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Se ha analizado, mediante un diseño cuasi-experimental con 19 sanitarios (33.7 ± 5.1 años), la importancia de la condición física, cognitiva y el rendimiento al portar un equipo de protección con mascarilla quirúrgica durante situaciones de entrenamiento en contextos significativos de intervención militar. Se midieron la frecuencia cardíaca y su variabilidad, los niveles de glucosa, la termorregulación, la fuerza explosiva y el esfuerzo percibido en tareas de rendimiento motor específicas (tapping test, torniquete, municionamiento), y de rendimiento cognitivo y decisional (triaje). Los resultados indican diferencias significativas (p < 05) en función de la condición física (glucemia y fuerza explosiva), del género (fuerza explosiva y torniquete), del hábito tabáquico (esfuerzo percibido) y del cuerpo de pertenencia (nivel de glucemia) en el grupo de estudio. Como conclusión, se destaca la importancia del entrenamiento físico y psicológico para la mejora de la respuesta operativa en situaciones sanitario-militares que requieren el uso de mascarilla quirúrgica.

IntroductionSpecialists in biology, medicine, and psychology need to pay special attention to theoretical and practical research on the implementation of the fight or flight mechanism in humans in conditions of war and hostilities. Adaptation mechanism of fight or flight is related to individual and social forms of behavior among people and animals, and is aimed at the homeostasis preservation in difficult living conditions. The evolutionary fight or flight mechanism in the functional connection with stress as a general adaptation syndrome and stress reactivity has individual features due to the strengthening of the functions of certain body systems. The systemic mechanism of fight or flight is accompanied by the corresponding functional and clinical symptoms and significantly influences physical and mental health of a person in various conditions of activity.ObjectivesIn this regard, the main goal of this work was to determine the relationship between the behavioral strategy of fighting or escaping under stress and during sports activities.MethodsThe following research methods were used to realize the goal of the work: theoretical analysis and generalization of literary sources and Internet data.ResultsIn our opinion, possible versions of Walter Cannon’s concept of the fight-or-flight mechanism are: 1) attack-or-flight mechanism; 2) defense or escape mechanism; 3) pursuit or escape mechanism. At the same time, it is advisable to consider aggression as a struggle, and escape as a struggle. In addition, in line with the concept of Walter Cannon and Hans Selye, it is possible to distinguish the stress of struggle and the stress of flight. Any intense muscle activity is accompanied by changes in the hormonal and nervous regulation of metabolism, as a result of which the body adapts to a certain physical load. In the athlete, these functional changes are observed even before the start of physical exercises, in particular, in the conditions of the pre-start and start state. The nature and reaction of neuro-endocrine mechanisms in the pre-start state depend on the nature of the load, as well as on the individual characteristics of the athlete (age, gender, type of nervous system, temperament, character, training, sports experience, etc.). It is important that the pre-start changes in metabolism contribute to the mobilization of the athlete’s functional potential even before the start of the corresponding physical activity. Moderate activation of the neuro-endocrine mechanisms of the athlete’s body (“combat readiness” state) is optimal. Functionally, it is less beneficial for the athlete’s body to have a sharp strengthening of neuro-endocrine mechanisms (“pre-start fever” state) or their paradoxical inhibition (“pre-start apathy” state).ConclusionsThus, in humans, sports activities include a behavioral mechanism of fight or flight in combination with physiological and psychological stress.Disclosure of InterestNone Declared

This text provides rich evidence of the relevance of the temporal aspects of behaviour. The generalized areas of learning, memory, operant scheduled behaviour, task performance, vigilance, mood and motivation and their rhythmic components are explored in varying detail. The particularized measures range from on-the-job errors, through reading efficiency to milliseconds of change in reaction time in the laboratory. The subjects range from ants to older persons. Across this range of settings, subjects, and behaviours, the message is clear: there is an interaction between time and behaviour.

