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# Sweat glands: secretion, salt reabsorption and acclimatization

- Mechanism
- Exam priority: medium

Sweat glands make a plasma-like fluid, then the duct pulls salt back out; heat training makes more sweat with less salt.

Updated Nov 13, 2026

Also called: Eccrine glands, Sweat chloride test, Heat acclimatization, Body insulation

## Key points

- Eccrine glands are innervated by sympathetic fibres that release acetylcholine onto muscarinic receptors: anticholinergics cause hot, dry skin.
- The duct reabsorbs Cl⁻ through CFTR and Na⁺ through ENaC; in cystic fibrosis sweat Cl⁻ stays high (sweat chloride ≥ 60 mmol/L supports the diagnosis).
- Sweat Na⁺ is lowest at low sweat rates (≈ 5 mEq/L) and rises toward ≈ 50–60 mEq/L at high rates in an unacclimatized person.
- Heat acclimatization (1–3 weeks) roughly doubles maximal sweating, expands plasma volume and, via aldosterone, cuts salt loss in sweat.
- Evaporating sweat removes ≈ 0.58 kcal per gram; dripping sweat that does not evaporate does not cool.

## What it is

Eccrine sweat glands cool the body by evaporation. The coiled secretory part makes a protein-free, plasma-like fluid under sympathetic cholinergic control; the duct then reabsorbs Na⁺ and Cl⁻ but little water, so final sweat is hypotonic. Faster sweating leaves less time for reabsorption, and aldosterone during heat acclimatization lowers the salt lost in it. Skin and subcutaneous fat insulate the core; skin blood flow sets how much heat reaches the surface.

## Key facts

- There are about 2–4 million eccrine glands, densest on palms, soles and forehead; palm and sole sweating also responds to emotion.
- Apocrine glands (axilla, groin, areola) open into hair follicles, start at puberty, respond to adrenergic stimuli and produce odour only after bacterial breakdown.
- The secretory coil loads Cl⁻ with a basolateral Na⁺–K⁺–2Cl⁻ cotransporter and releases it apically; Na⁺ and water follow.
- The duct is relatively impermeable to water, so salt reabsorption makes sweat hypotonic and concentrates urea, lactate and K⁺ at low flow.
- Unacclimatized people rarely exceed ≈ 1 L/h of sweat; acclimatized workers can reach ≈ 2–3 L/h.
- Skin and subcutaneous fat conduct heat poorly, about a third as well as other tissues; arteriovenous anastomoses in fingers, toes and ears control how much warm blood reaches the surface.

## How it works, step by step

- A rise in core or skin temperature activates the preoptic hypothalamus, which increases sympathetic cholinergic outflow to sweat glands.
- ACh on M₃ receptors raises intracellular Ca²⁺ in coil cells; Cl⁻ channels open and a protein-free, plasma-like fluid is secreted.
- In the duct, ENaC reabsorbs Na⁺ and CFTR lets Cl⁻ follow, while water mostly stays in the lumen.
- Slow flow allows near-complete NaCl reabsorption; fast flow leaves more NaCl in the sweat.
- Repeated heat exposure lowers body NaCl slightly, aldosterone rises and boosts ductal Na⁺ reabsorption; gland output capacity also increases.
- Sweat evaporates from the skin surface and removes heat; humidity and still air reduce evaporation.

