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Cited by 112Electrolyte and hormonal disordersThermoregulation and physiological responsesExercise and Physiological Responses

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Exercise-Associated Hyponatremia: 2017 Update

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Hew-Butler, Tamara, Loi, Valentina, Pani, Antonello, Rosner, Mitchell H.·2017·Frontiers in Medicine
DOI 10.3389/fmed.2017.00021PMC PMC5334560
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Abstract

Exercise-associated hyponatremia (EAH) was initially described in the 1980s in endurance athletes, and work done since then has conclusively identified that overdrinking beyond thirst and non-osmotic arginine vasopressin release are the most common etiologic factors. In recent years, EAH has been described in a broader variety of athletic events and also has been linked to the development of rhabdomyolysis. The potential role of volume and sodium depletion in a subset of athletes has also been described. This review focuses on the most recent literature in the field of EAH and summarizes key new findings in the epidemiology, pathophysiology, treatment, and prevention of this condition.

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Figure 1 Reported cases of exercise-associated hyponatremia (EAH) along the spectrum of pathophysiology. Cases of EAH per sport are superimposed upon the broad spectrum of volemic pathophysiology: (1) hypervolemia—overzealous drinking with arginine vasopressin (AVP) stimulated fluid retention and minimal sodium losses or sodium over-correction (black triangle); (2) euvolemia—moderate drinking with AVP stimulated fluid retention and mild (compensable) sodium losses (gold triangle); and (3) hypovolemia—moderate drinking (volemic thirst) with AVP stimulated fluid retention, and under-replaced sodium losses (red triangle).
Figure 1 Reported cases of exercise-associated hyponatremia (EAH) along the spectrum of pathophysiology. Cases of EAH per sport are superimposed upon the broad spectrum of volemic pathophysiology: (1) hypervolemia—overzealous drinking with arginine vasopressin (AVP) stimulated fluid retention and minimal sodium losses or sodium over-correction (black triangle); (2) euvolemia—moderate drinking with AVP stimulated fluid retention and mild (compensable) sodium losses (gold triangle); and (3) hypovolemia—moderate drinking (volemic thirst) with AVP stimulated fluid retention, and under-replaced sodium losses (red triangle).CC BY · PubMed Central
Figure 2 Pathogenic factors involved in the development of exercise-associated hyponatremia (EAH). EAH develops from multiple mechanisms and can occur in both states of volume excess and depletion with AVP secretion occurring in both cases. It is important to note that none of these mechanisms occur in isolation, and they can overlap in any given patients (for example, sodium loss and excess water intake can occur in the same patient) Abbreviations: Na, sodium; AVP, arginine vasopressin; GI, gastrointestinal; CNS, central nervous system; RAAS, renin–angiotensin–aldosterone system.
Figure 2 Pathogenic factors involved in the development of exercise-associated hyponatremia (EAH). EAH develops from multiple mechanisms and can occur in both states of volume excess and depletion with AVP secretion occurring in both cases. It is important to note that none of these mechanisms occur in isolation, and they can overlap in any given patients (for example, sodium loss and excess water intake can occur in the same patient) Abbreviations: Na, sodium; AVP, arginine vasopressin; GI, gastrointestinal; CNS, central nervous system; RAAS, renin–angiotensin–aldosterone system.CC BY · PubMed Central
Figure 3 Putative bidirectional relationship between exercise-associated hyponatremia (EAH) and rhabdomyolysis. EAH may lead to rhabdomyolysis through changes in the skeletal muscle membrane (osmotic shock) and activation of reactive oxygen species (ROS) along with increases in intracellular calcium (Ca) that activate intracellular proteases and lead to cellular breakdown. Rhabdomyolysis either through this mechanism or by other means leads to local and systemic inflammation and release of interleukin-6 (IL-6), which may increase arginine vasopressin (AVP) levels further lowering serum sodium. Non-steroidal anti-inflammatory drug use may also contribute to excess AVP release.
Figure 3 Putative bidirectional relationship between exercise-associated hyponatremia (EAH) and rhabdomyolysis. EAH may lead to rhabdomyolysis through changes in the skeletal muscle membrane (osmotic shock) and activation of reactive oxygen species (ROS) along with increases in intracellular calcium (Ca) that activate intracellular proteases and lead to cellular breakdown. Rhabdomyolysis either through this mechanism or by other means leads to local and systemic inflammation and release of interleukin-6 (IL-6), which may increase arginine vasopressin (AVP) levels further lowering serum sodium. Non-steroidal anti-inflammatory drug use may also contribute to excess AVP release.CC BY · PubMed Central
Figure 4 Treatment of exercise-associated hyponatremia (EAH) according to signs and symptoms. Evidenced-base treatment options for EAH associated with mild (yellow), moderate (orange), or severe clinical signs and symptoms.
Figure 4 Treatment of exercise-associated hyponatremia (EAH) according to signs and symptoms. Evidenced-base treatment options for EAH associated with mild (yellow), moderate (orange), or severe clinical signs and symptoms.CC BY · PubMed Central

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Citations

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Show all 101 references

Research works printed but not linked: 11

  1. 2008, Electrolyte Imbalance Blamed in Death of Football Player. Coroner’s Office Says Athlete Failed to Replenish Lost Sodium
  2. Blevins, 2014, Preps Sports Report
  3. Stevens, 2015, Update: Douglas County Football Player Has Died
  4. Baumgarder, 2009, Au Sable River Canoe Marathon Pushes Paddlers to the Limits
  5. Krabel, 2015, Athlete Dies after IM Frankfurt
  6. Vega, 2005, 8 Charged in Chico Hazing Death
  7. Sydney Morning Herald, 2012, Bushwalker Died from Drinking Too Much Water
  8. Gierer, 2016, Benning Soldier Dies after Falling Ill on First Day of Ranger School
  9. WIlber, 2005, District Officer Dies After Bike Ride. Over-hydration Cited as Factor
  10. Cruel, 2015, 12 Easy Ways to Drink More Water Every Day
  11. Associated Press, 2007, Woman Dies after Water Drinking Contest

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Metadata

Authors
Hew-Butler, T., Loi, V., Pani, A., & Rosner, M. H.
Affiliations
  • Azienda Ospedaliera G. Brotzu (IT)
  • University of Virginia Health System (US)
Corresponding author
Rosner, Mitchell H.
ORCID
Venue
Frontiers in Medicine
Publisher
Frontiers Media SA
Published
2017-03-03
Volume
4
Pages
21-21
ISSN
2296-858X (ISSN-L)
DOI
10.3389/fmed.2017.00021
PMC
PMC5334560
OpenAlex
W2594661228
Cited by
112
References
101
Citations by year
2026: 6 · 2025: 9 · 2024: 7 · 2023: 11 · 2022: 12 · 2021: 17 · 2020: 15 · 2019: 26 · 2018: 9
FWCI
2.49
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Medicine (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UNICA IRIS Institutional Research Information System (University of Cagliari) (submittedVersion, other-oa)
Topics
  • Health Sciences › Medicine › Nephrology › Electrolyte and hormonal disorders
  • Health Sciences › Medicine › Physiology (medical) › Thermoregulation and physiological responses
  • Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
Keywords
exercise-associated hyponatremia, endurance athletes, rhabdomyolysis, sodium depletion, hypovolemia, pathophysiology, prevention, treatment

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