Open access peer-reviewed chapter - ONLINE FIRST

Impacts of Environmental Stressors on Autonomic Nervous System

Written By

Mayowa Adeniyi

Submitted: November 26th, 2021 Reviewed: December 1st, 2021 Published: January 23rd, 2022

DOI: 10.5772/intechopen.101842

IntechOpen
Autonomic Nervous System - Special Interest Topics Edited by Theodoros Aslanidis

From the Edited Volume

Autonomic Nervous System - Special Interest Topics [Working Title]

Dr. Theodoros Aslanidis and M.Sc. Christos Nouris

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Abstract

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.

Keywords

  • stress
  • autonomic nervous system
  • hormonal stress markers
  • nonhormonal stress markers

1. Introduction

The autonomic nervous system is a nervous control saddled with the regulation of vegetative functions, moderating homeostatic processes in the body. It mediates growth, reproduction, digestion, respiration, blood pressure, heart rate, thermoregulation, osmoregulation, penile tumescence, maintenance of glucose, and electrolyte balance in the body. It connects the peripheral organs in the body with the central nervous system. The autonomic nervous consists of the parasympathetic nervous system and the sympathetic nervous system.

The parasympathetic nervous system plays important role in the homeostasis and restoration of homeostasis. It is evoked during rest and relaxation. Parasympathetic signals are transmitted from one neural cell to another cell through cholinergic nerve endings. Examples of such nerve endings include preganglionic cholinergic nerve fibers, postganglionic cholinergic nerve fibers, and preganglionic sympathetic cholinergic nerve fibers and postganglionic sympathetic cholinergic nerve fibers. The acetylcholine released by parasympathetic nerve fibers binds with muscarinic receptors (m1-m5) to elicit specific responses.

In some cases, parasympathetic activities are not directly mediated by acetylcholine but by other chemical messengers. For instance, the cholinergic nerve endings to cavernosal arterioles increase the expression of nitric oxide synthase leading to the secretion of nitric oxide causing vasodilation and increased blood flow to penile erectile tissues. Vagal nerve endings in the stomach secrete nitric oxide leading to expansion of the stomach before the arrival of bolus (receptive gastric relaxation) and relaxation of the stomach in the presence of bolus (adaptive gastric relaxation).

The parasympathetic nervous system originates from the cranial nerves and sacral segments of the spinal cord (craniosacral outflow). Usually, the preganglionic parasympathetic cell bodies are situated in the cranial nerves and sacral segments of the spinal cord. However, the parasympathetic ganglia are located close to the effector structures. This makes the postganglionic nerve fibers shorter. Examples are otic ganglion, sphenopalatine ganglion, submaxillary ganglion, ciliary ganglion, among others. Effects of parasympathetic innervation may either be excitatory (involving the development of excitatory postsynaptic potential) or inhibitory. Examples of the inhibitory effects of parasympathetic stimulation include decreased heart rate, the force of cardiac contractility, and blood pressure. Other effects include miosis, increased gastrointestinal motility and secretion, peripheral vasodilation, increased cutaneous blood flow, penile, and clitoral tumescence among others.

The sympathetic nervous system evolved to enable organisms to cope with the emergency, specifically, increased metabolic demand associated with an emergency, flight, and fight. The sympathetic nervous function is executed by the thoracolumbar outflow of the spinal cord and lower brain areas. Unlike the parasympathetic nervous system, the sympathetic ganglia are situated close to the spinal cord and from where postganglionic fibers originate to innervate effectors. The effect of sympathetic stimulation is mediated through binding with adrenergic receptors (alpha and beta receptors). The effects of sympathetic stimulation are increased heart rate and cardiac contractility, increased blood pressure, mydriasis, decreases gastrointestinal motility and secretion, peripheral vasoconstriction among others. It is interesting to note that many phenomena can elicit sympathetic nervous activity. One of them is stress.

