**1. Introduction**

Stress can be defined as any sensation that indicates physical, psychological, or physical-psychological discomforts [1–3]. Climaxing stress is the sensation of discomfort and the sensations may be described as unimodal when one major sensation of discomfort is involved [2]. Psychological sensations of discomfort may be characterized by emotional and behavioral swings [1]. When there is more than one strain sensation, stress is said to be polymodal. Examples of such are fluctuations in vital signs, body functions, and physical states manifesting as digestive disorders (diarrhea, vomiting, and nausea), headache, hyperthermia, palpitations, muscle fatigue, aches, and reduced libido [2] among others. Gravitational stress can cause dizziness, pedal pain, muscle fatigue, anger, and sleep deprivation. It is important to add that stress occurs when there is a deviation from what the body has perceived as normal or homeostatic. In fact, it is typically characterized by a non-specific response to any deviation from the homeostatic state.

Any strain sensations occurring either physically, psychological, or both in relation to one's job or profession is referred to as occupational stress [3]. Occupational stress is a type of stress that occurs when employees are overwhelmed by the dictates of their jobs or by institutional, organizational, and personal targets. Usually, the stress ensues when demands, expectations, and projections are incapable of being met at the set time. Switching from one job to another and exposure to long working periods are heavily implicated in occupational stress. Occupational stress also bouts where and when employees feel inadequately rewarded, appraised, and motivated [3]. During occupational stress, hemodynamic changes occur such that blood is diverted more to the central nervous system and some skeletal muscles at the expense of other body systems. This invariably results in cerebral vascular changes, and headache, among others culminating in increased sleep latency and delay in sleep onset. It is not unusual that the hypothalamo-hypophyseal-adrenal axis is activated leading to the release of cortisol. The sympatho-adrenal axis, the rapid response mechanism, is unarguably largely perturbed during occupational stress, manifesting as an increase in epinephrine, norepinephrine, and dopamine levels [4]. Non-hormonal consequences of sympatho-adrenal activation include increases in heart rate, respiratory rate and blood pressure, blood glucose, blood urea nitrogen, urine specific gravity, changes in heart rhythms, skin conductance, and sleep disturbances. Others include changes in brain activities and mood swings. Long-term exposure to occupational stress results in musculoskeletal impairments and cardiovascular adversities. Apart from musculoskeletal and cardiovascular impairments, occupational stress has a connection with posttraumatic stress syndrome, anxiety, depression, drug misuse, and insomnia [5]. Occupational stress is one of the underlying causes of morbidity and mortality [2], responsible for around 10% of job-induced ailments and diseases [6].

Sleep disruption, as one of the features of occupational stress, can be described as an impediment to normal sleep pattern. It has been implicated in occupational stress-induced injuries, accidents, and diseases [5, 6]. COVID-19 (severe acute respiratory syndrome-2) is a transmissible disease of the viral clan that belongs to the Coronaviridae family [7–10]. It is caused by a new coronavirus strain that was discovered in 2019 in Wuhan, China. COVID-19 has affected millions of people worldwide [7–9]. It has claimed many lives globally [7–10]. The disease is contagious and can be contracted through respiratory droplets, contact, and interface with COVID-19 contaminated surfaces [11, 12]. Currently, there is no specific cure but COVID-19 patients benefit from secondary treatments though vaccines are now available to induce an active artificial immune defense [12].

COVID-19 outbreak created huge pressure on frontline health workers owing to many reasons [12, 13]. First, the novelty of the disease elicited an unprecedented increase in the number of healthcare seekers from the usual counts. Since there was no specific forewarning and preparation across the globe in terms of boosting the

*Occupational Stress-Related Sleep Anomaly in Frontline COVID-19 Health Workers… DOI: http://dx.doi.org/10.5772/intechopen.109148*

capacity of healthcare providers, hospital facilities, diagnostic and management sectors, the whole tension mounted on healthcare personnel. In fact, there was a subjective increase in expectation of health seekers and the general public from the healthcare providers. Another important concern was the contagiousness of the disease. All of these culminated significantly in mounting tension on healthcare providers resulting in adverse health consequences including alteration in their normal sleep pattern. Many primary studies have been done to examine the sleep pattern of healthcare providers during COVID-19. The review was designed to highlight the possible mechanisms that underlie occupational stress-related sleep impairment in frontline healthcare workers during COVID-19 outbreak.

