Schmitt Daniel T, Stein Phyllis K, Ivanov Plamen Ch
Theoretische Physik, Universität Ulm, D-89069 Ulm, Germany.
IEEE Trans Biomed Eng. 2009 May;56(5):1564-73. doi: 10.1109/TBME.2009.2014819. Epub 2009 Feb 6.
Cardiac dynamics exhibit complex variability characterized by scale-invariant and nonlinear temporal organization related to the mechanism of neuroautonomic control, which changes with physiologic states and pathologic conditions. Changes in sleep regulation during sleep stages are also related to fluctuations in autonomic nervous activity. However, the interaction between sleep regulation and cardiac autonomic control remains not well understood. Even less is known how this interaction changes with age, as aspects of both cardiac dynamics and sleep regulation differ in healthy elderly compared to young subjects. We hypothesize that because of the neuroautonomic responsiveness in young subjects, fractal and nonlinear features of cardiac dynamics exhibit a pronounced stratification pattern across sleep stages, while in elderly these features will remain unchanged due to age-related loss of cardiac variability and decline of neuroautonomic responsiveness. We analyze the variability and the temporal fractal organization of heartbeat fluctuations across sleep stages in both young and elderly. We find that independent linear and nonlinear measures of cardiac control consistently exhibit the same ordering in their values across sleep stages, forming a robust stratification pattern. Despite changes in sleep architecture and reduced heart rate variability in elderly subjects, this stratification surprisingly does not break down with advanced age. Moreover, the difference between sleep stages for some linear, fractal, and nonlinear measures exceeds the difference between young and elderly, suggesting that the effect of sleep regulation on cardiac dynamics is significantly stronger than the effect of healthy aging. Quantifying changes in this stratification pattern may provide insights into how alterations in sleep regulation contribute to increased cardiac risk.
心脏动力学表现出复杂的变异性，其特征是与神经自主控制机制相关的尺度不变和非线性时间组织，这种机制会随着生理状态和病理状况而变化。睡眠阶段睡眠调节的变化也与自主神经活动的波动有关。然而，睡眠调节与心脏自主控制之间的相互作用仍未得到很好的理解。对于这种相互作用如何随年龄变化知之更少，因为与年轻受试者相比，健康老年人的心脏动力学和睡眠调节方面都有所不同。我们假设，由于年轻受试者的神经自主反应性，心脏动力学的分形和非线性特征在不同睡眠阶段呈现出明显的分层模式，而在老年人中，由于与年龄相关的心脏变异性丧失和神经自主反应性下降，这些特征将保持不变。我们分析了年轻和老年受试者在不同睡眠阶段心跳波动的变异性和时间分形组织。我们发现，心脏控制的独立线性和非线性测量值在不同睡眠阶段始终呈现相同顺序，形成了一个稳健的分层模式。尽管老年受试者的睡眠结构发生了变化且心率变异性降低，但这种分层令人惊讶地并未随着年龄增长而瓦解。此外，一些线性、分形和非线性测量在睡眠阶段之间的差异超过了年轻和老年之间的差异，这表明睡眠调节对心脏动力学的影响明显强于健康衰老的影响。量化这种分层模式的变化可能有助于深入了解睡眠调节的改变如何导致心脏风险增加。
