Fight-or-Flight Response and The Role of Adrenaline

10 Key excerpts on "Fight-or-Flight Response and The Role of Adrenaline"

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  Stress Management for Life

  A Research-Based Experiential Approach

  • Michael Olpin, Margie Hesson, Michael Olpin(Authors)
  • 2020(Publication Date)
  • Cengage Learning EMEA

    (Publisher)

  The cascade of nervous system activity and release of stress hormones cause immediate physiological responses that help a person deal with or avoid danger by either fighting or running. Harvard physiologist Walter Cannon coined the term fight-or-f light response to describe the body’s automatic response anytime we perceive a threat or danger. This primi- tive response gives us extra strength, power, and speed to avoid physical harm. As you read in Sarah’s story in the opening vignette, the fight-or-flight response can be activated to protect both others and us when we perceive danger. The fight-or-flight response is designed to help us do one thing, and only one thing: survive physical danger! Physiologically, the stress response is characterized by activation of the sympathetic nervous system, which results in the secretion of chemicals into the blood- stream, mobilizing the behavioral response. Whether the reaction culminates in “fight” or “flight” depends on whether we perceive the threat or stressor as surmountable or insur- mountable. Consequently, a stress response that works as it is designed is essential to sur- vival. Figure 3.1 illustrates the fight-or-flight response. Because we are designed for survival, our body systems react to protect us from pain and death in life-threatening or dangerous situations. In the short run, this response is a power- ful and useful process. Scientists use the term homeostasis (homeo 5 the same; stasis 5 standing) to define the physiological and emotional boundaries at which the body functions efficiently and comfortably. Stress disturbs homeostasis by creating a state of imbalance. When we are in homeostasis, we are in a state of balance. We disrupt the balance when something happens in our surroundings—something equivalent to a bear rampaging out of the forest. This per- ception of danger automatically activates the fight-or-flight response.

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  The Body Bears the Burden

  Trauma, Dissociation, and Disease

  • Robert Scaer(Author)
  • 2014(Publication Date)
  • Routledge

    (Publisher)

  The immediate effects of the arousal neurotransmitter norepinephrine on the brain include increased alertness and focus, immediate enhancement of short-term memory, dilatated pupils, increased muscle tone, and divergence (outward movement) of the eyes to expand the field of view. The immediate effects of body-based epinephrine and brain-based norepinephrine prepare the organism for the high-level neuromuscular activity required for ensuring survival in the face of threat—the fight/flight response. These effects promote short-term preparation of the brain for intense alertness, and the neuromuscular and cardiovascular systems for high-level short-term skeletal muscle and cardiac activity and energy expenditure. Activation of the fight/flight response, of course, may be triggered by excitement as well as by threat.

  FIGURE 2.2 Hypothalamic/pituitary/adrenal axis. Sensory input signaling stress or threat (see Figure 2.1 ) activates the hypothalamus, triggering release of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). These promote release of cortisol from the adrenal medulla. Cortisol inhibits further release of ACTH, modulates the basic noradrenergic arousal response, and mediates the long-term stress adaptation response to stress.

  The basic physiological sympathetic nervous system response of the prey in response to threat is mirrored by that of the predator as it prepares for attack. Pre-game jitters, stage fright, sexual arousal, and the thrill of the roller coaster ride all reflect the physical sensations associated with arousal in the face of threat. What separates the experience of the fight/flight response from that of anticipatory excitement, of course, is the meaning of the event to the participant. This piece of information processing takes place in the hippocampus (comparison of new information with past associative memories), and the orbitofrontal cortex (problem solving and planning).4

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  Handbook of Occupational Safety and Health

  • Danuta Koradecka(Author)
  • 2010(Publication Date)
  • CRC Press

    (Publisher)

  These processes enhance vigilance, improve reflexes, and allow quick adaptation of the muscular system to substantial effort requirements (Figure 5.1). The same changes were recorded by Release of noradrenaline from sympathetic neurons and the adrenal medulla Noradrenaline has an e ect mainly on the alpha receptors of e ector cells Response of the organism: - Contraction of vessels of the skin, intestines, and kidneys - Contraction of the spleen - Bristling up (in animals) - Less intense activity of the alimentary tract - Decrease of the concentration of glycogen Response of the organism: - Heart muscle contraction (stronger and faster) - Dilation of blood vessels in the heart and in the skeletal muscles - Dilation of alveoli - Increased activity of the alimentary tract - Decrease of the concentration of glycogen and fats Adrenaline has an e ect mainly on the beta receptors of e ector cells Release of adrenaline from the adrenal medulla ‘Fight or flight’ reactions FIGURE 5.1 Diagram showing stimulation of the adrenal medulla and its physiological consequences, or the ‘fight or flight’ reaction. 90 Handbook of Occupational Safety and Health Cannon after adrenaline injections, proving that this hormone was responsible for the preparation of the organism to respond to a stimulus. The role of adrenaline in the mobilisation of an organism under the influence of strong emotions had already been described by Napoleon Cybulski (1895), a Polish physician and scientist, in the late nineteenth century. Discoveries that laid the foundation for knowledge of the basic mechanisms of adaptation to environmen-tal conditions were popularised in the late twentieth century due to the efforts of a great scientist and physician, Hans Selye (1907–1982).

