31 Stress response
Learning Objectives
After reading this section you should be able to-
- Describe the three stages of stress (general adaptation syndrome)
- List the hormones released during short-term stress and describe the hormonal actions
- List the hormones released during long-term stress and describe the hormonal actions
The body responds in different ways to short-term stress and long-term stress following a pattern known as theĀ general adaptation syndrome (GAS). Stage one of GAS is called the alarm reaction. This is short-term stress, the fight-or-flight response, mediated by the hormones epinephrine and norepinephrine from the adrenal medulla. Their function is to prepare the body for extreme physical exertion. Once this stress is relieved, the body quickly returns to normal. The section on the adrenal medulla covers this response in more detail.
If the stress is not soon relieved, the body adapts to the stress in the second stage called the stage of resistance. If a person is starving for example, the body may send signals to the gastrointestinal tract to maximize the absorption of nutrients from food.
If the stress continues for a longer term however, the body responds with symptoms quite different than the fight-or-flight response. During the stage of exhaustion, individuals may begin to suffer depression, the suppression of their immune response, severe fatigue, or even a fatal heart attack. These symptoms are mediated by the hormones of the adrenal cortex, especially cortisol, released as a result of signals from the HPA axis.
More detail about each stage follows.
Alarm Stage
The alarm stage represents the body’s initial response to a stressor, characterized by the activation of the sympathetic nervous system and the release of stress hormones. When an individual encounters a threatening or stressful situation, whether physical or psychological, the body swiftly mobilizes resources to cope with the perceived threat. This phase is often referred to as the “fight-or-flight” response due to the body’s preparation for either confronting the stressor or escaping from it.
At the onset of the alarm stage, the hypothalamus, a region of the brain crucial for coordinating stress responses, detects the stressor and signals the sympathetic nervous system to initiate a cascade of physiological changes. The sympathetic nervous system stimulates the adrenal medulla, located atop the kidneys, to release catecholamines, including epinephrine (adrenaline) and norepinephrine, into the bloodstream.
Epinephrine and norepinephrine rapidly exert their effects throughout the body, eliciting a range of physiological responses that enhance the individual’s ability to cope with the stressor. These responses include increased heart rate and cardiac output, dilation of airways to improve oxygen intake, and redirection of blood flow away from non-essential organs like the digestive system and toward skeletal muscles, which may be needed for physical exertion.
Moreover, epinephrine and norepinephrine trigger the release of glucose from glycogen stores in the liver and muscles, providing an immediate source of energy for cells. This surge in blood glucose levels ensures that cells have sufficient fuel to meet the increased energy demands associated with the stress response.
Additionally, during the alarm stage, there is heightened arousal and vigilance, facilitating rapid sensory processing and reaction times. This heightened state of alertness allows individuals to assess and respond to the stressor more effectively, whether by confronting the threat head-on or initiating an escape strategy.
Overall, the alarm stage of GAS represents the body’s rapid and coordinated physiological response to stress, aimed at preparing the individual for immediate action and ensuring survival in the face of adversity. Understanding the intricacies of the alarm stage provides insight into the adaptive mechanisms that enable organisms to respond adaptively to challenging situations.
Resistance Stage
Following the initial alarm reaction, if the stressor persists or recurs over an extended period, the body enters the resistance stage of the GAS. Unlike the acute and immediate responses seen in the alarm stage, the resistance stage represents a more prolonged adaptation to the ongoing stressor.
During the resistance stage, the body endeavors to maintain a heightened state of readiness to cope with the sustained stressor while simultaneously conserving energy and resources. This phase is characterized by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, a neuroendocrine system crucial for orchestrating the body’s response to stress.
In response to persistent stress signals from the hypothalamus, the pituitary gland releases adrenocorticotropic hormone (ACTH) into the bloodstream. ACTH, in turn, stimulates the adrenal cortex, the outer layer of the adrenal glands, to produce and release glucocorticoids, primarily cortisol.
Cortisol plays a central role in the body’s adaptation to prolonged stress by modulating various physiological processes. One of its primary functions is to mobilize energy reserves to sustain prolonged physical and cognitive demands. Cortisol promotes gluconeogenesis, the synthesis of glucose from non-carbohydrate sources such as amino acids and glycerol, thereby ensuring a continuous supply of glucose to fuel cellular activities.
