Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O-2 uptake (VO2p) 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 VO2p kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Q(T)) following the onset of heavy-intensity exercise. We measured VO2p, Q(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 VO2p (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of VO2p (42 +/- 13 vs. 73 +/- 24 s) and Q. 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 VO2p kinetics compared with age-matched controls.