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Exercise Associated Hyponatremia

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Other Names

  • EAH
  • Exercise-Associated Hyponatremia
  • Exercise-associated Hyponatremic Encephalopathy
  • EAHE


  • Defined as hyponatremia which occurs during or up to 24 hours following physical activity[1]


  • <1% of individuals have a pre-race sodium below 135 mmol/L[2]
    • This is in the expected range for the general population
  • Asymptomatic EAH
    • Common with incidence ranging from 0-51%[3]
    • Most commonly seen in ultramarathons[4]
  • Symptomatic EAH
    • Rare and occurs with less frequency than asymptomatic EAH
    • Incidence estimated to be 0.06% - 1% in endurance events[5][6]
    • Incidence estimates range from 2 - 4 per 1000,000 person years in hikers[7], 4 - 13 cases per 100,000 person years in active duty military[8]
    • At least 14 documented deaths since 1981[1]


  • Definition
    • Hyponatremia: serum, plasma or blood sodium concentration below the normal reference range
    • In most labs, this is typically less than 135 mmol/L[9]
  • Determinants of serum sodium
    • Total body content of sodium
    • total body content of potassium
    • Total body water
  • Can occur due to relative loss of sodium, potassium, total body water or some combination of both[10]
  • Symptoms are directly proportional to magnitude of decrease from baseline and the rate at which the decrease occurs
  • Patients can become symptomatic at declines as low as 7-10% from baseline[11]
  • The role of thirst
    • Thirst should provide adequate stimulus for preventing excess dehydration, markedly reduces the risk of developing EAH
    • Defined as a “generalized, deep seated feeling of desire for water”[12]
    • Evolutionarily refined, finely tuned, regulatory mechanism serving to protect both plasma osmolality and circulating plasma volume[13]


  • Euvolemic (Euvolemic Hyponatremia)/ Hypervolemic (Hypervolemic Hyponatremia)
    • In most cases, hyponatremia is dilutional, occurring due to relative excess of total body water intake[14].
    • This occurs in excess of total body fluid losses which includes the sum of insensible (cutaneous, respiratory, and gastrointestinal), sweat and renal (urine) fluid losses
    • Excessive water intake increases release of vasopressin, overwhelming renal water clearance, subsequently leading to water retention
    • This cause is believed to be associated with all causes of morbidity and mortality associated with EAH
  • Hypovolemic (Hypovolemic Hyponatremia)
    • Defined by electrolyte depletion without expansion of total body water
    • Well described in medical literature in non-exercising individuals
    • More poorly defined in sports medicine literature, less commonly encountered
    • Seen in extreme events such as ultra-marathons and ironman distance triathlons[15]

Risk Factors

  • Male = Female[16]
  • Extrinsic risk factors[1]
    • Overdrinking (water, sports drinks, hypotonic beverages)
    • Weight gain while exercising
    • Duration of activity >4 hours
    • Inexperienced athlete
    • Inadequately trained athlete
    • Slow running or performance pace
    • High or low BMI
    • Readily available fluids (on athlete)
    • NSAID use: controversial[17]
  • Intrinsic risk factors
  • Sports and Activities
    • Endurance competitions including marathon, ironman, ultramarathon
    • Hiking
    • Military exercises
    • Police training[20]
    • Football[21]
    • Fraternity hazing[22]
    • Bikram yoga[23]
    • Lawn bowling[24]

Differential Diagnosis

Clinical Features

  • Asymptomatic
    • Occurs when serum sodium is less than < 135 mmol/L
    • Typically incidental when athlete participating in research protocol or blood work for other unrelated purpose
  • Mild EAH
    • Mild: Non-specific symptoms including lightheadedness, dizziness, nausea, puffiness, weight gain
  • Severe EAH/ EAHE
    • Typically present with headache, vomiting
    • Altered mental status (confusion, seizure, disorientation, obtundation, seizure, coma)
    • May due to cerebral edema (exercise-associated hyponatremic encephalopathy or EAHE)
    • Signs of impending herniation (decorticate posturing, mydriasis)
    • Frothly sputum, SOB, cough due to non-cardiogenic pulmonary edema