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  The Handbook of Stress

  Neuropsychological Effects on the Brain

  • Cheryl D. Conrad(Author)
  • 2011(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  A detailed outline of the integration and execution of the various components of the stress response is beyond the scope of this chapter, but what follows is an introduction to the fundamentals of the SNS and HPA axis in relation to stress. At the most basic level, the stress response involves a series of SNS and endocrine responses that aim to restore stability within the body and promote the ability of an organism to deal with a threat. A critical feature of these systems is to mobilize energy resources for instant use while simultaneously inhibiting body functions that are nonessential for immediate survival. Thus, heart rate, blood pressure, and blood glucose levels are elevated while digestive and reproductive processes are curtailed. Inflammation is reduced and pain perception is blunted. The immune response is immediately activated to promote defense, followed by processes put into place to prevent overshoot and the possibility of autoimmune damage. Components of the central nervous system (CNS) are activated, via neurotransmitter, neuropeptide, and hormonal messengers, to enhance learning and memory processes, and to further regulate maintenance of HPA output. Behavioral changes also occur, with organisms experiencing increased arousal and vigilance in order to identify and appraise threats within the environment.

  At the core of an acute stress response is the initiation of the fight-or-flight response, which is characterized by its sympathetic-adrenal medullary components that serve as the first response to prepare the body for the energy resources it will require. Upon experiencing a threatening or stressful situation, the SNS is engaged and stimulates rapid release of catecholamine hormones (i.e., epinephrine and norepinephrine [or noradrenaline]) to direct autonomic processes. Norepinephrine is released from postganglionic fibers onto target organs, providing a local release of norepinephrine (see Figure 1.2

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  Coward

  Why We Get Anxious & What We Can Do About It

  • Tim Clare(Author)
  • 2022(Publication Date)
  • Canongate Books

    (Publisher)

  * The hypothalamus can marshal all sorts of physiological responses throughout your body via the autonomic nervous system, which governs functions like breathing, blood pressure and heart rate. The autonomic nervous system has two branches – the sympathetic and the parasympathetic. The sympathetic nervous system is what gets us pumped up, energised, and ready for action. The parasympathetic nervous system helps settle us down afterwards. If the sympathetic nervous system is responsible for ‘fight or flight’, the parasympathetic deals with ‘rest and digest’ – healing, recovering and refuelling, all essential parts of survival too.

  Current models of the stress response go like this: the hypothalamus receives a signal from the amygdala that there’s a threat (you actually have two amygdalae, one in either hemisphere, but they tend to be referred to in the singular). First, the hypothalamus triggers the sympathetic nervous system, relaying a message to the adrenal glands* way down beside your kidneys to start pumping out adrenaline. Adrenaline speeds up your heart rate, releases stored glucose – thus raising your blood sugar – dilates small airways in your lungs and stimulates your desire to breathe. This process is near-instantaneous, giving us a sudden burst of energy and speed to deal with whatever the danger is.7

  The second part of the response is driven by a collaboration between the hypothalamus, the pituitary gland, and the adrenal gland – together known as the hypothalamic-pituitary-adrenal axis or HPA axis. Stress triggers a hormonal cascade – like a series of molecular dominoes. The hypothalamus releases vasopressin and corticotropin-releasing factor (CRF). CRF then stimulates the pituitary gland to release adrenocorticotropic hormone (or ACTH). ACTH stimulates the adrenal gland to produce glucocorticoids – one of which is cortisol.8

  For our purposes, it’s enough to remember: ‘Stress in – adrenaline and cortisol out’.

  Our heart rate increases. Our muscles tense. Our blood sugar rises. But unless strenuous physical activity follows quickly, these changes feel very uncomfortable. It’s like turning up the heating on an already hot day.

