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IOP Publishing, Physiological Measurement, 5(44), p. 054001, 2023

DOI: 10.1088/1361-6579/acce1f

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Model-based spectral causality of cardiovascular variability interactions during head-down tilt

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

Abstract Objective. Cardiovascular control mechanisms are commonly studied during baroreceptor unloading induced by head-up tilt. Conversely, the effect of a baroreceptor loading induced by head-down tilt (HDT) is less studied especially when the stimulus is of moderate intensity and using model-based spectral causality markers. Thus, this study computes model-based causality markers in the frequency domain derived via causal squared coherence and Geweke spectral causality approach from heart period (HP) and systolic arterial pressure (SAP) variability series. Approach. We recorded HP and SAP variability series in 12 healthy men (age: from 41 to 71 yrs, median: 57 yrs) during HDT at −25°. The approaches are compared by considering two different bivariate model structures, namely the autoregressive and dynamic adjustment models. Markers are computed in traditional frequency bands utilized in cardiovascular control analysis, namely the low frequency (LF, from 0.04 to 0.15 Hz) and high frequency (HF, from 0.15 to 0.4 Hz) bands. Main results. We found that: (i) the two spectral causality metrics are deterministically related but spectral causality markers exhibit different discriminative ability; (ii) HDT reduces the involvement of the baroreflex in regulating HP-SAP variability interactions in the LF band, while leaving unmodified the action of mechanical feedforward mechanisms in both LF and HF bands; (iii) this conclusion does not depend on the model structure. Significance. We conclude that HDT can be utilized to reduce the impact of baroreflex and to study the contribution of regulatory mechanisms different from baroreflex to the complexity of cardiovascular control in humans.