  • Primarily a clinical diagnosis supported by laboratory findings
  • Important to check sodium if clinical suspicion of EAH


  • Mild (>130 mmol/L)
  • Moderate (125 - 130 mmol/L)
  • Severe (<125 mmol/L)


  • Treatment should be directed primarily at the level of neurological impairment
  • Not simply just the sodium


  • Typically subclinical and found incidentally
  • No treatment required if not symptomatic
  • Post event, the athlete may be encouraged to avoid hypotonic fluid intake
  • Goal is to achieve urine production
    • Suggests vasopressin levels have fallen and urine is dilute
  • Could consider administering oral hypertonic fluids to prevent progression to symptomatic EAH


  • Less clear guidelines on patients with mild symptoms
  • Can observe and restrict hypotonic and isotonic fluids until urinating
  • Can administer oral Hypertonic Saline (HTS)
    • Concentrated bouillon (4 cubes in 125 mL or 1/2 cup of water
    • 3% Normal Saline 100 mL, preferably with flavoring
  • Oral sodium tablets thought to be less effective than oral HTS
    • More research is needed to better delineate this
  • Disposition: Can be discharged once symptoms have resolved and micturitionhas ocurred


  • Rapidly progressing, life threatening emergency
  • Administer IV Hypertonic Saline (HTS)
    • Typically, 3% Sodium Chloride
    • Dose is 100 mL bolus of 3%
    • Can use 8.4% NaHCO3 50 mL as an alternative
  • Because this is an acute process, there is no risk of osmotic demyelination syndrome
  • Repeated doses (every 10 minutes, up to 3 doses) should be administered until there is clinical improvement[25]
  • In certain clinical contexts, seizure, coma, etc, larger or more frequent doses should be considered
  • The safety of this approach is well documented with one runner receiving 950 mL of 3% over a 7 hour period without complications[26][27]
  • If symptoms are severe, it is reasonable to HTS bolus prior to measuring the sodium
  • Disposition: Goal is stabilize patient for transfer to advanced medical facility for further workup, monitoring and treatment
  • The diagnosis should be communicated to the accepting physician to avoid administration of hypotonic or isotonic fluids


  • Suspected diagnosis without the ability to measure sodium presents a common clinical conundrum
  • If history and exam is suspicious, treatment with HTS is justified
  • Can be a lifesaving therapy and unlikely to do harm
  • Expand intravascular volume, low risk for osmotic demyelination syndrome


  • Should receive immediate electrolyte evaluation
  • If severe, should be treated as above
  • Admission to critical care


Hydration Strategy

  • Fluid and electrolyte therapy should be considered ex-ante rather than ex-post facto
  • Individuals should be discouraged from drinking prior to feeling a thirst sensation as this can lead to EAH
    • Case series cites overdrinking water as a cause or contribution to the development of EAH
    • Body can tolerate loss of 3% body mass or 5% total body water without reduction in performance[28]
  • Body weight is a reasonable surrogate for hydration status when measured daily after sleep[29]
    • It is imprecise during athletic events where EAH is most likely to develop
  • Safest hydration strategy is to drink fluids when thirsty before, during and immediately following exercise
    • Studies have demonstrated individuals maintain plasma osmolality by drinking to thirst[30][31]
  • This persists in both hot[32]and cold[33]environments
  • Thus, drinking to thirst will, in most cases, prevent both dilutional EAH and performance decrements due to excessive dehydration
  • Sodium Supplementation
    • Can attenuate the fall in sodium over prolonged exercise[34]
    • Sodium containing drinks are still hypotonic and will not attenuate EAH in athletes who overdrink[35]

Education & Event Management

  • Safe hydration practices should be instituted and educational strategies disseminated
  • This includes reducing the emphasis on high fluid intakes
  • Example at one ironman competition[36]
    • Education program advised athletes of the risks incurred by overdrinking
    • Additionally decreased the number of fluid stations to limit the fluid availability reduced the incidence of EAH
  • In one 90 km footrace, education of safe drinking habits was shown to reduce the incidence of EAH[37]
  • Placing cycling stations 20 km apart in an ironman triathalon, 5 km apart in a standard marathon reduced EAH[38]
    • Need more studies to optimize spacing strategies
  • Some athletes will seek more quantitative measurements by measuring pre- and post-race weights