Stress is a perception of physical, psychological, or physico-psychological strains or discomforts. During stress, the discomfort perceived physically, psychologically or physical-psychologically represents deviations from what the human body has recognized as normal. Stress is characterized by a nonspecific physiological response to stressors, stress-inducing phenomena. Stress-inducing phenomena can be defined as environmental insults, such as perturbed levels of light, temperature, chemicals, ambient oxygen, and noise. In terms of rapidity of physiological response to stress, the chemical messenger-mediated sympathetic nervous system including the autonomic-adrenal axis plays a major role. Furthermore, the chemical messenger-mediated sympathetic nervous system is a determinant of nonhormonal effects which are often used as general stress markers, such as change in heart rate, heart rate variability, blood pressure, body temperature, blood glucose, baroreflex sensitivity, skin conductance, among others. The chapter looks at different forms of environmental stressors and their autonomic characterizations.

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2. Stress

Stress is a perception of physical, psychological, or physico-psychological strains or discomforts. Stress as a sensation of discomfort may be subjective, that is, qualitative. For instance, during a prolonged examination procedure, a student may report having muscle ache or nausea without any confirmatory screenings. In objective cases, medical assessments are done to ratify the existence of stress [1]. Examples of these include determinations of catecholamine, cortisol, prolactin, heart rate, blood pressure, body temperature, brain rhythm, cardiac rhythm, blood glucose, respiratory rate, peripheral oxygen saturation, urine specific gravity among others. During stress, the discomfort perceived either physically or psychologically or both represents deviations from what the human body has recognized as normal. For example, sudden standing elicits perception of physical and physico-psychological strains because of the sudden diversion of a large amount of blood to structures below the heart including the lower extremities at the detriment of other structures including the brain. Events such as driving a car, teaching a crowd of students, having sexual intercourse, exposure to high altitude or low atmospheric oxygen tension, exposure to noise, or running a 100meter race and nighttime study [2, 3] will result in the perception of physical and physico-psychological discomfort in naïve individuals. It is important to add that a measure of stress is beneficial for physical fitness and health status. This is simply known as eustress. An example of eustress is exercise, any programmed and purposeful physical activity. This invariably means that it is not all physical, psychological, and psychophysical sensations of discomfort that can be imaged as harmful. For instance, in order to be able to run a marathon race, a high V02 max is needed. Achieving this high V02 max through training is not unassociated with sensations of discomfort. The term “distress” comfortably describes all sensations of discomfort either physically, psychologically or both that are not beneficial to human health and survival [4].

Furthermore, sudden standing, driving a car for the first time, acute exposure to high altitude or low atmospheric oxygen tension, exposure to unfamiliar noise, or executing new physical tasks like running a 100meter race, clearly indicate that stress is part of man. If stress is part of man, then, are there natural defensive, protective, and modulatory mechanisms that come into play during stress? The human body was designed to respond to stress nonspecifically through two mechanisms and they are hormonal and nonhormonal mechanisms. Hormonal mechanisms operate through the autonomic-adrenal axis, hypothalamo-hypophyseal-adrenal axis, tuberoinfundibular dopamine axis, and autocrine, paracrine, and neurohormonal pathways. The nonhormonal mechanisms are outcomes of hormonal mechanisms. Examples include changes in heart rhythms, blood pressure, skin conductance, blood glucose, body temperature, respiratory rate, peripheral oxygen saturated among others.

