Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O2 uptake (V̇o2p) 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 V̇o2p kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Q̇t) following the onset of heavy-intensity exercise. We measured V̇o2p, Q̇t (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 V̇o2p ( r = −0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of V̇o2p (42 ± 13 vs. 73 ± 24 s) and Q̇t (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 V̇o2p kinetics compared with age-matched controls.

Background: Respiratory muscle unloading during exercise could improve locomotor muscle oxygenation by increasing oxygen delivery (higher cardiac output and/or arterial oxygen content) in patients with chronic obstructive pulmonary disease (COPD). Methods: Sixteen non-hypoxaemic men (forced expiratory volume in 1 s 42.2 (13.9)% predicted) undertook, on different days, two constant work rate (70-80% peak) exercise tests receiving proportional assisted ventilation (PAV) or sham ventilation. Relative changes (D%) in deoxyhaemoglobin (HHb), oxyhaemoglobin (O 2 Hb), tissue oxygenation index (TOI) and total haemoglobin (Hb tot ) in the vastus lateralis muscle were measured by nearinfrared spectroscopy. In order to estimate oxygen delivery (DO 2 est, l/min), cardiac output and oxygen saturation (SpO 2 ) were continuously monitored by impedance cardiography and pulse oximetry, respectively. Results: Exercise tolerance (Tlim) and oxygen uptake were increased with PAV compared with sham ventilation. In contrast, end-exercise blood lactate/Tlim and leg effort/Tlim ratios were lower with PAV (p,0.05). There were no between-treatment differences in cardiac output and SpO 2 either at submaximal exercise or at Tlim (ie, DO 2 est remained unchanged with PAV; p.0.05). Leg muscle oxygenation, however, was significantly enhanced with PAV as the exercise-related decrease in D(O 2 Hb)% was lessened and TOI was improved; moreover, D(Hb tot )%, an index of local blood volume, was increased compared with sham ventilation (p,0.01). Conclusions: Respiratory muscle unloading during highintensity exercise can improve peripheral muscle oxygenation despite unaltered systemic DO 2 in patients with advanced COPD. These findings might indicate that a fraction of the available cardiac output had been redirected from ventilatory to appendicular muscles as a consequence of respiratory muscle unloading.

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Measurements of excessive exercise ventilation which consider all data points maximize the usefulness of incremental cardiopulmonary exercise testing in the prognosis evaluation of PAH.

Impaired O(2) delivery relative to O(2) demands at the onset of exercise might influence the response profile of muscle fractional O(2) extraction (≅Δ[deoxy-Hb/Mb] by near-infrared spectroscopy) either by accelerating its rate of increase or creating an "overshoot" (OS) in patients with pulmonary arterial hypertension (PAH). We therefore assessed the kinetics of O(2) uptake [Formula: see text] Δ[deoxy-Hb/Mb] in the vastus lateralis, and heart rate (HR) at the onset of heavy-intensity exercise in 14 females with PAH (connective tissue disease, IPAH, portal hypertension, and acquired immunodeficiency syndrome) and 11 age- and gender-matched controls. Patients had slower [Formula: see text] and HR dynamics than controls (τ[Formula: see text] = 62.7 ± 15.2 s vs. 41.0 ± 13.8 s and t (1/2)-HR = 61.3 ± 16.6 s vs. 43.4 ± 8.8 s, respectively; p < 0.01). No study participant had a significant reduction in oxyhemoglobin saturation. In OS(-) subjects (6 patients and 7 controls), the kinetics of Δ[deoxy-Hb/Mb] relative to [Formula: see text] were faster in patients (p = 0.05). Larger area under the OS and slower kinetics (MRT) of the "downward" component indicated greater O(2) delivery-to-utilization mismatch in OS(+) patients versus OS(+) controls (477.4 ± 330.0 vs. 78.1 ± 65.6 a.u. and 74.6 ± 18.8 vs. 46.0 ± 17.0 s, respectively; p < 0.05). Resting pulmonary vascular resistance was higher in OS(+) than OS(-) patients (23.1 ± 12.0 vs. 10.7 ± 4.0 Woods, respectively; p < 0.05). We conclude that microvascular O(2) delivery-to-utilization inequalities slowed the rate of adaptation of aerobic metabolism at the start of heavy-intensity exercise in women with PAH.

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