Driving frequently exposes individuals to conditions triggering acute stress, but its effects on drivers’ visual behaviour remain insufficiently understood. We used the heart rate dynamics to label acute stress episodes in recordings from 881 participants who performed simulated and on-road driving. Considering acute stress as a phased process, we analysed eye gaze metrics during stress activation and stress resistance periods. In simulation, stress activation was accompanied by more frequent and shorter fixations, greater fixation area, higher stationary gaze entropy, and lower gaze transition entropy. In on-road driving, significant effects were more selective, with the most consistent changes observed for the horizontal diameter of fixation area and entropy-based gaze measures. During stress resistance, many measures partially returned toward non-stress levels, suggesting a transition from initial reactivity toward stabilisation. These findings support gaze-derived measures as candidate indicators of changes in visual behaviour related to acute stress during driving, while highlighting the importance of considering acute stress as a phased process. They also indicate that multimodal context-aware validation is needed for translation into real-time driver state monitoring and safety-relevant assistance applications.
The freeze-like response is a fundamental defensive mechanism that remains poorly understood despite its potential to impair functioning under acute threat. We examined its biological correlates using untargeted serum proteomics in participants exposed to ecologically valid simulated armed attacks, comparing untrained individuals (n = 20) with experienced police rapid response personnel (n = 20). Freeze-like responses, characterized by unresponsiveness to attack, were assessed via expert video analysis of participant performance during the scenarios. Serum samples collected before and after threat exposure were analyzed via LC‒MS/MS, identifying 1,238 protein groups. Experienced personnel demonstrated markedly greater resistance to freeze-like responses. No significant proteomic changes were observed from pre- to post-exposure in either group, suggesting that freeze-resistance may be associated with stable, trait-like signatures rather than acute stress-responsive processes. Weighted gene co-expression network analysis identified a module strongly correlated with freeze-resistance (r = 0.75, p = 4 × 10−9) and training status (r = 0.71, p = 6 × 10−8), which also correlated with skeletal muscle mass (r = 0.57, p = 8 × 10−5). This module was enriched for processes including extracellular matrix organization, muscle development, carbohydrate metabolism, and antioxidant activity. These molecular patterns may reflect the downstream effects of comprehensive training that integrates physical conditioning, operational experience, and psychological preparation. This study provides the first proteomic characterization of freeze-like response resistance under realistic threat conditions, supporting the view that resilience involves stable physiological adaptations rather than solely reactive stress mechanisms.
Suffering the stress of others (termed empathic stress or stress contagion) may affect an individual’s health and well-being. To understand the underlying hormonal processes of empathic stress, N = 108 opposite-sex dyads were tested, with one dyad partner passively observing the other undergoing a standardized psychosocial laboratory stressor. A positive link between oxytocin release and empathic stress response was hypothesized, while a negative relationship was expected for testosterone release. Associations of observer oxytocin and testosterone levels with two components of empathic stress were examined: stress resonance (i.e. synchronized observer–target responses) and vicarious stress (observer responses independent of target stress). During the passive observation of a stressed target, salivary oxytocin and testosterone levels increased by 16.64% and 23.00%, respectively, followed by a drop back to baseline levels. Supporting our hypotheses, increased observer oxytocin reactivity was linked to greater stress resonance in HF-HRV reactivity. This association was reversed in low oxytocin responders. Further, testosterone reactivity was negatively associated with stress resonance in heart rate activity. However, testosterone also showed a positive association with vicarious cortisol activity, which resembles the response pattern seen in first-hand stress exposure. We conclude that stress resonance may be the more empathy-dependent component of the empathic stress construct, aligning with previous work on the involvement of oxytocin and testosterone in empathy. To draw further conclusions about the role of oxytocin and testosterone in empathic stress response, future studies including a control group and hormone stimulation are needed.
Chronic stress induces neurobiological alterations within limbic circuits. The contribution of hippocampal histaminergic signaling to stress-related behavioral dysfunction remains insufficiently characterized. This study examined the comparative and combined effects of fluoxetine and treadmill exercise on anxiety- and depression-like behaviors and ventral hippocampal histamine H1 and H2 receptor expression in a chronic unpredictable mild stress (CUMS) rat model. Male Wistar rats were exposed to four weeks of CUMS and allocated to seven groups: Control, CUMS, Exercise (EXC), Fluoxetine (FLX), CUMS+EXC, CUMS+FLX, and CUMS+FLX+EXC. Anxiety-like behavior was assessed using the elevated plus maze (EPM) and open field test (OFT), while depressive-like behavior was evaluated using the forced swim test (FST). Hippocampal H1 and H2 receptor mRNA levels were quantified by real-time PCR. CUMS induced significant anxiety- and depression-like behaviors, evidenced by reduced central zone exploration and increased FST immobility. Fluoxetine significantly attenuated depressive-like behavior, while combined fluoxetine and exercise increased open-arm exploration in the EPM. CUMS significantly upregulated hippocampal H1 and H2 receptor mRNA expression relative to controls. Neither fluoxetine nor exercise alone significantly reversed these stress-induced elevations. Combined treatment produced partial attenuation of H1 receptor upregulation, whereas H2 receptor expression remained elevated across treatment conditions. These findings demonstrate that chronic stress induces robust hippocampal histaminergic remodeling that persists despite behavioral improvement, suggesting that histaminergic signaling is a stress-responsive molecular substrate only partially sensitive to conventional antidepressant strategies. The dissociation between behavioral recovery and receptor normalization identifies the hippocampal histaminergic system as a potential target for future therapeutic intervention in stress-related disorders.
Chronic stress facilitates the development and progression of multiple psychiatric disorders, including depression and addiction. The dysregulation of approach motivation has been proposed as a mechanism of chronic stress, but it is unclear how chronic stress is related to approach motivation. The current study sought to elucidate the relationship between chronic stress and resting-state electroencephalographic (EEG) measures of approach motivation. Sixty undergraduate students filled out the Perceived Stress Scale (PSS) and were recorded with resting-state EEG. Hierarchical regression analyses revealed significant quadratic (U-shaped) associations between mean-centered PSS scores and all three EEG measures: alpha frontal asymmetry (AFA) (β = 0.32, 95% CI [0.0001, 0.0018], p = 0.032), delta power (β = 0.33, 95% CI [0.0003, 0.0036], p = 0.021), and theta power (β = 0.31, 95% CI [0.0002, 0.0035], p = 0.030). All quadratic effects remained statistically significant after false discovery rate (FDR; Benjamini-Hochberg) correction (all adjusted ps < 0.05). These findings suggest that there is a nonlinear relationship between chronic stress and approach motivation, i.e. at both low and high chronic stress levels, resting-state activation of approach motivation is enhanced, whereas at moderate chronic stress levels, approach motivation is reduced, probably reflecting more efficient allocation and conservation of brain resources. More importantly, our findings demonstrate the necessity of examining the baseline neural state in addition to the task-evoked responses when assessing stress-related changes of approach motivation, thereby providing novel insights into the mechanisms of stress adaptation and their implications for psychological health.
