14.2 — Temperature Control and Sweat

Humans are among the best long-distance runners in the animal kingdom, and it is not because we are fast. It is because we can shed heat while moving, and almost nothing else can.

A horse, a dog or an antelope cools mainly by panting, which cannot be done efficiently while galloping. A human cools by sweating over a nearly hairless body, which works at any speed. Over a long enough distance in hot conditions, a trained human can run a horse into exhaustion — and persistence hunting, in which prey is pursued until it collapses from heat, is documented in several hunter-gatherer cultures.

Sweating is our defining physiological advantage, and it is the same mechanism that fails in heat stroke.

The balance

Core temperature is held near 37 °C, with a daily variation of about 0.5 °C — lowest around 4 to 6 a.m., highest in the early evening (Chapter 12.7).

"Normal" is a range rather than a number. The traditional 37.0 °C comes from a study of 25,000 measurements published in 1868; modern large datasets put the average closer to 36.6 °C, and there is evidence that average human body temperature has genuinely declined slightly over the past century, possibly from reduced chronic infection and inflammation.

And the measurement site matters by up to a degree. Rectal is the most accurate core measure; oral runs about 0.5 °C lower; axillary about 1 °C lower; and tympanic and forehead readings vary with technique. A fever threshold quoted without a site is incomplete.

Heat production — at rest, essentially all of it from basal metabolism, with the liver, brain, heart and kidneys producing the most per gram.

During exercise, muscle dominates, and heat production can rise ten to twentyfold. Muscle is only about 20 to 25 percent efficient (Chapter 1.6), so most of the energy becomes heat.

Heat loss happens by four routes.

Radiation — infrared emission to cooler surroundings. About 60 percent of resting loss, and it works without any air movement.

Conduction — direct contact. Small in air, and enormous in water: water conducts heat about 25 times faster than air, which is why immersion cools so rapidly and why hypothermia develops so fast in water even at moderate temperatures.

Convection — heat carried away by moving air. This is why wind chill is real, and why a fan helps.

Evaporation — about 22 percent at rest, from skin and breathing, and it becomes the dominant route in heat and exercise.

And there is a threshold that changes everything. When the environment is hotter than your skin, radiation, conduction and convection all reverse — they bring heat in.

Above about 35 °C ambient, evaporation is the only route left.

Sweating

2 to 4 million eccrine glands (Chapter 14.1), producing up to 1 to 2 litres per hour in an acclimatised person, and up to 10 to 12 litres a day in extreme conditions.

Evaporating one litre removes about 2,400 kilojoules — 580 kilocalories (Chapter 1.2).

And the critical point that is missed constantly: sweat only cools when it evaporates. Sweat that drips off has cost you water and salt and removed almost no heat.

Which is why humidity is the dangerous variable, not temperature.

At 100 percent humidity, evaporation stops entirely, and the body has no cooling mechanism at all above skin temperature.

This is why "wet bulb temperature" is used to assess heat danger. A wet bulb temperature above about 35 °C is survivable for only a few hours even for a healthy person resting in the shade with unlimited water, because there is no physical route for heat to leave the body. Such conditions have already occurred briefly in parts of the Persian Gulf and South Asia, and their expected increase is one of the more concrete health consequences of climate change.

Sweat composition: mostly water, with sodium chloride, potassium, and small amounts of urea and lactate.

Sweat is hypotonic — less salty than plasma — because sodium is reabsorbed as the sweat passes up the duct (Chapter 1.4).

And acclimatisation improves that reabsorption substantially. Over 10 to 14 days of heat exposure, an acclimatised person sweats earlier, sweats more, and loses far less salt — sodium concentration in sweat can fall by half or more.

Which is why the unacclimatised are at much greater risk, and why heat illness clusters in the first days of a heatwave and in newly arrived workers.

And it is why the CFTR chloride channel matters here (Chapter 1.4) — people with cystic fibrosis cannot reabsorb the salt, so their sweat is markedly salty, which is both the basis of the diagnostic test and a genuine risk of salt depletion in hot weather.

Responses to heat and cold

Getting hot:

Skin vessels dilate — free, and it works first. Sweating — expensive in water and salt. Reduced heat production — appetite falls, activity falls. Behaviour — shade, clothing, fluid, and this is by far the most powerful effector.

Getting cold:

Skin vessels constrict — reducing loss, and producing the pale cold extremities of a cold person.

And an elegant refinement: countercurrent heat exchange. In the limbs, arteries and veins run close together, so warm arterial blood pre-warms the returning venous blood and the heat never reaches the surface. In cold conditions blood returns via the deep veins beside the arteries; in warm conditions it returns via superficial veins instead, which is why hand veins become prominent in heat. A vascular thermostat with no moving parts.

Shivering — involuntary muscle contraction generating heat, increasing heat production three to fivefold. Voluntary movement generates more, which is why moving is better than shivering.

Non-shivering thermogenesis — brown fat, using the UCP1 uncoupler of Chapter 1.6. Important in newborns, who cannot shiver effectively, and present in adults in small amounts around the neck and shoulders.

Piloerection — goosebumps. In a furred animal this raises the hairs and traps an insulating air layer. In humans it does essentially nothing and is a vestige (Chapter 3.1).

Behaviour — again the most powerful response.

Heat illness

A spectrum, and recognising where a person sits on it determines what to do.

Heat cramps — painful muscle cramps during or after exertion in heat, associated with salt loss. Rest, cooling and oral salt-containing fluid.

Heat exhaustion — the body is coping, barely.

Heavy sweating, weakness, dizziness, nausea, headache, cramps, and a rapid weak pulse. Core temperature is raised but below about 40 °C. Mental state is essentially normal.