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  The Minder Brain

  How Your Brain Keeps You Alive, Protects You from Danger, and Ensures that You Reproduce

  • Joe Herbert(Author)
  • 2007(Publication Date)
  • WSPC

    (Publisher)

  Chapter 4

  The Brain and Stress

  The idea of a state of stress is not at all new. Suppose we were to measure the heart rate and blood pressure of several people: one had just been told he had lost his job; the other had been attacked by a mugger in the street; a third had just lost a great deal of blood from a bleeding vein; and a fourth was exploring a rather dark, strange place that he found frightening. In all cases we are likely to find that the pulse quickens, the blood pressure rises, the face may grow pale and, were we to measure it, blood levels of adrenaline, the hormone secreted from the inner part of the adrenal gland, had gone up. These changes in the body, all the result of the increasing activity of the sympathetic nervous system, would not tell us which person was which. The sympathetic nervous system is a network of nerves that pass from the brain and spinal cord to activate heart, blood vessels, lungs and gut—it is our general emergency system. Note that the nature of the emergency is not specified; it could be anything that threatens us. Also note that how we react to this threat is not specified either: for example, we could either attempt to deal with it in a variety of ways or try to avoid it and run away.

  This was what Walter Cannon meant, in a famous book published in 1932, when he described the sympathetic nervous system as being activated in readiness for either ‘fight or flight,’ the two very appropriate, but also very different, ways of tackling any (physical) threat. This system activates your heart, blood vessels and glands; it is not under your control. In an acute emergency, the body assumes that you will shortly need every muscle and every bit of attention to make sure you deal with the emergency as effectively as possible. You do not want to deflect unnecessary energy or resources onto parts of the body that are not essential for the immediate threat. This includes the gut: you can digest your lunch later. So you divert blood from other areas to the muscles, and increase your heart rate and blood pressure to drive more blood every precious minute through them. You increase your blood glucose to fuel them with extra energy, and make sure your brain is extremely alert. The sympathetic nervous system does all this for you, very quickly. Since many threats will need this pattern of emergency reaction, it can usefully occur irrespective of what exactly the threat might be. It is what physiologists call an ‘undifferentiated’ response. You do something at once, and work out the details later. Your brain gambles on getting it right (or right enough). The odds must be in favour, since this undifferentiated way of dealing with acute stress has evidently proved effective. Mostly, we and our mammalian cousins, who have very similar sympathetic responses to an acute threat, live to fight or flee another day.

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  Minder Brain, The: How Your Brain Keeps You Alive, Protects You From Danger, And Ensures That You Reproduce

  How Your Brain Keeps You Alive, Protects You from Danger, and Ensures that You Reproduce

  • Joe Herbert(Author)
  • 2007(Publication Date)
  • World Scientific

    (Publisher)

  Chapter 4 The Brain and Stress The idea of a state of stress is not at all new. Suppose we were to measure the heart rate and blood pressure of several people: one had just been told he had lost his job; the other had been attacked by a mugger in the street; a third had just lost a great deal of blood from a bleeding vein; and a fourth was exploring a rather dark, strange place that he found frightening. In all cases we are likely to find that the pulse quickens, the blood pressure rises, the face may grow pale and, were we to measure it, blood levels of adrenaline, the hormone secreted from the inner part of the adrenal gland, had gone up. These changes in the body, all the result of the increasing activity of the sympathetic nervous system, would not tell us which person was which. The sympathetic nervous system is a network of nerves that pass from the brain and spinal cord to activate heart, blood vessels, lungs and gut — it is our general emergency system. Note that the nature of the emergency is not specified; it could be anything that threatens us. Also note that how we react to this threat is not specified either: for example, we could either attempt to deal with it in a variety of ways or try to avoid it and run away. This was what Walter Cannon meant, in a famous book published in 1932, when he described the sympathetic nervous system as being activated in readiness for either ‘fight or flight,’ the two very appropriate, but also very different, ways of tackling any (physical) threat. This system activates your heart, blood vessels and glands; it is not under your control. In an acute emergency, the body assumes that you will shortly need every muscle and every bit of attention to make sure you deal with the emergency as effectively as possible. You do not want to deflect unnecessary energy or resources onto parts of the body that are not essential for the immediate threat. This includes the gut: you can digest your lunch 65

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  Stress and Addiction

  Biological and Psychological Mechanisms

  • Mustafa al'Absi(Author)
  • 2011(Publication Date)
  • Academic Press

    (Publisher)

