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.
Traumatic events engage stress physiology, with the hypothalamic-pituitary-adrenal axis and cortisol central to adaptation. In naturalistic trauma, physical injury and psychological distress often co-occur, complicating interpretation of acute cortisol changes. Stillbirth offers a natural contrast: it is physiologically similar to live birth but constitutes traumatic bereavement. This study tested whether psychological trauma elicited by stillbirth is associated with acute alterations in diurnal cortisol rhythm versus comparable physiological delivery stress. Fifty-seven postpartum women were included (stillbirth, 24; live birth, 33). Saliva samples were collected at seven fixed time points across the day following childbirth. Cosinor curve fitting yielded the midline estimating statistic of rhythm, amplitude, and acrophase. Traditional indices included area under the curve with respect to ground, area under the curve with respect to increase, and the cortisol awakening response. Group differences were tested using analyzes of variance. Both groups showed a coherent diurnal pattern. Compared with live birth, stillbirth was associated with a lower area under the curve with respect to ground, a lower area under the curve with respect to increase, and a lower midline estimating statistic of rhythm. Stillbirth was also exhibited associated with an earlier acrophase. Compared with comparable physiological delivery stress, stillbirth is linked to reduced total cortisol secretion, lower mean levels, and an advanced circadian phase in the acute postpartum period, suggesting that the psychological trauma of stillbirth may involve alterations in hypothalamic-pituitary-adrenal axis regulatory patterns and providing preliminary evidence for future work on early biological markers and supportive interventions.
Heat stress is a condition that develops when the body absorbs more heat than it can dissipate, leading to hyperthermia and problems such as gastrointestinal dysfunction. Past research suggests that gut dysfunction is highly temperature sensitive, and hyperthermia that alters the gut myoelectric activity should be studied properly through electrogastrography. Ten rats, 5 as controls and 5 as hyperthermic, were used in the experiment. For control conditions, a real-time electrogastrogram (EGG) recording was performed at room temperature, and for the induction of hyperthermia, a 42 +/- 1 degrees C temperature was maintained in a closed incubator for 60 min. The rectal temperature was also taken before and after the exposure. The FFT of a full-length recording and five segments, each of 15 min, were analyzed; the wave shift and total time of occurrence of each wave were closely observed. As per the experiment, more spike pattern waves were observed in the hyperthermic rat model (p < 0.01) compared to the control rat, as the heat stress triggers changes in autonomic nervous activity, particularly through the parasympathetic and sympathetic pathways. This imbalance could lead to increased or irregular gastric electrical activity, converting slow waves to spikes. More spike patterns in EGG were observed due to exposure to hyperthermic conditions, which may have occurred due to gut inflammation, altered gastric motility, as well as ion channel dysregulation. [GRAPHICS] .
