Stress can be described as the perception of discomforts physically, psychologically, or physico-psychologically. During stress, the perceived discomfort indicates there is a deviation from homeostasis. In stress, there is a nonspecific physiological response to stressors, a group of stress-inducing phenomena. Stress-inducing phenomena can be defined as environmental insults, such as perturbed levels of light, temperature, chemicals, ambient oxygen, and noise. Response to stress occurs via the chemical messenger-mediated sympathetic nervous system including the autonomic-adrenal axis. Furthermore, the chemical messenger-mediated sympathetic nervous system determines nonhormonal effects which are often devised as general stress markers. Examples of general stress markers include changes in heart rate, heart rate variability, blood pressure, body temperature, blood glucose, baroreflex sensitivity, among others.
Part of the book: Autonomic Nervous System
COVID-19 is a highly contagious viral illness that has claimed millions of lives worldwide. Since its emergence, it has exerted a negative impact on many sectors globally without the exception of frontline COVID-19 healthcare providers. Specifically, in frontline COVID-19 healthcare workers, occupational stress-related sleep disorders such as insomnia and daytime somnolence have been extensively reported and were characterized by neuro-immunological changes. However, the possible mechanisms that underlie the sleep disorders have not been elucidated. The review was designed to highlight possible sleep mechanisms responsible for insomnia and daytime somnolence reported in frontline COVID-19 health workers. Available evidence shows that emotional perturbation, hypertension, chronobiological disruption and prolonged exposure to artificial light are among the events orchestrating occupational-stress-related sleep disorders in frontline COVID-19 healthcare workers. Anxiety-associated sleep anomaly is attributable to stimulation of the reticular activating system which occurs as a result of activation of noradrenergic fiber and sympatho-adrenal axis. Another mechanism includes depletion of hippocampal and brain glycogen by anxiety-induced activation of corticotropin releasing hormone (CRH)-secreting brain neurons and hypothalamic-corticotropic-adrenal cortex axis. Spontaneous discharge of noradrenergic fiber during basal state and changes in normal secretory rhythm of hypnosis-related chemical messengers may be responsible for hypertension- and chronobiological disruption-induced sleep disorders, respectively. Lastly, prolonged light exposure-induced suppression of melatonin secretion may elicit disruption of normal circadian sleep.
Part of the book: Identifying Occupational Stress and Coping Strategies
Physiological processes exhibit distinct rhythmic patterns influenced by external cues. External cues such as photic signal play an important role in the synchronization of physiological rhythms. However, excess of or indiscriminate exposure to photic signals exerts profound effects on physiological processes, disrupting normal hormonal secretory rhythms, altering sleep/wakefulness cycle, and impairing reproductive function. Alteration in sleep/wakefulness cycle, impairment in reproductive cycle, and disruption of normal hormonal secretory rhythms characterize risk groups for photic stress such as night workers, trans-meridian travelers, and night-active people. Evidence from primary studies is increasing on the tendency of selenium to reset internal biorhythms by targeting circadian proteins and melatonin. The review highlights the chronobiological roles of selenium.
Part of the book: Selenium and Human Health