Toyofuku Mamoru, Takaki Hiroshi, Sugimachi Masaru, Kawada Toru, Goto Yoichi, Sunagawa Kenji
Division of Cardiology, Department of Medicine, National Cardiovascular Center, Suita, Japan.
Eur J Appl Physiol. 2003 Sep;90(1-2):76-82. doi: 10.1007/s00421-003-0856-9. Epub 2003 Jun 13.
Patients with reduced peak oxygen uptake (VO2) due to chronic heart failure (CHF) exhibit abnormal VO2 kinetics even during mild to moderate exercise. This is characterized by a reduced ratio of the VO2 increase to the work rate increment (DeltaVO2/DeltaWR) during ramp exercise, and by a slow increase in VO2 during constant work rate exercise. Because the slow kinetics alone is unlikely to explain the reduced DeltaVO2/DeltaWR on theoretical grounds, we can postulate that the linearity between work rate and VO2 may be impaired when exercise is imposed in a ramp fashion. The present study was designed to address this issue. In 21 CHF patients and 17 normal controls, we performed both symptom-limited exercise testing (15 W. min(-1) ramp) and a constant work rate exercise test (0 W followed by 50-W step). The VO2 step response was used to mathematically derive the hypothetical VO2 ramp response by time integration. Although peak VO2 and work rate were both significantly lower in patients, the attenuation in peak VO2 was more prominent ( p<0.05), which could be explained by a lower DeltaVO2/DeltaWR in patients compared with controls [8.1 (SD 1.0) and 9.8 (0.5) ml. min(-1). W(-1), p<0.01]. The hypothetical DeltaVO2/DeltaWR derived from the VO2 step response was also significantly lower in patients [8.7 (1.0) and 10.0 (0.7) ml. min(-1). W(-1), p<0.01]. The hypothetical and measured DeltaVO2/DeltaWR were highly correlated ( r=0.78, p<0.001). Thus, we can reasonably predict the VO2 ramp response from the VO2 response to a step increase in work rate, indicating that linearity between VO2 and work rate is held constant irrespective of loading patterns. Additional studies, such as those including evaluation of anaerobic bioenergetics, are needed to further elucidate the precise mechanism(s) of this phenomenon.
由于慢性心力衰竭(CHF)导致峰值摄氧量(VO2)降低的患者,即使在轻度至中度运动期间也表现出异常的VO2动力学。这表现为在递增运动期间VO2增加与工作率增量的比率(DeltaVO2/DeltaWR)降低,以及在恒定工作率运动期间VO2缓慢增加。由于仅缓慢的动力学在理论上不太可能解释DeltaVO2/DeltaWR的降低,我们可以假设当以递增方式进行运动时,工作率与VO2之间的线性关系可能受到损害。本研究旨在解决这个问题。在21名CHF患者和17名正常对照中,我们进行了症状限制性运动测试(15 W·min(-1)递增)和恒定工作率运动测试(0 W随后50-W阶跃)。VO2阶跃反应用于通过时间积分数学推导假设的VO2递增反应。尽管患者的峰值VO2和工作率均显著较低,但峰值VO2的衰减更为突出(p<0.05),这可以通过与对照组相比患者较低的DeltaVO2/DeltaWR来解释[8.1(标准差1.0)和9.8(0.5)ml·min(-1)·W(-1),p<0.01]。从VO2阶跃反应推导的假设DeltaVO2/DeltaWR在患者中也显著较低[8.7(1.0)和10.0(0.7)ml·min(-1)·W(-1),p<0.01]。假设的和测量的DeltaVO2/DeltaWR高度相关(r=0.78,p<0.001)。因此,我们可以合理地从VO2对工作率阶跃增加的反应预测VO2递增反应,表明VO2与工作率之间的线性关系与负荷模式无关保持恒定。需要进行更多研究,如包括评估无氧生物能学的研究,以进一步阐明这种现象的确切机制。