Any agents or conditions that orchestrate deviations from what the human body has recognized as normal or homeostatic are known as a stressor. They are stress-inducing situations and events [1]. These agents may be exogenous, chemical, and biological. Information made available by Study.com indicates hyperthermia results in discomfort. In diurnal mammals, secretions of melatonin predicates photic signals. Hence, disruption of photic signal and photic stress impairs melatonin secretion resulting in circadian desynchronization, impaired glucose homeostasis [2, 3], weight gain, diabetes mellitus, sexual disorder, and breast cancer [3]. Thermal changes, unfamiliar noise, job-related mental and physical exertions [4], job loss, increase in expected work output, overcrowding, marital problem, irregular lighting, bereavement, barotrauma, traveling, exposure to low atmospheric oxygen, economic hardship, heightened family needs and demands, drug and chemical use, and abuse are stressors. Hence, they demonstrate a huge tendency of triggering certain effects. The effects produced depend on the type of stressor. For instance, metabolic perturbation and cytokine production can be produced by chemical stressors. Intake of tobacco brings about an increase in metabolic rate causing tachycardia, palpitation, tachypnea among others. Alcohol induces secretions of cytokines such as dopamine, endorphin, and serotonin secretion resulting in motivation and addiction. Direct and indirect trauma on the body tissues such as epithelium, muscles, connective tissues, and neural structures and pain-mediating cytokines such as substance P and glutamate are results of both physical and chemical stressors. Both physical and chemical stressors may activate hormonal mechanisms through the autonomic-adrenal axis, hypothalamic hypophyseal-adrenal axis, tuberoinfundibular dopamine axis, autocrine, paracrine, and neurocrine pathways resulting in the release of norepinephrine, dopamine, cortisol, prolactin, prostaglandins interleukin-6, leptin, dehydroepiandrosterone, salivary alpha-amylase, alpha tumor necrosis factor, ghrelin, and growth hormone. As widely believed, human existence has always revolved around not only the surroundings but also the conditions of the environment (Psychology second course) [5].

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3. Effect of photic stress on autonomic nervous system

Indiscriminate and prolonged exposure to light has a great deal of impact on the autonomic nervous system. Yasushi et al., [6] examined the effect of exposure to bright light (5000 lux) on sympathetic nervous activity for a period of 20 minutes. The authors reported that exposure increased heart rate while no change was noticed in blood pressure. Muscle sympathetic nerve activity was found to increase after exposure. Sleep is an autonomic phenomenon, Katsanis et al., [7] reported that exposure to color light stimulation shortened time for sleep onset and influence heart rate variability in healthy humans. Specifically, color light preference was found to lower frequency/high-frequency ratio. The study simply indicated that color light preference induces parasympathetic nervous stimulation leading to enhancement of sleep.

To demonstrate the role of dynamic lighting system after fatigue, Maietta et al., [8] utilized a self-reported questionnaire and heart rate variability to measure the autonomic nervous system. There was a rise in parasympathetic nervous mechanisms in the dynamic lighting system within 25 minutes. Heart rate variability means interbeat time interval. Usually, heart rate variability is inversely related to heart rate. This implies the higher the heart rate variability, the small the heart rate. Schaefer and Kraft [9] studied the impacts of light stress courtesy of illumination with a colored fluorescent light on autonomic regulation and heart rate variability. He studies the exposure of 12 healthy individuals to red, blue, and green light (700 lux) for 10 minutes. With a green light, there was a reduction in high-frequency components; thus indicating that illumination with colored light can affect heart rate variability.

Glucose metabolism is influenced by the autonomic nervous system. The islet, the birthplace of insulin and glucagon. is innervated by autonomic nerve fibers. Target tissues, such as the liver, muscles, and adipose tissues, express receptors for these hormones. The expression of these receptors is necessary for the hormone to exert its effects. Hormone resistance or hormone tolerance occurs when there is a reduction in the levels of expressed hormone receptors. Sympathetic stimulation of islet is widely known to increase glucagon secretion. Usually, glucagon, when secreted, is in immature form (preproglucagon) which will become activated through intracellular mechanisms. On the other hand, sympathetic stimulation brings about the breakdown of hepatic glycogen and gluconeogenesis. Exposure to light at night was found to increase glucose intolerance in rats. Specifically, the green light was shown to exert more glucose intolerance. However, blue and red lights did influence glucose intolerance. At 50 and 150 lx, greater glucose responses were produced than 5–20 lx [10]. The study results clearly showed that the intensity of light exposure affects glucose homeostasis.

