Thermoregulation by the skin
Also known as: temperature regulation, sweating, cutaneous vasodilation, vasoconstriction, heat loss
The skin is the main effector organ of temperature regulation: under hypothalamic control it varies blood flow and sweating to lose or conserve heat, keeping core temperature near 37 °C.
Overview
Thermoreceptors in the skin (free nerve endings) and in the core (hypothalamus, spinal cord, viscera) feed the preoptic area of the anterior hypothalamus, which compares body temperature with a set point (≈37 °C) and drives effectors through the sympathetic nervous system.
Heat loss. At rest in a comfortable environment ≈60% of heat is lost by radiation, ≈15% by conduction/convection and ≈20–25% by evaporation (insensible loss from skin and airways plus sweat). When too hot, sympathetic vasoconstrictor tone is withdrawn and the active vasodilator system opens skin vessels, bringing warm core blood to the surface; eccrine sweating (sympathetic cholinergic) wets the skin, and each gram evaporated removes ≈2.4 kJ. When ambient temperature exceeds skin temperature, evaporation becomes the only effective route, so high humidity is dangerous. Heat acclimatisation over ≈1–2 weeks increases sweat rate, starts sweating at a lower temperature and lowers sweat NaCl (aldosterone).
Heat conservation. When cold, noradrenergic vasoconstriction of dermal arterioles and AV anastomoses shrinks skin blood flow and the countercurrent arrangement of deep limb veins and arteries returns heat to the core; piloerection (arrector pili) is vestigial in humans; subcutaneous fat insulates. Heat production increases by shivering (skeletal muscle) and non-shivering thermogenesis (brown fat, thyroid hormones) — effectors outside the skin.
Function
- Maintain core temperature ≈37 °C (±0.6 °C) despite environmental and metabolic changes
- Dissipate exercise heat (up to 10–20 × resting heat production)
- Conserve heat in the cold by cutaneous vasoconstriction and insulation
- Regulation
Preoptic anterior hypothalamus → sympathetic outflow: cholinergic to eccrine glands; noradrenergic vasoconstrictor and cholinergic vasodilator fibres to skin vessels; adrenergic to arrector pili. Pyrogens (IL-1, IL-6, TNF via PGE2) raise the set point in fever.
Clinical significance
Heat exhaustion and heat stroke
Heat exhaustion: fatigue, headache, nausea and syncope from salt and water depletion; core temperature <40 °C, mental state normal. Heat stroke: core temperature >40 °C with CNS dysfunction (confusion, seizures, coma); classic (elderly, hot weather, often anhidrotic) or exertional. A medical emergency requiring rapid cooling (cold-water immersion).
Hypothermia and frostbite
Core temperature <35 °C causes shivering, then confusion, bradycardia, J (Osborn) waves on ECG and arrhythmias. Frostbite is freezing of tissue in vasoconstricted extremities (fingers, toes, ears, nose).
Fever
Cytokine-induced prostaglandin E2 raises the hypothalamic set point; the body feels cold, vasoconstricts and shivers (rigors) until the new set point is reached, then vasodilates and sweats when the fever "breaks".
Compiled from standard anatomy and physiology references — see the Integumentary System sources. For education only; not medical advice.