Key Points Perhaps the most well-replicated biological finding in post-traumatic stress disorder (PTSD) is higher autonomic (heart rate and skin conductance) and facial electromyography responding during internal, mental imagery of the traumatic event and upon exposure to external, trauma-related cues. Higher heart rate responding to sudden loud tones in PTSD probably reflects an acquired sensitization of the nervous system. Diminished volumes of the hippocampus and anterior cingulate cortex are the most frequently replicated neuroanatomic findings in patients with PTSD. These do not appear to be fully explained by comorbid conditions such as substance abuse and depression. Some evidence exists to support both pre-existing vulnerability and neurotoxicity as origins of brain volume reductions in PTSD. On the basis of present data, it is going too far to say that stress damages the brain, but there is no doubt that it changes it. Functional neuroimaging studies suggest that the amygdala and dorsal anterior cingulate cortex are hyper(re)active, whereas the ventral medial prefrontal cortex is hypo(re)active, in PTSD. These abnormalities are likely to underlie the attentional bias towards threat, impaired emotion regulation and persistence of fear memories in this disorder. The classic model of stress based on chronic hyperactivity of the hypothalamus–pituitary–adrenal cortical axis does not characterize PTSD. A number of neurotransmitters and neuroendocrinological factors interact to influence PTSD risk, symptom profiles and severity. These factors vary across individuals owing to genetic and epigenetic factors, as well as within individuals over time in response to environmental influences, including exposure to psychological trauma. As with other mental disorders, genetic vulnerability to PTSD is likely to involve the sum of contributions from multiple alleles, each with small effects. The full range of molecular genetic factors, which include genotype, methylation, histone deacetylation and gene expression, probably influence or accompany the development of PTSD. However, at this time, there are no definitive findings for any one gene or gene system in the aetiology of the disorder. Animal models have identified important molecular pathways that are likely to contribute to the pathophysiology of PTSD and may constitute promising therapeutic targets. Post-traumatic stress disorder is associated with changes in psychophysiological, neuroimaging, endocrinological and genetic measures. Animal studies have begun to elucidate its neurobiological mechanisms. Pitman and colleagues review these findings and discuss directions for research aimed at identifying risk factors, biomarkers and preventive and therapeutic interventions. Post-traumatic stress disorder (PTSD) is the only major mental disorder for which a cause is considered to be known: that is, an event that involves threat to the physical integrity of oneself or others and induces a response of intense fear, helplessness or horror. Although PTSD is still largely regarded as a psychological phenomenon, over the past three decades the growth of the biological PTSD literature has been explosive, and thousands of references now exist. Ultimately, the impact of an environmental event, such as a psychological trauma, must be understood at organic, cellular and molecular levels. This Review attempts to present the current state of this understanding on the basis of psychophysiological, structural and functional neuroimaging, and endocrinological, genetic and molecular biological studies in humans and in animal models.

\"The blush is a ubiquitous yet little understood phenomenon which can be triggered by a number of self-conscious emotions such as shame, embarrassment, shyness, pride and guilt. The field of psychology has seen a recent surge in the research of such emotions, yet blushing remains a relatively neglected area. This unique volume brings together leading researchers from a variety of disciplines to review emerging research on the blush, discussing in depth issues that have arisen and stimulating new theorising to indicate future directions for research. Topics covered include: the psychophysiology of the blush; developmental aspects; measurement issues; its evolutionary significance and the role of similar colour signals in the social life of other species; its relation to embarrassment, shame and social anxiety; and the rationale for and clinical trials of interventions to help people suffering from blushing phobia\"-- Provided by publisher.

The presentation shows the basic principles of exposure as it is used in cognitive behavior therapy. One of the possibilities is to expose phobic subjects to virtual material/video. This presentation discusses the pros and cons of this approach. A solution to one problem is the ability of Procomp Infiniti device to measure the actual level of arousal by psychophysiological measurement and to adapt exposure material based on this measurement. The approach can solve the same problems of virtual exposure by our created stimulus materials provided on CD.

For the most part bodies have been neglected and ignored in psychology, thought of merely as a taxi for the mind, dwarfed by the study of observable behaviour, of action and agency, motivation and performance, or of cognition and emotion. 'Embodied' is a fascinating guide to how we experience our bodies and how our bodies experience the world.

Abstract Introduction: Insomnia has been characterized by state of hyperarousal. Patients with psychophysiological insomnia (PI) worry excessively about not being able to sleep. It disturbs relaxation and PI patients are less and less likely to fall asleep. In current study, we aimed to investigate intrinsic functional connectivity in patients with PI, especially in frontostriatal regions which is known as major nodes of circuit associated with arousal regulation. Methods: Thirteen patients with psychophysiological insomnia (51.0 ± 10.2y, 10 females) and 18 healthy good sleepers (42.7 ± 12.3y, 14 females) underwent resting-state functional MRI scan. We implemented seed-to-voxel functional connectivity analysis using the Harvard-Oxford Atlas as frontostriatal seed regions. Results: Compared with the good sleepers, PI patients showed increased frontal connectivity with the right lateral occipital, right occipital fusiform, right/left lingual gyrus and left amygdala. In addition, increased connectivity between right thalamus and right superior frontal, between right thalamus and right frontal pole, and between right pallidum and precuneus showed in PI patients. Decreased functional connectivity found between right caudate and right frontal pole, and between right pallidum and left lateral occipital in PI patients compared with the good sleepers. The strength of connectivity between the right pallidum and the precuneus in PI patients was positively correlated with the PSQI score (r = .67, p < .05). Conclusion: Current findings provide changes of intrinsic functional connectivity between various corticostriatal regions in patients with psychophysiological insomnia. Particularly, increased couplings with frontal cortex may support the hyperarousal theory in psychophysiological insomnia. Support (If Any): This research was supported by Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education (Study No.: 2013R1A1A2062517) and the Brain Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (Study No.: NRF-2016M3C7A1904336).