# Pathophysiology and treatment of exercise-associated hyponatremia

**Authors:** Barbara Altieri, Irene Aini, Giuseppe Cannavale, Caterina Magnelli, Camilla Mancini, Virginia Zamponi, Andrea M. Isidori, Annamaria Colao, Antongiulio Faggiano, Alessandro Peri

PMC · DOI: 10.1007/s40618-025-02673-7 · Journal of Endocrinological Investigation · 2025-09-06

## TL;DR

Exercise-associated hyponatremia (EAH) is a dangerous condition caused by low sodium levels during exercise, often due to excessive fluid intake and can lead to severe symptoms requiring treatment with hypertonic saline.

## Contribution

This paper provides updated insights into the pathophysiology and treatment of EAH, emphasizing the importance of fluid intake strategies to prevent the condition.

## Key findings

- EAH is caused by excessive fluid intake and non-osmotic vasopressin secretion, not primarily by sodium loss through sweat.
- Treatment of EAH depends on symptom severity, with hypertonic saline solutions recommended for severe cases.
- Prevention strategies should focus on drinking when thirsty rather than in anticipation of thirst.

## Abstract

Exercise associated hyponatremia (EAH) is a medical condition that can occur during physical exertion. Initially, EAH was considered to be restricted to extreme endurance activities, such as ultramarathons and Ironman triathlons. However, it has been more recently recognized in a variety of sports, including team sports and in shorter-duration events. The pathophysiology of EAH is multifactorial and includes excessive fluid intake and non-osmotic arginine vasopressin secretion, which is induced by physical activity. Sodium loss through sweat appears to play a less important role in contributing to EAH. The clinical presentation may vary, depending on the degree of serum sodium reduction. Symptoms, which are due to increased intracranial pressure, may vary from nausea, vomiting, headache, confusion to severe alterations in cognitive functions, decorticate posturing, respiratory distress, coma and even death. It is of pivotal importance to differentiate EAH from other conditions that may present with similar signs/symptoms, such as for instance hypoglycemia, orthostatic hypotension, vasovagal syncope, heat stroke. The treatment of EAH depends on the severity of symptoms. In life-threatening situations intravenous infusion of hypertonic saline solution (3%NaCl) is recommended. In less severe situations oral hypertonic saline solutions can be administered, as an alternative to intravenous hypertonic saline, when tolerated by patients. When symptoms are negligible, the treatment can be limited to fluid restriction. Effective strategies to prevent EAH would be important to reduce the risk of incurring in potentially life-threatening situations. In particular, recommendations to drink in anticipation of thirst during physical exertions should be replaced by the “drinking when thirsty” strategy.

## Linked entities

- **Diseases:** hypoglycemia (MONDO:0004946), orthostatic hypotension (MONDO:0005469)

## Full-text entities

- **Genes:** AVP (arginine vasopressin) [NCBI Gene 551] {aka ADH, ARVP, AVP-NPII, AVRP, VP}
- **Diseases:** orthostatic hypotension (MESH:D007024), heat stroke (MESH:D018883), confusion (MESH:D003221), vasovagal syncope (MESH:D019462), headache (MESH:D006261), coma (MESH:D003128), vomiting (MESH:D014839), death (MESH:D003643), hypoglycemia (MESH:D007003), respiratory distress (MESH:D012128), EAH (MESH:D007010), nausea (MESH:D009325)
- **Chemicals:** Sodium (MESH:D012964)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC12847173/full.md

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Source: https://tomesphere.com/paper/PMC12847173