How the Acute Psychosocial Stress Response Ends: A Post-Stressor Transition Model of Glucocorticoid Feedback, Vagal Re-Engagement, and Frontolimbic Context Updating
- 1Department of Psychology, Henan Medical University, Xinxiang 453003, China
- 2Mental Illness and Cognitive Neuroscience Key Laboratory of Xinxiang, Henan Medical University, Xinxiang 453003, China
Abstract
Objective stressor offset does not mark a common onset of recovery: cardiovascular activation may be waning while cortisol is still rising and threat-related cognition persists. This structured narrative review integrates molecular, autonomic, neural, cognitive, and immune evidence on the post-stressor interval, primarily in adult psychosocial-stress paradigms. We propose the Post-Stressor Transition Model (PSTM) as an operational extension of existing recovery and allostatic accounts, not as a newly discovered biological system. Three regulatory functions organize the synthesis: updating whether threat remains current, changing cardiac autonomic influence, and regulating continuing hypothalamic–pituitary–adrenocortical output. Glucocorticoid receptor signaling, catecholamines, endocannabinoids, oxytocin, and vasopressin contribute across these functions. The framework distinguishes objective offset from system-specific extrema, physiological resolution from demonstrated adaptation, and shared timing from directional coupling. Eight propositions specify outcomes, temporal windows, competing explanations, and prespecified effect bounds. Measurement recommendations address cortisol nonresponse, respiratory influences on heart rate variability, assessment reactivity, and multirate sampling. Hormonal state and development modify candidate parameters rather than define fixed response types. No universal recovery threshold or clinically validated transition profile is claimed. The model is useful only if its additional parameters are identifiable, improve independent prediction, and withstand phase-specific experimental tests.
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BibTeX
@article{liu2026acute,
title = {{How the Acute Psychosocial Stress Response Ends: A Post-Stressor Transition Model of Glucocorticoid Feedback, Vagal Re-Engagement, and Frontolimbic Context Updating}},
author = {Congcong Liu and Ronglian Zheng and Yihan Wu and Meng Zhang},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27209047},
url = {https://www.mdpi.com/1422-0067/27/20/9047},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - How the Acute Psychosocial Stress Response Ends: A Post-Stressor Transition Model of Glucocorticoid Feedback, Vagal Re-Engagement, and Frontolimbic Context Updating
AU - Congcong Liu
AU - Ronglian Zheng
AU - Yihan Wu
AU - Meng Zhang
PY - 2026
DA - 2026/10/12
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27209047
UR - https://www.mdpi.com/1422-0067/27/20/9047
AB - Objective stressor offset does not mark a common onset of recovery: cardiovascular activation may be waning while cortisol is still rising and threat-related cognition persists. This structured narrative review integrates molecular, autonomic, neural, cognitive, and immune evidence on the post-stressor interval, primarily in adult psychosocial-stress paradigms. We propose the Post-Stressor Transition Model (PSTM) as an operational extension of existing recovery and allostatic accounts, not as a newly discovered biological system. Three regulatory functions organize the synthesis: updating whether threat remains current, changing cardiac autonomic influence, and regulating continuing hypothalamic–pituitary–adrenocortical output. Glucocorticoid receptor signaling, catecholamines, endocannabinoids, oxytocin, and vasopressin contribute across these functions. The framework distinguishes objective offset from system-specific extrema, physiological resolution from demonstrated adaptation, and shared timing from directional coupling. Eight propositions specify outcomes, temporal windows, competing explanations, and prespecified effect bounds. Measurement recommendations address cortisol nonresponse, respiratory influences on heart rate variability, assessment reactivity, and multirate sampling. Hormonal state and development modify candidate parameters rather than define fixed response types. No universal recovery threshold or clinically validated transition profile is claimed. The model is useful only if its additional parameters are identifiable, improve independent prediction, and withstand phase-specific experimental tests.
SN - 1422-0067
ER -