Stress: Dynamic state within the body resulting from the interaction of the body with the stressor.

Stressors: Stimuli that impose strain on body homeostasis.

Types of stressors:


  • pregnancy
  • adolescence
  • mating
  • ageing


  • orthostasis (upright standing position)
  • exertion
  • trauma
  • infection


  • hypoxia
  • hypoglycemia
  • acidosis

External/ Environmental

  • loud noise
  • air polution
  • bright light
  • threats


  • anger
  • excitement

Psychosocial behavioural

  • peer pressure
  • fitting in

Body’s Response to Stress


  • Nocireceptor: pain
  • Thermo: temperature
  • Mechano: physical
  • Baro: blood pressure
  • Chemo: glucose, acid, O2
  • In Special senses: sight, smell

Ascending sensory pathways:

Action potential go to..

  • -> hypothalamus (neuroendocrine response)
  • -> somatic sensory cortex (perception/stress)
  • -> motor cortex (voluntary action response)
  • -> limbic cortex (emotions)

During stress:

  • Increase in CRH – ACTH
  • Increase in GHRH, Decrease in somatostatin– Growth Hormone
  • Decrease in PIH – Increase in Prolactin
  • Decrease in TRH – TSH
  • Decrease in GnRH – Gonadotropin

Increase ACTH, GH & Prolaction


Mental stress: ACTH is high.


Physical stress: Cold pressor test (immersion of hand in cold water for 3 minutes). Blood pressure & Heart rate Increased.

Flight Fight Reaction (hypothalamo-sympatho-adrenalmedullary axis activation)

Stressor: External stress
Afferent Sensory Pathway: Limbic cortex (perception of stress)
Efferent Sensory Pathway:

  • sympathetic nervous system –>Hypothalamus (release noradrenaline)
  • Adrenal medulla (release A, NA, dopamine & opioid peptides) prolong effects of hypothalamus (EMERGENCY FUNCTION)

Target organs: Skeletal muscles

  • Increased energy demands by skeletal muscles
  • more fuel & O2 needed for aerobic production of ATP
  • More blood flow to skeletal msucles (supply o2, fuels, elimination of products of metabolism & heat)

Effects of sympatho-adrenal axis activation (fight flight/LION rule):

Increase BP

  • increase HR & contractility (increase stroke volume)
  • vasoconstriction (increase TPR)
  • vasoconstriction in skin & splanchnic regions (diversion of blood flow to skeletal muscles, heart muscles & brain)
  • Venoconstriction & skeletal muscle pump (increase venous return)
  • Accumulation of vasodilator metabolites in skeletal muscles (vasodilation in skeletal muscles)

Increase ventilation

  • bronchodilation (decrease airway resistance –> increase tidal volume)
  • increase O2 supply –> increase aerobic metabolism –> increase ATP production for skeletal muscle activity.

Increase fuel supply for ATP production

  • muscle glycogenolysis –> increase glucose for local use (muscle)
  • liver glycogenolysis –> increase plasma glucose
  • lipolysis –> increase plasma FA
  • Decrease GIT activity –> less energy demand

Decrease urination

  • Renal vasoconstriction


  • Activation of brainstem reticular activating system

Pupil dilation (mydriasis)

  • Stimulate dilator pupillae

Decrease bleeding/heat loss

  • Skin vasoconstriction

Decrease pain

  • Release of opioid peptides by adrenal medulla
  • decrease pain transmission & perception (stress analgesia)
  • euphoria

General Adaptation Syndrome (Hypothalamo-pituitary-adrenocortical axis activation)



Based on 1st graph,

Alarm state/Compensation phase:

  • When the stressor is noticed, there will be onset of shock and decreased resistance.
  • During this time, both sympatho-adrenal & hypothalamo-pituitary-adrenocortical axis are activated.

Resistance phase:

  • Resistance to the stressor increased as animal adapted & coped with it
  • Lasts for as long as the animal can support this heightened resistance.

Exhaustion/Decompensation phase:

  • Resistance has exhausted


Stress hormones


  • emergency function of sympatho-adrenal axis

Noradrenalin & Adrenaline

  • equally potent in increasing alertness (adrenaline evokes more anxiety & fear)
  • Known familiar stress –> more Noradrenaline
  • Unknown stress – > more Adrenaline

Glucocorticoids (Cortisol)

  • Stimulate protein catabolism –> liver uptake of amino acids –> conversion to glucose (gluconeogenesis)
  • **Anti-insulin action on muscle (own local supply) & adipose tissue (inhibit uptake of glucose)
  • Increase glucose supply to brain
  • TG breakdown –> glycerol + FA (fuel for muscle activity)
  • Increase plasma AA, glucose, glycerol & FA
  • Permissive effects (gives permission) for:
    -Catecholamines (vasoconstriction, bronchodilation, lipolysis)
    -Glucagon (gluconeogenesis)
  • Antiallergic effect
  • Increase RBC count
  • Increase neutrophil count

Due to the permissive actions for catecholamines & glucagon, secretion of ACTH & glucocorticoids (cortisol) are essential for survival when stress is severe.

Renin-angiotensin-aldosterone system

  • Angiotensin 2: generalised vasoconstriction
  • Aldosterone: Na+ & water reabsorption in distal nephron (increase blood volume & BP)

Vasopressin (ADH/AVP)

  • Increase ACTH secretion
  • Increase water reabsorption (increase blood volume & BP)
  • Generalised vasoconstriction
  • Liver glycogenolysis (in large amounts)

Growth Hormone

  • Lipolysis (FA for muscle activity)
  • Anti-insulin action (decrease glucose uptake in peripheral tissues, direct to brain)


Effect of stress on performance


Therefore, moderate stress is advantageous for optimum performance.

Effect of PROLONGED stress on health

  • Repeated episodes can cause cardiovascular disease.
  • Glucocorticoids in large amounts can suppress the immune system and increase protein catabolisme (muscle loss)
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Terri is obsessed with making medical school as painless as possible. She studies and compiles medical school notes in a concise, easy-to-understand format. She also enjoys reading contributions by others. She is an investor in sustainability projects. Her ideal weekend is wine tasting and experimenting on bread-making. She has yet to master the art of Sourdough baking.


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