American Journal of Physiology-Regulatory, Integrative and Comparative PhysiologyNeurosciencePeer-reviewed journal article
Dynamic fluctuations in ascending heart-to-brain modulations under mental stress elicitation
Diego Candia‐RiveraiD, Kian Norouzi, Thomas Zoëga RamsøyiD, Gaetano ValenzaiD
Abstract
Dynamical information exchange between central and autonomic nervous systems, as referred to functional brain-heart interplay, occurs during emotional and physical arousal. It is well documented that physical and mental stress lead to sympathetic activation. Nevertheless, the role of autonomic inputs in nervous-system-wise communication under mental stress is yet unknown. In this study, we estimated the causal and bidirectional neural modulations between EEG oscillations and peripheral sympathetic and parasympathetic activities using a recently proposed computational framework for a functional brain-heart interplay assessment, namely the sympathovagal synthetic data generation model. Mental stress was elicited in 37 healthy volunteers by increasing their cognitive demands throughout three tasks associated with increased stress levels. Stress elicitation induced an increased variability in sympathovagal markers, as well as increased variability in the directional brain-heart interplay. The observed heart-to-brain interplay was primarily from sympathetic activity targeting a wide range of EEG oscillations, whereas variability in the efferent direction seemed mainly related to EEG oscillations in the gamma band. These findings extend current knowledge on stress physiology, which mainly referred to top-down neural dynamics. Our results suggest that mental stress may not cause an increase in sympathetic activity exclusively as it initiates a dynamic fluctuation within brain-body networks including bidirectional interactions at a brain-heart level. We conclude that directional brain-heart interplay measurements may provide suitable biomarkers for a quantitative stress assessment and bodily feedback may modulate the perceived stress caused by increased cognitive demand.
- organism: human
- assay: electronic health records
- research focus: cell type annotation
- approach: statistical model
- Citations
- 24
- FWCI
- 4.72
- Field percentile
- top 4%
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