## Reference values (adult)

| Parameter | Value | Note |
| --- | --- | --- |
| Primary (coil) fluid Na⁺ / Cl⁻ | ≈ 140 / 105 mEq/L | like plasma, no protein |
| Final sweat Na⁺, low rate | ≈ 5–10 mEq/L | |
| Final sweat Na⁺, high rate, unacclimatized | ≈ 50–60 mEq/L | |
| Maximal sweat rate | ≈ 1 L/h (up to ≈ 2–3 L/h acclimatized) | |
| Sweat chloride test | ≤ 29 normal; 30–59 intermediate; ≥ 60 mmol/L consistent with CF | |
| Heat removed by evaporation | ≈ 0.58 kcal/g water | |

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

## Eccrine and apocrine glands

| Feature | Eccrine | Apocrine |
| --- | --- | --- |
| Location | Almost all skin; most on palms, soles, forehead | Axilla, groin, perineum, areola |
| Opens onto | Skin surface | Hair follicle |
| Main nerve signal | Sympathetic, cholinergic (muscarinic) | Adrenergic |
| Secretion | Watery, hypotonic | Thicker, lipid- and protein-rich |
| Main role | Cooling by evaporation | Scent; little role in cooling |
| Onset | From infancy | At puberty |

## Clinical notes

- Cystic fibrosis: defective CFTR blocks ductal Cl⁻ (and so Na⁺) reabsorption, giving salty-tasting skin and risk of salt depletion in hot weather.
- The sweat test stimulates local sweating with pilocarpine (a muscarinic agonist) applied by iontophoresis, then measures chloride.
- Anticholinergic toxicity blocks sweating, so heat cannot be shed: hot, flushed, dry skin with fever.
- In classic heat stroke, especially in older adults, sweating can fail and core temperature rises rapidly.

## Memory aid

The coil pours salt water; the duct is a salt thief that works best when the tap runs slowly. Aldosterone trains the thief; CF ties its hands.

## Test yourself

Think of the answer, then tap the question to see it.

## Sweat glands are sympathetic targets. Why does atropine stop sweating?

Eccrine glands are an exception: their sympathetic postganglionic fibres release acetylcholine onto muscarinic receptors, which atropine blocks.

## Why is sweat chloride high in cystic fibrosis while airway secretions are thick and dry?

In the sweat duct CFTR is needed to reabsorb Cl⁻, so salt stays in sweat; in the airway CFTR is needed to secrete Cl⁻ and water, so mucus is dehydrated.

## Why does sweat contain more sodium when a person sweats heavily?

Fluid flows through the duct faster, leaving less contact time for Na⁺ and Cl⁻ reabsorption, so more salt stays in the final sweat.

## Which hormone lowers sweat sodium during heat acclimatization, and what triggers it?

Aldosterone, released when repeated sweating slightly lowers body NaCl and volume; it increases Na⁺ reabsorption in the sweat duct and kidney.

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## Connections

## Related topics 5

- [Body temperature regulation](https://durgical.com/en/physiology/body-temperature-regulation/)
- [Heat exhaustion and heat stroke](https://durgical.com/en/physiology/heat-exhaustion-and-heat-stroke/)
- [Skin blood flow](https://durgical.com/en/physiology/skin-blood-flow/)
- [Adrenergic and cholinergic receptors](https://durgical.com/en/physiology/adrenergic-and-cholinergic-receptors/)
- [Aldosterone: actions and control](https://durgical.com/en/physiology/aldosterone-actions-and-control/)

## Related conditions 3

- [Cystic fibrosis](https://durgical.com/en/conditions/cystic-fibrosis/)
- [Heat stroke and heat exhaustion](https://durgical.com/en/conditions/heat-stroke-and-heat-exhaustion/)
- [Anticholinergic toxicity (incl. scopolamine «burundanga»)](https://durgical.com/en/conditions/anticholinergic-toxicity/)

## In Pharmacology 1

- [Atropine](https://durgical.com/en/pharmacology/atropine/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [Physiology, Integument](https://www.ncbi.nlm.nih.gov/books/NBK554386/) (StatPearls (NCBI Bookshelf), 2025); [Sweat electrolytes test: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/003630.htm) (MedlinePlus, US National Library of Medicine, 2025); [Cystic fibrosis: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000107.htm) (MedlinePlus, US National Library of Medicine, 2025).

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Representative model, for educational purposes only.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/sweat-glands-secretion-salt-reabsorption-and-acclimatization/