Department of Surgery & Anaesthesia, University of Otago, Wellington, New Zealand.
Exp Physiol. 2010 Jul;95(7):788-97. doi: 10.1113/expphysiol.2010.052910. Epub 2010 Apr 9.
The respiratory component of heart rate variability (respiratory sinus arrhythmia, RSA) has been associated with improved pulmonary gas exchange efficiency in humans via the apparent clustering and scattering of heart beats in time with the inspiratory and expiratory phases of alveolar ventilation, respectively. However, since human RSA causes only marginal redistribution of heart beats to inspiration, we tested the hypothesis that any association between RSA amplitude and pulmonary gas exchange efficiency may be indirect. In 11 patients with fixed-rate cardiac pacemakers and 10 healthy control subjects, we recorded R-R intervals, respiratory flow, end-tidal gas tension and the ventilatory equivalents for carbon dioxide and oxygen during 'fast' (0.25 Hz) and 'slow' paced breathing (0.10 Hz). Mean heart rate, mean arterial blood pressure, mean arterial pressure fluctuations, tidal volume, end-tidal CO(2), and were similar between pacemaker and control groups in both the fast and slow breathing conditions. Although pacemaker patients had no RSA and slow breathing was associated with a 2.5-fold RSA amplitude increase in control subjects (39 +/- 21 versus 97 +/- 45 ms, P < 0.001), comparable (main effect for breathing frequency, F(1,19) = 76.54, P < 0.001) and reductions (main effect for breathing frequency, F(1,19) = 23.90, P < 0.001) were observed for both cohorts during slow breathing. In addition, the degree of (r = 0.36, P = 0.32) and reductions (r = 0.29, P = 0.43) from fast to slow breathing were not correlated to the degree of associated RSA amplitude enhancements in control subjects. These findings suggest that the association between RSA amplitude and pulmonary gas exchange efficiency during variable-frequency paced breathing observed in prior human work is not contingent on RSA being present. Therefore, whether RSA serves an intrinsic physiological function in optimizing pulmonary gas exchange efficiency in humans requires further experimental validation.
心率变异性的呼吸成分(呼吸窦性心律失常,RSA)已被证明可以通过心跳在吸气和呼气阶段分别与肺泡通气的相应阶段明显聚集和分散,从而提高人类的肺气体交换效率。然而,由于人体 RSA 仅导致心跳向吸气的轻微重新分配,我们检验了这样一个假设,即 RSA 幅度与肺气体交换效率之间的任何关联可能是间接的。在 11 名带有固定心率起搏器的患者和 10 名健康对照者中,我们记录了 R-R 间期、呼吸流量、呼气末气体张力以及二氧化碳和氧气的通气等效值,在“快速”(0.25 Hz)和“缓慢”(0.10 Hz)起搏呼吸期间。在快速和缓慢呼吸条件下,起搏器患者和对照组的平均心率、平均动脉血压、平均动脉压波动、潮气量、呼气末 CO2 和均相似。尽管起搏器患者没有 RSA,并且缓慢呼吸导致对照组 RSA 幅度增加 2.5 倍(39 ± 21 与 97 ± 45 ms,P < 0.001),但在两组中均观察到相似的(呼吸频率的主要效应,F(1,19) = 76.54,P < 0.001)和减少(呼吸频率的主要效应,F(1,19) = 23.90,P < 0.001)。此外,从快速呼吸到缓慢呼吸的幅度增加(r = 0.36,P = 0.32)和减少(r = 0.29,P = 0.43)与对照组 RSA 幅度增强的程度无关。这些发现表明,在先前的人体工作中观察到的变频率起搏呼吸期间 RSA 幅度与肺气体交换效率之间的关联并不取决于 RSA 的存在。因此,RSA 是否在优化人体肺气体交换效率方面发挥内在生理功能需要进一步的实验验证。