A network physiology framework investigated how coordinated interactions among multiple organ systems collectively support the preservation of cerebral bioenergetic function and better distinguish adaptive from maladaptive responses to hypoxia. Twelve healthy males were passively exposed to 6 h of normoxia (21% O2) and hypoxia (12% O2) in a randomised, single-blind, crossover design. Venous blood was assayed for oxidative-nitrosative stress (OXNOS, spectroscopy/chemiluminescence) and neurovascular unit (hs-ELISA) biomarkers. Global cerebral delivery of O2 and glucose were determined by duplex ultrasound. Clinical acute mountain sickness (AMS+) was diagnosed in five participants. Cerebral substrate delivery was well maintained in both hypoxia and AMS+ (p < 0.05 vs normoxia and AMS-) despite marked arterial hypoxemia. Bioenergetic defence coincided with pronounced elevations in the spectral amplitude and phase synchronisation of very low-frequency oscillations (VLFOs, 0.03-0.06 Hz), which were evident across multiple organ systems and most prominent within the cerebral network. Systemic VLFOs were further exaggerated and more functionally connected in AMS+ in the absence of exaggerated systemic OXNOS or structural damage/destabilisation of the neurovascular unit (both p < 0.05 vs normoxia and AMS-). Collectively, these findings suggest that AMS, while characterised by debilitating symptomatology, may reflect a neuroprotective adaptive as opposed to pathologically maladaptive phenotype.

Dynamic cerebral autoregulation (dCA) stabilises cerebral blood flow (CBF) against rapid fluctuations in perfusion pressure and may serve as a key physiological mediator of cognitive function. Inhibitory executive function, a core domain essential for goal-directed behaviour, is influenced by modifiable lifestyle factors such as physical activity and dietary behaviours, yet the mechanisms linking these behaviours to inhibitory executive function remain poorly understood. This review synthesises evidence examining the relationship between dCA and inhibitory executive function in response to feasible behavioural interventions. Acute aerobic exercise (AE) preserves dCA and enhances inhibitory control, whereas exhaustive AE impairs both. Similarly, dietary behaviours such as breakfast skipping or post-prandial hyperglycaemia acutely reduce dCA and inhibitory executive performance, suggesting a potential mechanistic link between vascular regulation and cognitive outcomes in short-term contexts. Long-term effects of physical activity on the dCA-inhibitory executive function relationship are less clear, likely reflecting complex interactions among vascular, metabolic and neural systems. While causal pathways remain to be fully elucidated, impaired dCA may contribute to reduced inhibitory control, highlighting its potential role as a physiological mediator. Conversely, maintaining intact dCA may be critical for supporting cognitive performance. Understanding how modifiable behaviours influence both dCA and inhibitory control provides novel insights into the physiological mechanisms underlying cognitive health. These findings could inform lifestyle-based strategies aimed at optimising inhibitory executive function and preserving cognitive performance across the lifespan.

Combat sports provide a unique human model in which cerebral ischaemia-reperfusion stress, adaptive neuroprotection, and impact-induced neurodegenerative risk coexist. Across striking and grappling disciplines, exercise-induced metabolic and redox stress, repetitive head impacts and transient cerebral ischaemia-reperfusion during vascular neck restraints expose the brain to competing adaptive and injurious stimuli. Cerebral ischaemic preconditioning (cIPC) research demonstrates that brief, sublethal reductions in cerebral blood flow (CBF) activate a conserved hormetic programme involving modulation of oxidative-inflammatory-nitrosative stress (OXINOS), reduced glutamate excitotoxicity, mitochondrial stabilisation, anti-apoptotic and autophagic pathways, and metabolic reprogramming. These responses preserve glucose-and lactate-dependent bioenergetics, neurovascular unit integrity, and cognitive function. Repetitive sportive strangulations may engage cIPC-like mechanisms, potentially explaining elevated basal CBF reported in elite Brazilian jiu-jitsu athletes (~500 pre-syncopal exposures per year). In contrast, repetitive impacts and rotational shear in boxing and mixed martial arts initiate neurometabolic cascades marked by axonal injury, exaggerated OXINOS, mitochondrial dysfunction, and neurovascular disruption, promoting tau pathology associated with chronic traumatic encephalopathy. By integrating cerebral bioenergetics, hormesis, ischaemic tolerance and traumatic brain injury, this review positions combat sports as a translational model for defining cerebral resilience and the balance between adaptive neuroprotection and cumulative neurological risk.

