Stress Response and General Adaptation Syndrome

Stress Response

• Homeostasis is the state where all systems are balanced at a specific "set-point."
• Allostasis is the process of adapting to maintain survival and well-being.
• Stress is the sum of biological responses when homeostasis is disrupted.
• Stressors are agents or conditions that cause stress and initiate allostasis.

General Adaptation Syndrome (GAS)

• Hans Selye theorized GAS in the 1920s.
• GAS has three stages: alarm, resistance, and exhaustion.

GAS: Alarm Stage

• The "fight-or-flight" response.
• A surge in energy and physical changes to either run or confront danger.
• The hypothalamus senses a threat (internal or external, physical or emotional).
• Hypothalamus activates the sympathetic nervous system (SNS).
• Adrenal medulla releases catecholamines (epinephrine and norepinephrine), enabling the body to fight or flee.
• Corticotropic-releasing hormone (CRH) from hypothalamus stimulates anterior pituitary gland to release adrenocorticotropic hormone (ACTH).
• ACTH triggers adrenal cortex to release glucocorticoids, especially cortisol.
• Hypothalamic-pituitary-adrenal (HPA) axis is activated.
• Alarm stage happens in full force; cannot be deactivated once the pituitary gland is activated.
• Prolonged activation leads to permanent body damage.
• SNS, adrenal medulla, and cortex fully function during alarm stage.

GAS: Resistance Stage

• Allostatic return to homeostasis.
• SNS activity, catecholamine and glucocorticoid secretion get normalized.
• Body returns to a steady state if stressors are adequately addressed and resolved.
• Body has "adapted" or "increased resistance" to the stressor.

GAS: Exhaustion Stage

• Body cannot return to homeostasis.
• Adaptive energy stores are depleted.
• Body cannot adapt further.
• Pathological triad (hypertrophy of adrenal glands, atrophy of lymphoid tissues, and bleeding GI ulcers).
• Death is possible if homeostasis is not restored.

Allostatic Overload

• When adaptive mechanisms are inadequate, allostatic overload may occur.
• Many physiological and psychological effects occur from excessive stress.

Neurohormones of Stress and Adaptation

• Catecholamines: Norepinephrine (NE) and epinephrine (Epi).

  • Released from the CNS in response to stressors.
  • NE released by sympathetic neurons near organs/tissues.
  • NE and Epi released from adrenal medulla into bloodstream to enhance the SNS.

• Norepinephrine and epinephrine:

  • Norepinephrine is a primary blood vessel constrictor, regulating blood flow and maintaining blood pressure.
  • It reduces GI activity, dilates the iris, and relaxes ciliary muscles for better vision.
  • Epinephrine increases heart rate, myocardial contractility, venous return, and raises cardiac output/blood pressure.
  • Epinephrine also increases glycogenolysis and blood flow to the brain, enhancing mental attention and alertness.

• Adrenocortical steroids (cortisol and aldosterone):

  • Have regulatory roles in cardiovascular system, fluid volume, metabolism, immunity, inflammatory responses, brain function, and reproduction.
  • Cortisol is a lipid-soluble hormone and its effects last longer than catecholamines.
  • Cortisol supports catecholamines by promoting epinephrine synthesis and controlling blood pressure/cardiac output.
  • Cortisol increases liver protein synthesis but has a catabolic effect on other tissues, stimulating gluconeogenesis (liver) for glucose availability (especially to nerve cells). It also promotes appetite and suppresses inflammation and acute-phase responses.
  • Aldosterone is a primary mineralocorticoid that's released in response to stimulation of the SNS to enhance sodium reabsorption in kidneys, increasing ECF volume and blood pressure.

• Other neurohormones (endorphins, enkephalins, and sex hormones):

  • Endogenous opioids (endorphins, enkephalins) inhibit pain naturally by raising pain threshold, producing sedation, and euphoria. They are released in response to stressors, e.g., by laughter, massage, or acupuncture.
  • Sex hormones (e.g., cortisol) affect stress, and vice versa. For instance, cortisol inhibits the female reproductive system (luteinizing hormone, estrogen, progesterone) but androgens(testosterone, DHEA) oppose the catabolic effects of cortisol and lower levels of stress related depression. Stress often lowers testosterone levels.
  • Oxytocin, combined with estrogen, is calming during stress. Oxytocin is also produced during childbirth, lactation, and orgasm, promoting bonding and social attachment.

• Growth hormone and Prolactin:

  • Released during intensely stressful physical/psychological stimuli.
  • Growth hormone enhances protein synthesis, fat mobilization, and decreases carbohydrate utilization, impacting immune function.
  • Prolactin is also released during stress, sexual activity, and breast feeding with functions similar to growth hormone, including immune regulation.

• Stressors:

  • External (e.g., pollution, accidents).
  • Internal (e.g., low blood sugar, feelings of threat).
  • Physical/Chemical/Biological/Social (e.g., injury, exhaust fumes, viruses, bad relationships).
  • Psychological (e.g., sadness).
  • Emotional stressors can be present or anticipated.
  • Can be low-intensity impacting over time.

• Risk factors: increase the likelihood of experiencing a stressor.