When C57Bl/6 J mice were placed on constant light in a bid to understand how constant length–induced circadian rhythm abnormality affects energy metabolism and insulin sensitivity, Coomans et al.,[11] showed a pronto decline in the amplitude of circadian rhythm. Energy expenditure fell by −13% and food intake rose by +26% culminating in pronto weight gain. Energy metabolisms, insulin sensitivity, and endocrine functions of the islet are autonomically controlled processes. Parasympathetic stimulation of the pancreatic islet through m4 receptors results in a CAMP-mediated increase in the secretion of preproinsulin, which will then be converted to insulin. In the quantification of insulin sensitivity, it is not only insulin secretion that receives consideration. Insulin sensitivity which examines the responsiveness of target tissues to insulin is essential. Insulin sensitivity involves both the reception of insulin by target tissue and associated transduction.

Similarly, a study by Abulmeaty et al.,[12] investigated the impact of prolonged continuous exposure on energy homeostasis as well as adropin expression, RORα, and Rev-erb-α nuclear receptors in 32 rats over a period of 3 months. Continuous light exposure was found to raise total energy expenditure. Lowered respiratory quotient and Rev-erb-α hepatic and renal nuclear receptors coupled with elevation in RORα and plasma levels of adropin and expressions. The study indicated the possible involvement of adropin, RORα, and plasma levels of adropin in energy homeostasis. The parasympathetic nervous system is a component of the autonomic nervous system concerned with energy restoration and homeostasis.

Melatonin secretion is an autonomically dependent process. The pineal-innervating postganglionic fibers from the superior cervical ganglion are known to secrete norepinephrine. Elsaid and Fahim [13] showed that maternal exposure to excess artificial light using female rabbits orchestrated a decline in maternal melatonin. In addition, epidermal vacuolation, swollen mitochondria, and shrunken indented nuclei were gotten. As far as the fetus was concerned, reduced thickness of the epidermis, decreased hair follicle number, raised collagen surface area, suppressed proliferating cell nuclear antigen-positive cells were gotten. It is possible that excess light-induced suppression of melatonin is responsible for maternal and fetal histological changes in the study. Furthermore, light also influences body temperature and the reproductive cycle. Specifically, in rodents’ study, exposure to light stress has been shown to lengthen the estrous cycle and estrous cycle ratio [2, 3, 14] and impairs body temperature rhythm [15]. Light exposure may also influence the activities of antioxidant enzymes. At least, a study has shown that ovarian glutathione peroxidase increased in light-deprived rats [16].

Sleep is another autonomically controlled mechanism. Sympathetic nervous stimulation through activation of alpha or beta receptors results in increased cortical activities, thereby promoting alertness. On the other hand, the parasympathetic nervous system elicits a reduction in cortical activities, eliciting rest and sleep. Stenvers et al.,[17] reported a novel means of creating circadian desynchronization in rats. In their study, they exposed rats to 12-hour of light with the intensity of 150–200 lux and natural 12 hours of dark or 12-hour light (150–200 lux) and 12-hour dark (5 lux). The amplitude of REM and NREM sleep rhythms was attenuated with 12 hour-light (150–200 lux) and 12-hour dark (5 lux). Although 12-hour light (150–200 lux) and 12 hour-dark (5 lux) did not affect glucose tolerance and body weight, there was a reduction in suprachiasmatic expression of the clock gene and desynchronized locomotive activity.

Ishida et al., [18] showed that exposure to light orchestrated the expression of the adrenal gland gene and the underlying mechanism involved suprachiasmatic nucleus-sympathetic nervous system connection. One of the most extensively documented suprachiasmatic nucleus-sympathetic nervous system connections is the retinohypothalamic-pineal gland pathway, through which ambient light passes through intrinsically photosensitive mesopic retinal ganglionic cells to the suprachiasmatic nucleus of the anterior hypothalamus and from there to the pineal gland via superior cervical ganglion. Before the advent of the electric bulb in 1860, human functions were governed by the natural light/dark cycle that consisted of 12 hours of daylight and 12 hours of dark. Cailotto et al., [19] reported that exposure to nocturnal light exerted a rapid effect on peripheral clock gene expression with autonomic hepatic innervation being found to be essential for the photic signals from the suprachiasmatic nucleus.