Treatment: move to a cool place, lie down with legs raised, remove excess clothing, cool actively, and give oral fluids with salt. It resolves.

Heat stroke — the emergency.

Core temperature above 40 °C with altered mental state, and this is the defining feature.

Confusion, agitation, slurred speech, seizures, or unconsciousness.

And the classic teaching that the skin is hot and dry is only half true. In classic heat stroke — an elderly person during a heatwave — the skin is often dry. In exertional heat stroke — an athlete or soldier — the person is usually still sweating profusely.

So the absence of dry skin does not exclude heat stroke. The mental state is the sign that matters. Anyone confused in the heat has heat stroke until proven otherwise.

The mechanism of harm is protein denaturation (Chapter 1.3) plus a systemic inflammatory response resembling sepsis, with multi-organ failure, rhabdomyolysis (Chapter 6.7), clotting failure and brain injury.

Mortality is around 10 to 50 percent, and it depends almost entirely on how fast the temperature is brought down.

The treatment is immediate aggressive cooling, and it takes priority over everything else including transport.

Cool first, transport second. The evidence is strongest for cold water immersion, which achieves cooling rates several times faster than any other method and, in exertional heat stroke treated with immersion within about 30 minutes, produces mortality close to zero.

Where immersion is impossible: cold wet sheets with continuous fanning, ice packs to the neck, armpits and groin, and cool intravenous fluid.

Target around 38.5 °C, then stop, to avoid overshoot.

And antipyretics do not work (Chapter 13.4). Paracetamol lowers the set point, and in heat stroke the set point is normal. Chapter 23.10.

The people who die in heatwaves are predictable, which is what makes prevention effective: the elderly, particularly those living alone; people on drugs that impair sweating (anticholinergics, antipsychotics) or fluid balance (diuretics); people with dementia or immobility; infants; and outdoor workers and athletes who are unacclimatised.

And the most effective intervention in a heatwave is checking on people — the excess deaths in the 2003 European heatwave, estimated at over 70,000, were concentrated among isolated elderly people, and the countries that responded best did so through active contact rather than through medical treatment.

Hypothermia

Core temperature below 35 °C.

Mild (32 to 35 °C) — shivering, cold and pale, poor coordination, confusion, and often paradoxical undressing, in which a hypothermic person removes their clothes. The explanation is that the vasoconstricted vessels suddenly dilate as regulation fails, producing an intense sensation of heat. It is a well-documented finding at scenes of hypothermic death, and it has led to wrongful suspicion of assault.

Moderate (28 to 32 °C) — shivering stops, which is an ominous rather than a reassuring sign. Consciousness declines, muscles stiffen, and the heart slows.

Severe (below 28 °C) — unconscious, very slow or undetectable pulse and breathing, rigid, and at high risk of ventricular fibrillation.

And the rules for handling severe hypothermia are specific and counter-intuitive.

Handle gently. A cold heart is extremely irritable, and rough movement can precipitate ventricular fibrillation. This includes moving the person, and it is why they are lifted horizontally rather than sat up.

Check the pulse for a full minute before concluding there is none, because it may be very slow and very weak.

And most importantly: "nobody is dead until they are warm and dead."

Hypothermia protects the brain by reducing metabolic demand (Chapter 8.6). Full neurological recovery has been documented after prolonged cardiac arrest in severe hypothermia — the record involves a core temperature below 14 °C and hours of resuscitation.

So resuscitation is continued far longer than in normothermic arrest, and death is not declared until the person has been rewarmed. Rewarming in severe cases is done with extracorporeal circulation where available, which both rewarms and supports the circulation.

Rewarming has its own hazard. Afterdrop — cold blood from the periphery returning to the core as the limbs are warmed, lowering the core temperature further. Which is why rewarming focuses on the trunk rather than the limbs, and why the person is not given a hot bath or vigorously rubbed.

And alcohol makes hypothermia worse while making it feel better. It dilates skin vessels, so the person feels warm while losing heat faster, and it impairs shivering and judgement. The traditional brandy for a cold rescue is actively harmful.

Therapeutic hypothermia turns the mechanism to advantage. Cooling to 32 to 36 °C after cardiac arrest improves neurological outcomes, by reducing the brain's metabolic demand during the vulnerable period after circulation is restored. The optimal target has been debated and refined, and the principle holds.

Sweating disorders

Hyperhidrosis — excessive sweating — affects around 1 to 3 percent of people.

Primary hyperhidrosis affects specific sites — palms, soles, armpits, face — is usually symmetrical, starts in adolescence, and stops during sleep. It is genuinely disabling socially and occupationally, and it is frequently dismissed.

And it is treatable, in a clear ladder: strong aluminium chloride antiperspirants; iontophoresis, passing a weak current through water; botulinum toxin injections, which block the acetylcholine release to the glands and last 4 to 6 months (Chapter 6.2); anticholinergic tablets; and surgery to divide the sympathetic nerves as a last resort — which frequently causes compensatory sweating elsewhere and should not be undertaken lightly.

Secondary hyperhidrosis is generalised, may occur at night, and points to an underlying cause: hyperthyroidism, infection, lymphoma, phaeochromocytoma, menopause, diabetes, or drugs.

And the distinction matters. Generalised sweating, particularly with night sweats and weight loss, warrants investigation; palm and armpit sweating since adolescence does not.

Anhidrosis — inability to sweat — is dangerous rather than convenient. It causes heat intolerance and heat stroke risk, and it occurs in some inherited conditions, in extensive burn scarring, in autonomic neuropathy (Chapter 11.9), and with anticholinergic drugs.

What the next page fixes

Two structures grow out of the skin and are made of the same protein as its outer layer. Chapter 14.3 covers hair and nails — how they grow, why hair loss follows the patterns it does, and what nails reveal about the rest of the body.