Jerath Ravinder, Edry John W, Barnes Vernon A, Jerath Vandna
Augusta Women's Center, 2100 Central Avenue, Suite 6 & 7, Augusta, GA 30904, USA.
Med Hypotheses. 2006;67(3):566-71. doi: 10.1016/j.mehy.2006.02.042. Epub 2006 Apr 18.
Pranayamic breathing, defined as a manipulation of breath movement, has been shown to contribute to a physiologic response characterized by the presence of decreased oxygen consumption, decreased heart rate, and decreased blood pressure, as well as increased theta wave amplitude in EEG recordings, increased parasympathetic activity accompanied by the experience of alertness and reinvigoration. The mechanism of how pranayamic breathing interacts with the nervous system affecting metabolism and autonomic functions remains to be clearly understood. It is our hypothesis that voluntary slow deep breathing functionally resets the autonomic nervous system through stretch-induced inhibitory signals and hyperpolarization currents propagated through both neural and non-neural tissue which synchronizes neural elements in the heart, lungs, limbic system and cortex. During inspiration, stretching of lung tissue produces inhibitory signals by action of slowly adapting stretch receptors (SARs) and hyperpolarization current by action of fibroblasts. Both inhibitory impulses and hyperpolarization current are known to synchronize neural elements leading to the modulation of the nervous system and decreased metabolic activity indicative of the parasympathetic state. In this paper we propose pranayama's physiologic mechanism through a cellular and systems level perspective, involving both neural and non-neural elements. This theoretical description describes a common physiological mechanism underlying pranayama and elucidate the role of the respiratory and cardiovascular system on modulating the autonomic nervous system. Along with facilitating the design of clinical breathing techniques for the treatment of autonomic nervous system and other disorders, this model will also validate pranayama as a topic requiring more research.
调息法，定义为对呼吸运动的一种调控方式，已被证明会引发一种生理反应，其特征为耗氧量降低、心率下降、血压降低，以及脑电图记录中θ波振幅增加，副交感神经活动增强，并伴有警觉和恢复活力的体验。调息法如何与神经系统相互作用从而影响新陈代谢和自主功能的机制仍有待明确。我们的假设是，自主的缓慢深呼吸通过拉伸诱导的抑制性信号和通过神经及非神经组织传播的超极化电流在功能上重置自主神经系统，这些信号和电流使心脏、肺、边缘系统和皮层中的神经元件同步。在吸气过程中，肺组织的拉伸通过慢适应性牵张感受器（SARs）的作用产生抑制性信号，并通过成纤维细胞的作用产生超极化电流。已知抑制性冲动和超极化电流都会使神经元件同步，从而导致神经系统的调节以及代谢活动的降低，这表明处于副交感神经状态。在本文中，我们从细胞和系统层面的角度提出调息法的生理机制，涉及神经和非神经元件。这一理论描述阐述了调息法背后的共同生理机制，并阐明了呼吸和心血管系统在调节自主神经系统方面的作用。除了有助于设计用于治疗自主神经系统及其他疾病的临床呼吸技术外，该模型还将验证调息法作为一个需要更多研究的课题。