  I . INTR ODUC TI O N Stress is a common condition of life and is significantly involved in the maintenance of health or the development of disease. In response to stress, different regulatory sys-tems of the body are activated to improve the ability of the organism to adapt to internal or external challenges. Adaptive responses can be specific to the stressor or can be gen-eralized and nonspecific (see Chrousos and Gold, 1992). The major physiological com-ponents of the stress response system are the corticotropin-releasing hormone (CRH) and the locus coeruleus (LC)-noradrenaline/ autonomic system with their peripheral effectors, the pituitary-adrenal axis, and the autonomic system. They trigger the release of glucocorticoids (e.g., cortisol in humans) from the adrenal cortex and catecholamines (adrenaline and noradrenaline) from the sympathetic nerves and adrenal medulla, C H A P T E R 1 B i o l og i ca l Bases o f t h e St r ess R es p o n se B R I G I TTE M . KU DI ELKA AN D C LEMEN S K I R SC H B AUM 3 Stress and Addiction: Biological and Psychological Mechanisms Edited by Mustafa al’Absi, Ph.D. Copyright © 2007, Elsevier Ltd. All rights reserved. 4 1 . BIOLO G IC A L B A SES O F THE ST R ESS R ES P O N SE respectively (see Axelrod and Reisine, 1984; Chrousos and Gold, 1992). There are numer-ous interactions among the components of the hypothalamus-pituitary-adrenal (HPA) axis and the LC-noradrenaline/autonomic (sympathetic) system and other brain ele-ments involved in the regulation of emo-tion, cognitive function, and behavior (see Axelrod and Reisine, 1984; Chrousos and Gold, 1992). The stress system also interacts with other important physiological systems like the immune system and other classi-cal endocrine axes, which are responsible for reproduction, growth, or thyroid func-tion (see below).

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  Body Awareness Workbook for Trauma

  • Yau, Julie Brown(Authors)
  • 2019(Publication Date)
  • Reveal Press

    (Publisher)

  Connection with others who are safe, with whom we can engage, allows us to stay present even during a crisis or traumatic event. Of course, in a frightening situation there may not be someone close by who is safe. Sometimes the person who is meant to be safe is actually hurting you. Your next line of defense is to call for help. This response is connected to your sympathetic nervous system (SNS) and the panic circuits of your brain. If no one safe arrives, your innate flow of defenses then prepares you to flee. In this state of hyperarousal, the fear circuits of your brain are recruited to help you get out of the situation. 15 During a severe traumatic event, the activation of the fear response shuts down 80 to 90 percent of the brain’s function. 16 It’s very confusing and frightening when you cannot access your usual brain functioning. The next line of defense if you cannot flee to safety is the fight response, in which the anger circuits of your brain are activated. In this hyperaroused state, your heart rate, respiration, and blood pressure elevate. The hyperarousal induces a cascade of released stress hormones. Often a traumatic impact happens so quickly that, like Jonathan in his car accident, you’re unable to respond with any of these innate defenses, and they may remain stuck within you. If you cannot act on your instinctual mobilizing responses of fight or flight, and you cannot reach safety, your next resort is the freeze response. Your muscle tone is rigid; your eyes may dart around scanning for danger and escape routes, looking for possible lifesaving actions. However, if you cannot act, and the fear continues, your energy-saving parasympathetic nervous system (PNS) is triggered into action, creating a state of hypoarousal, or immobility, with lowered heart rate and blood pressure and slower respiration along with the release of pain-numbing endogenous opioids—should the threat be fatal, these make death more painless.

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  The Principles and Practice of Human Physiology

  • O.G. Edholm(Author)
  • 2012(Publication Date)
  • Academic Press

    (Publisher)

  Conclusion There is little left to add to what has been written in the preceding sections about the functional significance in emergency of the defence reaction and its various components. The diverse visceral and hormonal features seem best regarded as the preparatory stage of a reflex, which, in THE PHYSIOLOGY OF STRESS—EMOTION 419 civilised man, may be expressed in this way alone. Curiously enough, Cannon regarded these reactions none the less as homoeostatic, for he was emphasising the long-term view; in the short run, though, they are the very antithesis, since they establish a new equilibrium only made possible by an interruption of short-term homoeostatic mechanisms. This was illustrated in dealing with the pattern of cardiovascular response by reference to the inhibition of the baroreceptor reflex, which would otherwise interfere. Some of the consequences of release of ACTH and adrenaline also are incom-patible with short-term homeostasis. The powerful effects of such hormones can greatly disturb the internal milieu, particularly if no muscular exertion occurs. Their potentially harmful effect in prolonged or chronic reactions should not need to be reiterated. Thus, though responses of the organism leading to changes of the internal milieu may still be physiological, they entail unavoidable risks. This does not detract from the imaginative hypotheses that Cannon deployed and to which reference has frequently been made here. As for the bodily responses themselves, it need hardly be said that there are still uncertainties about matters of fact, as well as of significance, and that these are multiplied with the increasing range of bodily responses to be discussed.

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