Why the study?
Conventional heart rate variability summaries use static indices over fixed windows, which cannot show how cardiac autonomic regulation persists, transitions, responds to perturbation, and recovers. This study developed a dynamical systems theory of cardiac-autonomic trajectories and equilibria observed through RR intervals to define what such a model can and cannot claim.
Does a dynamical resilience descriptor measuring sustained return after a perturbation pulse discriminate between monostable and bistable cardiac-autonomic systems better than static baseline variability or peak displacement in simulated replicates?
Does a dynamical resilience descriptor measuring sustained return after a perturbation pulse discriminate between monostable and bistable cardiac-autonomic systems better than static baseline variability or peak displacement in simulated replicates?
Answers are grounded in this paper and cite their sources.
This theoretical and computational study demonstrates that static baseline heart rate variability and peak perturbation displacement can fail to distinguish distinct underlying cardiac-autonomic dynamical architectures that exhibit vastly different post-perturbation recovery rates (100% vs. 7%).
Heart rate variability (HRV) is conventionally summarized with static indices computed over fixed windows, which cannot show how cardiac autonomic regulation persists, transitions, responds to perturbation, and recovers. We develop the Systems Theory of Cardiac-Autonomic Trajectories and Equilibria (STATE), in which autonomic regulation is a low-dimensional latent stochastic dynamical system observed only through RR intervals, and we derive what the theory can and cannot claim. First, we prove that for isotropic linear dynamics the sympathetic and parasympathetic coordinates are not separately identifiable from a scalar RR signal, whereas distinct time scales or coupling restore observability. Second, we derive exact properties of a minimal bistable system (stationary law, mean escape time, critical forcing), and a Monte Carlo simulation agreed with the exact escape time within 6%. Third, in 2000 simulated replicates of a monostable and a bistable system that share the same linearization at rest, baseline variability (area under the receiver operating characteristic curve, AUC, 0.56) and peak displacement at the pulse used (AUC 0.42) did not discriminate the systems, yet sustained return after an identical pulse differed: 100% versus 7%. We define resilience as a multidimensional response profile, show that recovery descriptors depend on analyst-chosen tolerances that must be fixed a priori, and state four falsifiable hypotheses with the result that would refute each. The work is theoretical and computational; no empirical recordings were used.
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Castillo-Aguilar et al. (2026) studied Cardiac autonomic regulation (theoretical and computational simulation) (n=4,000). Bistable cardiac-autonomic dynamical system (System B) subjected to a transient perturbation pulse (15.8 times critical forcing) vs. Monostable cardiac-autonomic dynamical system (System A, linearization of System B at rest) subjected to an identical transient pulse was evaluated on Sustained return to the resting regime after an identical transient perturbation pulse (with stability tolerance delta = 150.7 ms).
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