Cargando…

The control mechanisms of heart rate dynamics in a new heart rate nonlinear time series model

The control mechanisms and implications of heart rate variability (HRV) under the sympathetic (SNS) and parasympathetic nervous system (PNS) modulation remain poorly understood. Here, we establish the HR model/HRV responder using a nonlinear process derived from Newton’s second law in stochastic sel...

Descripción completa

Detalles Bibliográficos
Autor principal: He, Zonglu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075874/
https://www.ncbi.nlm.nih.gov/pubmed/32179768
http://dx.doi.org/10.1038/s41598-020-61562-6
Descripción
Sumario:The control mechanisms and implications of heart rate variability (HRV) under the sympathetic (SNS) and parasympathetic nervous system (PNS) modulation remain poorly understood. Here, we establish the HR model/HRV responder using a nonlinear process derived from Newton’s second law in stochastic self-restoring systems through dynamic analysis of physiological properties. We conduct model validation by testing, predictions, simulations, and sensitivity and time-scale analysis. We confirm that the outputs of the HRV responder can be accepted as the real data-generating process. Empirical studies show that the dynamic control mechanism of heart rate is a stable fixed point, rather than a strange attractor or transitions between a fixed point and a limit cycle; HR slope (amplitude) may depend on the ratio of cardiac disturbance or metabolic demand mean (standard deviation) to myocardial electrical resistance (PNS-SNS activity). For example, when metabolic demands remain unchanged, HR amplitude depends on PNS to SNS activity; when autonomic activity remains unchanged, HR amplitude during resting reflects basal metabolism. HR parameter alterations suggest that age-related decreased HRV, ultrareduced HRV in heart failure, and ultraelevated HRV in ST segment alterations refer to age-related decreased basal metabolism, impaired myocardial metabolism, and SNS hyperactivity triggered by myocardial ischemia, respectively.