Sperandio Priscila Abreu, Borghi-Silva Audrey, Barroco Adriano, Nery Luiz Eduardo, Almeida Dirceu R, Neder J Alberto
Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo (UNIFESP), São Paulo.
Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1720-8. doi: 10.1152/ajpheart.00596.2009. Epub 2009 Sep 4.
Impaired muscle blood flow at the onset of heavy-intensity exercise may transiently reduce microvascular O(2) pressure and decrease the rate of O(2) transfer from capillary to mitochondria in chronic heart failure (CHF). However, advances in the pharmacological treatment of CHF (e.g., angiotensin-converting enzyme inhibitors and third-generation beta-blockers) may have improved microvascular O(2) delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O(2) uptake (Vo(2)) kinetics. We assessed the rate of change of pulmonary Vo(2) (Vo(2)(p)), (estimated) fractional O(2) extraction in the vastus lateralis (approximately Delta[deoxy-Hb+Mb] by near-infrared spectroscopy), and cardiac output (Qt) during high-intensity exercise performed to the limit of tolerance (Tlim) in 10 optimally treated sedentary patients (ejection fraction = 29 + or - 8%) and 11 controls. Sluggish Vo(2)(p) and Qt kinetics in patients were significantly related to lower Tlim values (P < 0.05). The dynamics of Delta[deoxy-Hb+Mb], however, were faster in patients than controls [mean response time (MRT) = 15.9 + or - 2.0 s vs. 19.0 + or - 2.9 s; P < 0.05] with a subsequent response "overshoot" being found only in patients (7/10). Moreover, tauVo(2)/MRT-[deoxy-Hb+Mb] ratio was greater in patients (4.69 + or - 1.42 s vs. 2.25 + or - 0.77 s; P < 0.05) and related to Qt kinetics and Tlim (R = 0.89 and -0.78, respectively; P < 0.01). We conclude that despite the advances in the pharmacological treatment of CHF, disturbances in "central" and "peripheral" circulatory adjustments still play a prominent role in limiting Vo(2)(p) kinetics and tolerance to heavy-intensity exercise in nontrained patients.
在重度高强度运动开始时，肌肉血流受损可能会使慢性心力衰竭（CHF）患者的微血管氧分压暂时降低，并降低氧从毛细血管向线粒体的转运速率。然而，CHF药物治疗的进展（如血管紧张素转换酶抑制剂和第三代β受体阻滞剂）可能已在一定程度上改善了微血管氧输送，以至于肌细胞内代谢惰性可能成为氧摄取（Vo₂）动力学限制的主要部位。我们评估了10例经最佳治疗的久坐不动患者（射血分数 = 29±8%）和11例对照在进行至耐受极限（Tlim）的高强度运动期间肺Vo₂（Vo₂(p)）的变化率、股外侧肌的（估计）氧分数提取（通过近红外光谱法测定的约Δ[脱氧血红蛋白+肌红蛋白]）以及心输出量（Qt）。患者中缓慢的Vo₂(p)和Qt动力学与较低的Tlim值显著相关（P < 0.05）。然而，患者中Δ[脱氧血红蛋白+肌红蛋白]的动力学比对照组更快[平均反应时间（MRT） = 15.9±2.0秒对19.0±2.9秒；P < 0.05]，且仅在患者中发现随后的反应“超调”（7/10）。此外，患者的tauVo₂/MRT - [脱氧血红蛋白+肌红蛋白]比值更高（4.69±1.42秒对2.25±0.77秒；P < 0.05），并与Qt动力学和Tlim相关（分别为R = 0.89和 - 0.78；P < 0.01）。我们得出结论，尽管CHF药物治疗取得了进展，但在未经训练的患者中，“中枢”和“外周”循环调节紊乱在限制Vo₂(p)动力学和对重度高强度运动的耐受性方面仍起着重要作用。
