto Neder4*
1 Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo, Sao Paulo; Cardiology Division, Hospital de Clinica de Porto Alegre, Sao Paulo, Sao Paulo, Brazil
2 Physiotherapy, Federal University of Sao Carlos, Sao Paulo, Brazil
3 Physiology, University of kentucky, Lexington, Kentucky, United States
4 Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo, Sao Paulo, SP, Brazil
5 Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo,, Sao Paulo, Brazil
* To whom correspondence should be addressed. E-mail: albneder{at}pneumo.epm.br.
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 oxygenation 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 (Tlim) by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. The Tlim was significantly (P < 0.05) lower in patients and related to the kinetics of VO2p (r = -0.70; P < 0.05). Compared to controls, COPD patients displayed slower kinetics of VO2p (in s; 42 ± 13 vs. 73 ± 24) and QT (in s; 67 ± 11 vs. 96 ± 32), and faster overall kinetics of muscle deoxy-Hb (in s; 19.9 ± 2.4 vs. 16.5 ± 3.4). Consequently, 
VO2p/MRT-[deoxy-Hb] was significantly greater in patients, suggesting a slower kinetics of microvascular O2 delivery. In conclusion, our data shows 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 slowing of VO2p kinetics compared to age-matched controls.