Kalsbeek et al., [20] identified gamma aminobutyric acid (GABA) as the endogenous mechanism involved in the transmission of photic signals from the suprachiasmatic nucleus to the pineal gland. In the study, the authors showed the role of the chemical messenger by administering GABA antagonist to some parts of the suprachiasmatic nucleus. The presence of GABAergic projection between ventrolateral and dorsolateral parts of the suprachiasmatic nucleus has also previously been reported.

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4. Effect of thermal stress on autonomic nervous system

Exposure to thermal stress has a profound effect on the autonomic nervous system. Niimi et al., [21], in a study, examined the effect of heat stress on the sympathetic nervous system in human subjects on the sympathetic nervous system. Nine subjects were deployed for the study and they were exposed to heat stress through the rise in environmental temperature gradually from 290°C to 400°C. Muscle sympathetic nerve activity, tympanic temperature, plasma arginine vasopressin, cutaneous blood flow, heart rate, blood pressure, cardiac output, and mean arterial blood pressure were monitored. The rise in muscle sympathetic nerve activity, tympanic temperature, cardiac output, mean arterial blood pressure, and cutaneous blood flow were recorded when heat stress was applied. Crandall et al., [22] exposed seen subjects to whole-body heating through the infusion of 15 ml/kg of warm water. Skin blood flow, heart rate, arterial blood pressure, muscle sympathetic nerve activity, and sublingual temperature were measured. The authors observed that thermal exposure raised muscle sympathetic nerve activity but central venous blood and mean arterial blood pressure were unaffected. However, mean arterial pressure was found to increase when the effect of arterial baroreceptor loading on muscle sympathetic nerve activity during heat stress was conducted. Low et al., [23] examined the possibility that a shift from moderate to severe thermal stress would raise muscle sympathetic nerve activity and sympathetic nerve activity continuously. Thirteen subjects were made to undergo passive thermal stress that raised body temperature by 1.3°C. There was a rise in mean cutaneous temperature. Mean body temperature, heart rate, and skin vascular conductance by thermal stress exposure. There was also a transient increase in muscle sympathetic nerve activity with thermal stress. Cui et al., [24] investigated the role of thermal stress in the alleviation of muscle sympathetic nerve activity during gravitational stress. The authors found that there was a rise in sublingual temperature, sweat rate, cutaneous blood flow, heart rate, and muscle sympathetic nerve activity during whole-body heating. However, the rise in muscle sympathetic nerve activity which occurred in response to gravitational stress was not assuaged by thermal stress in human subjects. Cutaneous heating depressed the high-frequency component of heart rate variability but raised the ratio of low-to-high frequency component and mayer waves. However, there was no increase in baroreflex sensitivity with cutaneous heating [25]. Kaho et al., [26] investigated how thermal stress affects heart rate variability in freely moving ruminant animals. They measured autonomic nervous system markers such as heart rate variability, temperature-humidity index, among others. Heart rate variability was reported to decline with temperature-humidity index. Their study showed that high thermal stress may affect the autonomic equilibrium of ruminant organisms by inducing the sympathetic nervous system nonlinearly. Wilson and Ray, [27] reported that whole-body heating raised heart rate, internal temperature, and muscle sympathetic nerve activity but mean arterial blood pressure was unaffected.

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5. Effect of chemical stress on autonomic nervous system