Psychological stress is a recognised, yet mechanistically unresolved, risk factor for cardiovascular disease (CVD) partly through its association with a hypercoagulable state. Free radical-mediated oxidative stress has been proposed as a key upstream driver of this haemostatic imbalance. In this randomised cross-over study we investigated whether acute psychological stress promotes systemic radical formation and prothrombotic alterations in clot microstructure in eight healthy males. The Trier Social Stress Test was used to induce psychological stress. Antecubital venous blood was collected to measure the ascorbate free radical (A•-, electron paramagnetic resonance spectroscopy) and clot microstructure (Df, Fourier transform rheology), alongside standard coagulometry. Compared with the control condition (quiet sitting), psychological stress increased A•- (P = 0.042) and Df (P = 0.008), the latter reflecting larger, denser and more fibrin-rich networks. We also observed selective shortening of activated partial thromboplastin time (aPTT) (P = 0.018), indicating activation of the intrinsic coagulation pathway. This study provides the first in vivo evidence that acute psychological stress triggers systemic free radical formation and drives prothrombotic remodelling of clot architecture. These findings identify oxidative stress as a mechanistic link between psychological stress and CVD risk and highlight it as a compelling target for prevention and therapy. KEY POINTS: Although psychological stress is a recognised risk factor for cardiovascular disease (CVD), its mechanistic association with a hypercoagulable state remains unresolved. Acute psychological stress, induced by the Trier Social Stress Test (TSST), significantly increased systemic free radical formation, as measured by elevated levels of ascorbate free radical (A•-) via electron paramagnetic resonance (EPR) spectroscopy, and was associated with the formation of larger, denser, more fibrin-rich clots confirmed by increased fractal dimension (Df). The concurrent increase in A•- and Df suggests that free radical-mediated oxidative stress is an upstream driver of psychological stress-induced activation of haemostasis, specifically altering clot quality. The TSST selectively shortened activated partial thromboplastin time (aPTT), indicating activation of the intrinsic/contact coagulation pathway. There were no changes in prothrombin time (PT) or D-dimer, suggesting haemostatic activation occurred without engaging fibrinolysis. The findings demonstrate that even a brief episode of emotional stress can increase thrombotic potential in healthy individuals and identify oxidative stress as a key mechanistic link and a potential therapeutic target for treating stress-related CVD.

Background:Point-of-care ultrasound (POCUS) is integral to emergency department (ED) and pre-hospital medicine, yet evidence comparing its diagnostic and operational performance across environments remains fragmented, especially in cardiovascular emergencies. This review aimed to evaluate and compare the diagnostic performance, workflow impact, and clinical influence of POCUS for six major cardiovascular emergencies across pre-hospital and ED settings, while examining the effects of operator training, device technology, and governance structures. Methods:A structured scoping review search was conducted using multiple electronic databases to identify adult studies evaluating pre-hospital or ED POCUS in cardiac arrest, cardiac tamponade, acute heart failure, shock, pneumothorax, and aortic dissection. Eligible designs included randomised, prospective, and observational studies reporting diagnostic accuracy, process efficiency, management impact, or outcomes. Data were synthesised comparatively rather than pooled. Results:ED POCUS demonstrated high diagnostic accuracy (typically >85-90%) and shortened time to diagnosis or intervention by 30-70 minutes in acute heart failure, pneumothorax, tamponade, and dissection representing meaningful process improvements. However, as seen in conditions like undifferentiated shock, these process gains do not consistently translate into improved patient-centred outcomes such as survival or reduced hospital length of stay. Pre-hospital POCUS achieved adequate views in 70-90% of cases and frequently changed triage or destination decisions (10-50%), though mortality effects were neutral across studies with follow-up data. Cardiac-arrest POCUS provided strong prognostic value but required disciplined choreography to avoid interrupting compressions. Device miniaturisation and brief targeted training enabled field feasibility, while structured curricula, image archiving, and quality assurance (QA) underpinned safety and accuracy. Conclusions:POCUS consistently improves diagnostic efficiency and decision-making in both ED and pre-hospital settings. However, evidence that these gains translate into improved patient-centred outcomes remains limited. Future research should focus on protocolised POCUS pathways integrated with governance structures and system-level responses.

