The stress response is a complex, coordinated system of physiological, cognitive, and behavioral reactions that occur when an individual perceives an event or situation as demanding, overwhelming, or threatening to their well-being. While acute stress responses evolved as adaptive survival mechanisms, chronic activation can have severe consequences for human health.
Stress is a biological and psychological response experienced upon encountering a threat that we feel we do not have the resources to deal with.
Fight-or-Flight Response
First articulated by Harvard physiologist Walter Cannon in the early 20th century, the fight or flight response is the body’s rapid, built-in mechanism to confront or escape from a perceived physical threat.
A stressor is a stimulus (or threat) that causes stress, e.g., an exam, divorce, the death of a loved one, moving house, or loss of job.
When a stressor is encountered, the sympathetic nervous system is immediately activated, causing a cascade of physiological changes:
- Pupils dilate to increase visual sensitivity.
- Heart rate, blood pressure, and respiration rate (breathing) accelerate to deliver more oxygen and nutrients to the muscles.
- Digestion and salivation are inhibited, redirecting energy to where it is needed most.
- The liver releases stored glucose to provide an immediate energy boost.
The physiological execution of the stress response relies on two primary systems that work in tandem:
| Feature | SAM System | HPA Axis |
| Type of Stress | Acute (Immediate, short-term) | Chronic (Sustained, long-term) |
| Speed of Response | Rapid (Seconds) | Slow (Minutes to hours) |
| System Involved | Nervous system → Endocrine system | Purely Endocrine (Hormonal) system |
| Adrenal Part | Adrenal Medulla (Inner core) | Adrenal Cortex (Outer shell) |
| Primary Hormones | Adrenaline & Noradrenaline | Cortisol (and CRH/ACTH) |
SAM Pathway
Accute stress response: Sympathetic Adrenal Medullary (SAM) Pathway
While the HPA axis handles long-term, chronic stress, the Sympathetic Adrenal Medullary (SAM) system is your body’s rapid-response unit.
It drives the immediate fight-or-flight response, preparing your body for sudden, intense physical action within milliseconds of perceiving a threat.
3-Step Pathway
The SAM system bridges the nervous system and the endocrine (hormonal) system in a lightning-fast pathway:
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Perception of Threat: The brain detects a stressor and instantly activates the sympathetic branch of the Autonomic Nervous System (ANS).
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Signal to the Adrenal Glands: Electrical nerve impulses travel down the spinal cord directly to the adrenal medulla (the inner core of the adrenal glands sitting on top of the kidneys).
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Hormone Release: The adrenal medulla immediately secretes the hormones adrenaline (epinephrine) and noradrenaline (norepinephrine) directly into the bloodstream.
Physiological Effects: Preparing for Action
Adrenaline and noradrenaline act as sympathomimetics, meaning they mimic and prolong the effects of the sympathetic nervous system.
While the initial nerve impulse is instantaneous, these hormones keep the body highly alert for a short period.
They trigger a coordinated emergency reaction across the body:
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Cardiovascular: Heart rate and blood pressure increase sharply to pump oxygenated blood rapidly to the muscles.
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Respiratory: The airways (bronchi) dilate (widen) to increase oxygen intake.
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Energy Mobilization: Glycogen stored in the liver is converted into glucose and released into the blood for immediate muscle fuel.
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Diversion of Resources: Blood flow is shunted away from “non-essential” systems like digestion and skin, and directed toward the brain and skeletal muscles (this is why you get pale and experience a “dry mouth” when scared).
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Temperature Regulation: Sweating increases to prevent the body from overheating during physical exertion.
Bringing it Back to Baseline: The Parasympathetic Branch
If the threat passes quickly, the parasympathetic nervous system (the “rest and digest” branch of the ANS) takes over.
It acts as a brake, lowering heart rate, restoring digestion, and returning the body to its normal baseline (homeostasis).
However, if the stressor persists, the initial surge of the SAM system fades, and the slower, longer-lasting HPA axis takes over to sustain the stress response.
HPA Axis
Chronic stress response: hypothalamic-pituitary-adrenal (HPA) axis.
While your SAM pathway handles the immediate, split-second fight-or-flight response, the Hypothalamic-Pituitary-Adrenal (HPA) axis takes over for long-term, ongoing stress.
It operates more slowly but provides a sustained biological reaction to keep you coping.
The 3-Step Cascade
The HPA axis relies on a chain reaction between three main glands:
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Hypothalamus: When a stressor is perceived, the hypothalamus releases a hormone called Corticotropin-Releasing Hormone (CRH).
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Pituitary Gland: CRH travels through a local blood network directly to the anterior pituitary gland, triggering it to secrete Adrenocorticotropic Hormone (ACTH) into the general bloodstream.
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Adrenal Glands: ACTH travels down to the adrenal cortex (the outer layer of the adrenal glands sitting on top of the kidneys). This stimulates the release of glucocorticoids, primarily cortisol.