Furthermore, cortisol exerts anti-inflammatory and immunosuppressive effects, dampening the body’s immune response to prevent excessive inflammation and tissue damage. While beneficial in the short term, chronic exposure to elevated cortisol levels during the resistance stage may impair immune function and increase susceptibility to infections and inflammatory conditions.
Moreover, cortisol influences metabolism, promoting the breakdown of fat stores for energy and conserving protein by inhibiting protein synthesis. This metabolic shift helps to preserve essential tissues and organs during prolonged stress, ensuring the body’s survival over an extended period.
In addition to hormonal adaptations, the resistance stage may also involve behavioral and psychological adjustments to cope with ongoing stressors. Individuals may develop coping strategies, resilience, and adaptive behaviors to mitigate the impact of stress and maintain psychological well-being.
Overall, the resistance stage of GAS represents the body’s adaptive response to sustained stress, characterized by hormonal, metabolic, and behavioral adjustments aimed at promoting survival and maintaining homeostasis in the face of prolonged adversity.
Exhaustion Stage
The exhaustion stage represents the final phase of the GAS, occurring when the body’s resources become depleted after prolonged exposure to stressors and adaptive mechanisms fail to maintain homeostasis. This stage is characterized by a decline in physiological and psychological functioning, leaving the individual vulnerable to various health issues and potential collapse.
During the exhaustion stage, the body’s adaptive responses, which were initially beneficial for coping with stress, become maladaptive as resources are depleted. Prolonged activation of the hypothalamic-pituitary-adrenal (HPA) axis and continuous release of stress hormones, particularly cortisol, lead to dysregulation of physiological processes and impairments in immune function, metabolism, and cardiovascular function.
The persistent elevation of cortisol levels during the exhaustion stage can have detrimental effects on the body’s tissues and organs. Chronic exposure to high cortisol levels may result in muscle wasting, bone density loss, and impaired wound healing. Moreover, cortisol-induced immunosuppression increases susceptibility to infections and delays recovery from illness or injury.
Furthermore, the exhaustion stage is often accompanied by psychological symptoms such as depression, anxiety, and cognitive deficits. Prolonged stress and hormonal dysregulation can alter neurotransmitter levels in the brain, affecting mood regulation, cognition, and emotional well-being. Individuals may experience feelings of hopelessness, helplessness, and emotional exhaustion as they struggle to cope with persistent stressors.
Moreover, during the exhaustion stage, the body’s energy reserves are depleted, leading to profound fatigue, lethargy, and diminished physical performance. Metabolic imbalances, including disruptions in glucose regulation and energy metabolism, further contribute to feelings of exhaustion and weakness.
Additionally, the exhaustion stage may manifest as an increased risk of cardiovascular events, such as heart attacks or strokes, due to prolonged strain on the cardiovascular system. Chronic stress can elevate blood pressure, increase heart rate, and promote inflammation, predisposing individuals to cardiovascular disease and other related complications.
In summary, the exhaustion stage of GAS represents a state of physiological and psychological depletion resulting from prolonged exposure to stressors.
Additional Hormones and Their Actions
In addition to epinephrine, norepinephrine, and cortisol, other hormones contribute to the body’s response to stress. One such hormone is epinephrine which is released from the adrenal medulla during the fight-or-flight response. Epinephrine acts on various tissues to increase heart rate, dilate airways, and redirect blood flow to vital organs, all of which are essential for immediate physical exertion in response to stressors.
Adapted from Anatomy & Physiology by Lindsay M. Biga et al, shared under a Creative Commons Attribution-ShareAlike 4.0 International License, chapter 17.
the physiological changes that occur as the body responds to stress
the first stage of the general adaptation syndrome, characterized by increased levels of epinephrine and norepinephrine as the body prepares for extreme physical exertion
the second stage of the general adaptation syndrome, characterized by the body attempting to recover or adapt to ongoing stress
the last stage of the general adaptation syndrome, characterized by the depletion of the body's resources after prolonged exposure to stressors and failed homeostatic adaptive mechanisms