This narrative review compares and contrasts the most commonly encountered environmental stressors on human cerebrovascular functioning. From high altitude and space, extreme apnoea, heat and cold stress, the impact of these stressors on the regulation of cerebral blood flow (CBF) and oxygen metabolism ( CM R O 2 ${\mathrm{CM}}{{\mathrm{R}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ ) is discussed. As long as consciousness remains, CM R O 2 ${\mathrm{CM}}{{\mathrm{R}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ and oxygen delivery ( C D O 2 ${\mathrm{C}}{{\mathrm{D}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ ) remain stable during acute and chronic exposure to poikilocapnic hypoxia. Such a response is possible with alterations in CBF to maintain a relatively stable C D O 2 ${\mathrm{C}}{{\mathrm{D}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ . Likewise, the elevations in CBF during exercise in conditions of acute and chronic hypoxia seem to be appropriate to maintain stable CM R O 2 ${\mathrm{CM}}{{\mathrm{R}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ . In freedivers, prolonged periods of apnoea during breath-hold reflect marked hypoxaemia and acidosis. At these extremes in elite human freedivers, although elevations in CBF seem to maintain C D O 2 ${\mathrm{C}}{{\mathrm{D}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ , there is evidence of reductions in CM R O 2 ${\mathrm{CM}}{{\mathrm{R}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ . In contrast to hypoxia, heat- or cold-induced hyperventilation and related hypocapnic-induced vasoconstriction, marked reductions in CBF and C D O 2 ${\mathrm{C}}{{\mathrm{D}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ can occur. In the cold, however, the reductions in CBF seem to be partly compensated by elevations in blood pressure and haemoconcentration. In the heat, Q10-mediated elevations in CM R O 2 ${\mathrm{CM}}{{\mathrm{R}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ are challenged by cerebral vasoconstriction and limited C D O 2 ${\mathrm{C}}{{\mathrm{D}}_{{{\mathrm{O}}_{\mathrm{2}}}}}$ , especially when hyperventilation is pronounced. Furthermore, intracranial velocity seems stable during spaceflight despite elevations in P aC O 2 ${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ . The implications of these changes in CBF and metabolism during environmental stressors are considered in the context of neuropsychological functioning. Finally, the limited research on cross-exposures on cerebrovascular function is reviewed, and future research directions are proposed.

Background Acute type B aortic dissection (TBAD) has traditionally been classified as either complicated or uncomplicated, guiding management toward urgent intervention or optimal medical therapy with surveillance. However, growing evidence suggests that this binary framework inadequately captures the biological and haemodynamic heterogeneity of the disease. A subset of patients initially classified as uncomplicated demonstrates clinical or radiological features associated with adverse outcomes, commonly described as "high-risk" uncomplicated TBAD.Methods A structured narrative review was conducted to synthesise contemporary evidence relating to clinical predictors, imaging markers, and outcome data in TBAD. Major observational studies, meta-analyses, guideline statements, and recent registry data were evaluated to examine the pathophysiological basis and prognostic significance of high-risk features and their implications for disease classification and management.Results Accumulating data indicate that TBAD represents a dynamic continuum of haemodynamic and morphological instability rather than discrete clinical categories. Clinical markers such as refractory pain and persistent hypertension provide early indicators of potential instability but demonstrate limited specificity. In contrast, imaging findings, including false lumen diameter, entry tear geometry, true lumen compression, and aortic diameter, more reliably reflect underlying biomechanical stress and risk of progression. Contemporary outcome studies and meta-analyses suggest that thoracic endovascular aortic repair promotes favourable aortic remodelling and may improve survival in selected patients with high-risk disease, although heterogeneity in patient selection remains substantial.Conclusions High-risk uncomplicated TBAD likely represents a transitional phenotype within a broader spectrum of disease progression. Moving beyond binary classification toward integrated clinical, imaging, and haemodynamic risk stratification may enable more precise identification of patients who would benefit from early intervention while avoiding overtreatment in stable disease.

Dr Florence Buchanan (1867-1931) was one of physiology's foundational women. Trained as a zoologist at University College London (UCL), she became an exacting physiologist whose studies of muscle bioelectricity, reflexes, cardiac rhythm and exercise helped shape twentieth-century physiology. She was the first woman to attend a meeting of The Physiological Society, one of its first six women members, a collaborator of Nobel laureates Charles Sherrington and August Krogh, and author of the first paper in The Quarterly Journal of Experimental Physiology, now Experimental Physiology. A Physiological Society 'Blue Plaque' at Oxford commemorates her. Yet although her papers and institutional importance survived, no authenticated photograph was known. We report the discovery of a captioned portrait in a 1941 Buchanan family memoir held by the National Library of Scotland. The memoir restores Dr Buchanan to view as daughter, sister, aunt, friend, teacher, cyclist, colleague and scientist despite her progressive visual impairment. Most strikingly, it records that she dictated her 1901 paper on the electrical response of muscle during three months of enforced bed rest for severe eye disease. We describe the portrait's provenance and memoir evidence, and consider an 1887 UCL practical-zoology classroom photograph with Ray Lankester documenting her training environment. Because she studied there during this period, she may be among the three women students pictured, but no individual can be identified as her. The discovery restores not only a face but scale, texture and presence to a scientist whose work endured more visibly than our knowledge of the woman herself.