The Role of Cortisol: Meeting the Energy Demand
Cortisol is the primary hormone responsible for mobilizing the body’s resources during chronic stress:
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Increases Blood Sugar: It converts stored proteins into glucose (gluconeogenesis) and mobilizes fats to provide immediate energy.
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Suppresses Non-Essential Systems: It temporarily downregulates “luxury” systems like digestion, reproduction, and the immune system to conserve energy for survival.
Regulation: The Negative Feedback Loop
Too much cortisol is toxic to the body, so the HPA axis regulates itself using a strict negative feedback loop.
Because cortisol is a lipid-soluble hormone, it easily crosses the blood-brain barrier.
High levels of circulating cortisol bind to receptors in both the hypothalamus and pituitary gland.
signals them to stop producing CRH and ACTH, effectively shutting off the stress response once the threat has passed.
The Brain’s “Push-Pull” System
Two key brain structures control this feedback mechanism:
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The Amygdala (The “Gas Pedal”): Processes emotional threats and fear. It stimulates the HPA axis to start the stress response.
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The Hippocampus (The “Brake”): Responsible for memory. It has a high density of cortisol receptors. When it detects cortisol, it sends signals to inhibit the hypothalamus, shutting the system down.
Note for Exam Prep: Neurochemicals also modulate this. Oxytocin (the bonding hormone) dampens the HPA response, while vasopressin amplifies it.
Here is the version tailored for your A-Level studies, focusing on Hans Selye’s General Adaptation Syndrome (GAS). This is a classic model in A-Level Psychology and Biology, often used to show how short-term stress responses (SAM) transition into long-term ones (HPA), and eventually lead to illness.
GAS
General Adaptation Syndrome (GAS): The Universal Stress Response
Developed by Hans Selye in the 1930s, General Adaptation Syndrome (GAS) is a three-stage biological model describing how the body responds to stress.
Selye exposed rats to various harsh stressors (extreme cold, excessive exercise, or injury) and found they all developed the exact same physical symptoms: enlarged adrenal glands, shrunken immune organs (thymus and lymph nodes), and bleeding stomach ulcers.
From this, Selye concluded that the body’s physiological response to stress is non-specific—meaning the exact same universal physical response occurs regardless of what the stressor actually is.
3 Stages of GAS
Selye outlined this universal response in three distinct chronological stages:
[Alarm Reaction] ──> [Stage of Resistance] ──> [Stage of Exhaustion]
(SAM Activated) (HPA Activated) (Resources Depleted)
1. The Alarm Reaction (Immediate)
This is your immediate response to a sudden threat. It is divided into two quick phases:
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Shock Phase: The initial impact where the body’s resistance to the stressor temporarily drops.
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Countershock Phase: The SAM system instantly kicks in. The sympathetic nervous system stimulates the adrenal medulla to release adrenaline and noradrenaline, triggering the “fight-or-flight” response to manage the immediate crisis.
2. The Stage of Resistance (Long-Term)
If the stressor continues, the body tries to adapt and cope with the ongoing threat.
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The intense adrenaline rush from the alarm stage levels off, but the body remains on high alert.
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The HPA axis takes over. The anterior pituitary releases ACTH, stimulating the adrenal cortex to secrete cortisol.
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This cortisol maintains high blood glucose levels via gluconeogenesis, keeping energy levels up to fight the prolonged stressor.
3. The Stage of Exhaustion (Resource Depletion)
If the stressor continues indefinitely, the body’s physical resources eventually become completely depleted.
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The adrenal glands wear out and can no longer produce hormones effectively; blood sugar levels plummet.
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The immune system is severely suppressed.
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The body suffers severe wear and tear, leaving the individual highly vulnerable to “diseases of adaptation” (psychophysiological illnesses) such as high blood pressure, heart disease, and stomach ulcers.
Evaluation of Selye’s GAS Model
While Selye’s work was revolutionary for linking chronic stress to physical illness, modern psychology identifies several limitations:
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Ignores Cognitive Appraisal (The Role of Thought): Selye used animals (rats), so his model is purely biological and ignores cognitive processes. Richard Lazarus argued that human stress depends heavily on our psychological appraisal—how we mentally interpret a threat. If we perceive we can handle a situation, it doesn’t trigger the severe stress response Selye described.
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The “Non-Specific” Assumption is Flawed: Selye claimed the body reacts exactly the same way to every stressor. Modern research shows this isn’t strictly true; different stressors (e.g., a public speaking task vs. a physical injury) actually produce slightly different hormonal and physiological profiles.
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Strong Biological Evidence: Selye provided concrete physical proof of the link between chronic stress and illness, laying the groundwork for understanding how prolonged HPA axis activation physically damages the body.
References
Currie, A. R., & Symington, T. (1955). The pathology of the pituitary and adrenal glands in systemic disease in man. Proceedings of the Royal Society of Medicine, 48(11), 908.
