Temperature Regulation
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Direct answer
Body temperature is defended around a set point of about 37 degrees Celsius, controlled by the preoptic-anterior hypothalamus as the thermosensitive "heat loss centre" and the posterior hypothalamus as the integrator of heat conservation and production. Afferent information streams in from cutaneous warm and cold receptors and from deep thermoreceptors of the spinal cord and abdomen; effectors include skin blood flow (from near zero to several litres per minute), sweating, shivering, piloerection and, in neonates, brown-fat non-shivering thermogenesis. Fever is a regulated upward shift of the set point by pyrogen-driven prostaglandin E2, which is fundamentally different from hyperthermia, where the set point is normal and the cooling mechanisms are simply overwhelmed.
What you must remember
- Normal core temperature 36.5–37.5 degrees Celsius, with a daily variation of about 0.6 degrees; rectal reading runs roughly 0.6 degrees above oral.
- Heat production: basal metabolism, thyroid hormone (long-term calorigenic effect), muscular activity — shivering can raise production several-fold — sympathetic activation, and brown adipose tissue non-shivering thermogenesis in neonates through the uncoupling protein thermogenin (UCP1).
- Heat loss at comfortable room temperature: roughly 60% radiation, most of the rest convection-conduction and evaporation; evaporation becomes the only route in extreme heat.
- Insensible loss is about 600–700 mL per day through skin and respiration; maximal sweating reaches about 1.5 litres per hour, and acclimatisation raises volume while aldosterone lowers its salt content.
- Vasomotor responses can vary skin blood flow from around 0.5 to as much as 7–8 litres per minute — the dominant fine control.
- Fever pathogenesis: exogenous pyrogens (bacterial LPS) stimulate macrophages to release IL-1, IL-6 and TNF-alpha, which induce PGE2 in the preoptic area, raising the set point.
- Antipyretics (paracetamol, NSAIDs) inhibit cyclooxygenase and hence PGE2, lowering the set point — they do nothing in heat stroke, where the set point is normal.
- Heat stroke: core above 40 degrees with altered sensorium and (in the classic type) absent sweating — a cold-water cooling emergency.
- Neonates cannot shiver effectively and rely on brown fat, which is why kangaroo mother care under India's National Health Mission prevents hypothermia in low-birth-weight infants.
Fever worked through, phase by phase
Watch the physiology of a malaria rigor. The set point is suddenly raised to 39 degrees. The body's current 37 degrees is now read as too cold: cutaneous vessels constrict (pale, cold skin), piloerection follows, and the patient shivers — the chill or rigor — generating heat by muscle activity. This is the stage at which the patient piles on blankets, and it is pointless to tepid-sponge him, because the thermostat demands the higher temperature. When the set point is reached, the plateau begins: skin becomes warm and dry, pulse and respiratory rate rise, and the patient is flushed.
Then the parasite cycle ends or the antipyretic blocks PGE2 formation, and the set point falls back. Now the body is hotter than the thermostat wants: sweating, flushing and vasodilation appear (defervescence or crisis), and fluid loss can be substantial. Contrast the same 40 degrees in heat stroke: the set point was never moved, the PGE2 pathway was never engaged, and the patient's sweating machinery has failed from exhaustion — antipyretics are useless, active external or evaporative cooling is the treatment, and every minute of delay cooks the brain, liver and kidneys.
Where students slip
The classic error is calling every high temperature "fever" and reaching for paracetamol; distinguish regulated fever (set point raised, treat the cause, antipyretics work) from hyperthermia (set point normal, cool the body physically, dantrolene if malignant hyperthermia from ryanodine receptor failure). Second, remember that the hypothalamus itself senses temperature — it is not merely a relay — so direct hypothalamic lesions (tumour, surgery, haemorrhage) can produce central fever or poikilothermia, the loss of temperature control seen after high cervical cord transection. A viva favourite: why do neonates get cold stress so easily — high surface area to mass ratio, no shivering, thin subcutaneous fat, so brown fat sympathetic stimulation is their only heater, and its exhaustion converts into hypoxia and hypoglycaemia.
Frequently asked questions
Which hypothalamic region acts as the body thermostat?
The preoptic-anterior hypothalamus, rich in warm-sensitive neurons, initiates heat loss; the posterior hypothalamus integrates heat conservation and production responses.
How do pyrogens raise body temperature?
Endotoxin stimulates cytokine release (IL-1, IL-6, TNF-alpha), which drives prostaglandin E2 synthesis in the preoptic area, elevating the hypothalamic set point.
Why are antipyretics ineffective in heat stroke?
Heat stroke is hyperthermia with a normal set point — the problem is failed heat dissipation, not PGE2-mediated set-point elevation, so physical cooling is required.
What is non-shivering thermogenesis and where does it occur?
Sympathetic stimulation of brown adipose tissue, where UCP1 uncouples oxidative phosphorylation to release heat directly; the principal heat source in neonates.
Which heat loss mechanism is preserved in extreme environmental heat?
Evaporation, since radiation and convection reverse direction and add heat when ambient temperature exceeds skin temperature.