### **2. Methodology**

A narrative literature search was done using Web-based databases like Google Scholar, Pubmed, Scopus, and Web of Science. The search was done using several terms and text words such as occupational stress, COVID-19, sleep, sleep disorders relating to occupational stress, sleep mechanisms and stress. Inclusion and exclusion criteria were set to filter relevant articles. Articles that were not directly related with the topic are excluded. Each of the filtered articles was independently examined to ascertain the eligibility to the study.

### **3. Structure of human stress control**

Although stress response is not specific, there are distinct neural and non-neural mechanisms that are in charge. These can be divided into intrinsic and extrinsic stress controls with the latter modulated by the former.

### **4. Intrinsic stress control**

The intrinsic stress control includes brainstem, hypothalamus, noradrenergic neurons, histaminergic neurons, orexinergic neurons, opioid peptide-secreting neurons, serotonergic neurons, corticotropin releasing hormone (CRH)—secreting neurons, cholinergic neurons and dopaminergic neurons of the brain [14, 15].

Dopaminergic pathways including the mesolimbic and tuberoinfundibular dopamine pathway are influenced by stress. Signal from tuberoinfundibular dopamine pathway is widely known to cause inhibition of prolactin secretion. This is mediated through the interaction of dopamine with the D2 receptor on the surface of lactotrophs via decreased cyclic adenosine monophosphate. The absence of dopamine removes inhibition on prolactin secretion.

Conversely, increased prolactin secretion occasioned by stress represents a response to an increase in metabolic demand and hypoglycemia [16]. Although the specific contribution of prolactin during stress is not well understood, the hormone may increase blood glucose. It may also act on the brain and elicits a euphoric state, thereby helping relieve stress [17]. Despite insufficiency of evidence from human studies, a study has shown that prolactin may increase erythrocyte count in mice [18]. An increase in erythrocytes during stress is an important compensatory mechanism as it leads to an improvement in tissue oxygen supply.

Ghrelin level has been reported to increase during stress [19]. Ghrelin acts on the hypothalamus to induce secretion of growth hormone releasing hormone (GHRH) and inhibit growth hormone inhibiting hormone (somatostatin). GHRH in turn binds with its receptors on somatotroph causing growth hormone secretion. Growth hormone mobilizes free fatty acid and reduces peripheral tissue utilization of glucose. These actions help in maintaining blood glucose for ATP production. Another hormone elicited by stress is glucagon. Like growth hormone, glucagon helps in maintaining blood glucose levels.

Other intrinsic stress controls include increased levels of prostaglandins E2 [20], arginine vasopressin, heat shock proteins, interleukins-6, 10, and 19 [21] and adrenal progesterone [22]. Increased level of adrenal progesterone during stress might help in improving blood flow since progesterone is a vasodilator. However, it is unlikely the increased adrenal progesterone affects extracellular progesterone significantly under physiological conditions especially during active reproductive life. Like progesterone, adenosine is another chemical messenger that has been reported to increase during stressful situations [23].

The outcomes of stimulation of intrinsic stress control include modulation of stress which can manifest as increase in mood, stress-alleviating behavioral changes (like swaying or sitting down after prolonged standing), alterations in consciousness and sensory perception, change in blood flow, and maintenance of energy production among others.

### **5. Extrinsic stress control**

The extrinsic component consists of autonomic-adrenal medulla axis, which connects the spinal cord and lower brain areas to peripheral organs through adrenal medulla. Epinephrine and norepinephrine secreted from the medium exert their effect on peripheral organs by binding with adrenergic receptors [4] and the effects are discussed in **Table 1**.

Another part of the extrinsic neural stress control is the hypothalamic-corticotropin-adrenal cortex axis. The parvocellular neurosecretory cells of the paraventricular nucleus of the anterior hypothalamus communicate via arginine vasopressin with the corticotroph of adenohypophysis to form a central unit [15, 24]. Unlike the autonomic-adrenal medulla axis, the axis connects the control area with the peripheral organs through the adrenal cortex. Glucocorticoid and dehydroepiandrosterone sulfate (DHEAS) released from the adrenal cortex bind with their expressed receptors in the peripheral organs.
