Chiappa Gaspar R, Borghi-Silva Audrey, Ferreira Leonardo F, Carrascosa Claúdia, Oliveira Cristino Carneiro, Maia Joyce, Gimenes Ana Cristina, Queiroga Fernando, Berton Danilo, Ferreira Eloara M V, Nery Luis Eduardo, Neder J Alberto
Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Diseases, Department of Medicine, Federal University of São Paulo-Paulista School of Medicine, Rua Professor Francisco de Castro 54, Vila Clementino, São Paulo, Brazil.
J Appl Physiol (1985). 2008 May;104(5):1341-50. doi: 10.1152/japplphysiol.01364.2007. Epub 2008 Mar 20.
Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O(2) uptake (Vo(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 Vo(2)(p) 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 Vo(2)(p), 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 Vo(2)(p) (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of Vo(2)(p) (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 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 Vo(2)(p) kinetics compared with age-matched controls.
慢性阻塞性肺疾病（COPD）患者在运动期间肺氧摄取（Vo(2)(p)）动力学减慢，这可能源于肌肉氧输送不足。然而，目前尚不清楚COPD如何影响运动期间全身和微血管氧输送与摄取之间的动态关系。我们检验了以下假设：除了Vo(2)(p)动力学减慢外，COPD患者在高强度运动开始后肌肉脱氧动力学更快，但心输出量（Qt）动力学更慢。我们对10例中重度COPD患者和11例年龄匹配的久坐对照者进行了至耐受极限的高强度运动，期间测量了Vo(2)(p)、Qt（阻抗心动图）和肌肉脱氧情况（近红外光谱法）。通过标准非线性回归方程分析变量。患者运动不耐受时间显著更低（P < 0.05），且与Vo(2)(p)动力学相关（r = -0.70；P < 0.05）。与对照组相比，COPD患者Vo(2)(p)动力学（42 ± 13 vs. 73 ± 24秒）和Qt动力学（67 ± 11 vs. 96 ± 32秒）更慢，而肌肉脱氧血红蛋白的总体动力学更快（19.9 ± 2.4 vs. 16.5 ± 3.4秒）。因此，患者氧摄取与脱氧血红蛋白浓度平均反应时间的时间常数比显著更大，表明微血管氧输送动力学更慢。总之，我们的数据表明，中重度COPD患者在高强度运动开始后中枢和外周心血管调节受损。这些心脏循环障碍对氧输送和利用的动态匹配产生负面影响，可能导致与年龄匹配的对照组相比Vo(2)(p)动力学更慢。