Chemical stressors such as exogenous chemicals have an influence on the autonomic nervous system. Geraldes et al., [28] reported increased chemosensitivity as well as baroreceptor reflex disruption, sympathetic hyper-excitation, increased heart rate, and high blood pressure. Shvachiy et al., [29] investigated the impact of intermittent exposure to lead on autonomically controlled body functions such as cardiovascular and respiratory functions. High blood pressure, impaired baroreflex sensitivity and tachypnea were recorded following intermittent exposure to lead. In addition to the fact that chemical stressors suppressed parasympathetic actions in infancy and childhood, the effect may be scourged even during intrauterine life. Jurczyk et al., [30] in their review showed that prenatal exposure to alcohol decreased heart rate variability. Prolonged alcohol exposure has been linked with an increased risk of heart disease [31]. Decreased heart rate variability implies a high heart rate. Yu et al., [32] intended to examine the association between blood lead and autonomic nervous activity (heart rate variability and median nerve conduction velocity in 328 adult males aged 28 years. The authors found no association between blood level concentration and autonomic nervous activity. Liao et al., [33] reported that there was an association between exposure to airborne heavy metals and autonomic dysfunction in 82 young adults. Other airborne chemical stressors which have been reported to impair autonomic nervous activity, raising systolic blood pressure and diastolic blood pressure and disturbing other autonomically controlled structures include dust [34], cadmium [35], aluminum [36], lead [37], and oil spillage [38].

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6. Effect of hypoxic stress on autonomic nervous system

The environment is the primary source of oxygen in the body. Hypoxic stress represents the sensation of discomfort associated with exposure to the low partial pressure of oxygen. Exposure to high altitudes (3000–4000 m) has been reported to lead to depression of heart rate variability power spectra [39]. Exposure to hypoxia and hypercapnia has been reported to raise sympathetic burst frequency. However, hypoxia was found to produce a long-lasting effect on sympathetic activation in human subjects than exposure to hypercapnia [40]. Excessive hypoxia also causes disruption of peripheral chemoreceptors and hyperviscosity. Hyperviscosity leads to increased pulmonary blood pressure, right cardiac failure, inadequate brain perfusion, and death [41].

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7. Effect of noise stress on autonomic nervous system

Unlike note, noise is produced when sound waves are emitted from multiple sources. Noise has been reported to impact autonomic nervous activity. Goyal et al., [42] exposed 200 adult males to noise intensity of greater than 80 dB for about 6 months. Noise exposure increased heart rate and systolic blood pressure. Idrobo-Ávila et al., [43] in their systematic review noted that noise exposure increased heart rate and blood pressure and caused alteration in both high frequency and low frequency/high-frequency ratio. Chen et al., [44] examined the connection between occupational exposure to noise and high blood pressure using 1390 workers exposed to occupational noise. The authors reported that noise exposure caused an increase in systolic blood pressure and diastolic blood pressure. According to the study, the prevalence of high blood pressure was found as 17.8% in those who were exposed to noise and 9% in those who were not exposed to noise. Hey also claimed that there existed a stronger regression coefficient between diastolic blood pressure and noise exposure. Noise intensity, cumulative noise exposure, and years of exposure were related to high blood pressure risk. de Souza et al., [45] claimed that exposure to noise was associated independently with high blood pressure at 75–85 dB. The study recruited 1729 subjects who were petrochemical workers. The authors also found that age, body mass index, and gender were associated with high blood pressure independently. A study by Brahem et al., [46] was conducted on 120 electricity workers who were exposed to noise. Prevalence of high blood pressure was found in workers who were exposed to noise. Systolic blood pressure and diastolic blood pressure were higher in workers who were exposed to noise. Kuang et al., [47] showed that increasing years of exposure to occupational noise increased systolic blood pressure and diastolic blood pressure.

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8. Summary

Environmental stressors such as ambient threshold changes in light, heat, noise atmospheric oxygen, and chemical phenomena have a great impact on the autonomic nervous system causing impairment in general stress markers. Environmental stressors orchestrated an increase in systolic blood pressure, diastolic blood pressure, mean arterial blood pressure and disrupted baroreflex sensitivity in both males and females. Derangement in body temperature and blood glucose and suppression of melatonin were also consequences of environmental stressors in both human beings and animals. Future studies will examine in detail the molecular mechanisms that underlie environmental stressor-induced changes in general stress markers.

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Written By

Mayowa Adeniyi

Submitted: November 26th, 2021 Reviewed: December 1st, 2021 Published: January 23rd, 2022