Rehab and Return to Play


  • Needs to be updated

Return to Play

  • No clear guidelines


See Also


  1. 1.0 1.1 1.2 Hew-Butler, Tamara, et al. "Statement of the third international exercise-associated hyponatremia consensus development conference, Carlsbad, California, 2015." Clinical Journal of Sport Medicine 25.4 (2015): 303-320.
  2. Tam N, Hew-Butler T, Papadopoulou E, et al.. Fluid intake and changes in blood biochemistry, running speed and body mass during an 89km mountain trail race. Medicina Sportiva. 2009;13:108–115.
  3. Lebus DK, Casazza GA, Hoffman MD, et al.. Can changes in body mass and total body water accurately predict hyponatremia following a 161-km running race? Clin J Sport Med. 2010;20:193–199.
  4. Cairns RS, Hew-Butler T. Incidence of exercise-associated hyponatremia and its association with nonosmotic stimuli of arginine vasopressin in the GNW100s ultra-endurance marathon. Clin J Sport Med. 2014;25:347–354.
  5. Hoffman MD, Hew-Butler T, Stuempfle KJ. Exercise-associated hyponatremia and hydration status in 161-km ultramarathoners. Med Sci Sports Exerc. 2013;45:784–791.
  6. Noakes TD, Sharwood K, Speedy D, et al.. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci U S A. 2005;102:18550–18555.
  7. Backer HD, Shopes E, Collins SL, et al.. Exertional heat illness and hyponatremia in hikers. Am J Emerg Med. 1999;7:532–539.
  8. 76. O'Brien KK, Montain SJ, Corr WP, et al.. Hyponatremia associated with overhydration in U.S. Army trainees. Mil Med. 2001;166:405–410.
  9. Hew-Butler TD, Ayus JC, Kipps C, et al.. Statement of the second international exercise-associated hyponatremia consensus development conference, New Zealand, 2007. Clin J Sport Med. 2008;18:111–121.
  10. Edelman IS, Leibman J, O'Meara MP, et al.. Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. J Clin Invest. 1958;37:1236–1256.
  11. Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med. 1992;117:891–897.
  12. Robertson GL. Abnormalities of thirst regulation. Kidney Int. 1984;25:460–469.
  13. Fitzsimons JT. Angiotensin, thirst, and sodium appetite. Physiol Rev. 1998;78:583–686.
  14. Spasovski G, Vanholder R, Allolio B, et al.. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014;170:G1–G47.
  15. Owen BE, Rogers IR, Hoffman MD, et al.. Efficacy of oral versus intravenous hypertonic saline in runners with hyponatremia. J Sci Med Sport. 2014;17:457–462.
  16. Almond CS, Shin AY, Fortescue EB, et al.. Hyponatremia among runners in the Boston Marathon. N Engl J Med. 2005;352:1550–1556.
  17. Wharam PC, Speedy DB, Noakes TD, et al.. NSAID use increases the risk of developing hyponatremia during an Ironman triathlon. Med Sci Sports Exerc. 2006;38:618–622.
  18. Smith HR, Dhatt GS, Melia WM, et al.. Cystic fibrosis presenting as hyponatraemic heat exhaustion. BMJ. 1995;310:579–580.
  19. Brown MB, Haack KK, Pollack BP, et al.. Low abundance of sweat duct Cl- channel CFTR in both healthy and cystic fibrosis athletes with exceptionally salty sweat during exercise. Am J Physiol Regul Integr Comp Physiol. 2011;300:R605–R615.
  20. Wilber DQ, Brown D. District officer dies after bike ride. Over-hydration cited as factor. Washington Post. 2005.
  21. Herfel R, Stone CK, Koury SI, et al.. Iatrogenic acute hyponatraemia in a college athlete. Br J Sports Med. 1998;32:257–258.
  22. Vega C. 8 charged in Chico hazing death. SFGate. 2005. http://www.sfgate.com/cgi-bin/article.cgi?file=/c/a/2005/03/04/HAZING.TMP. Accessed April 28, 2015.
  23. Reynolds CJ, Cleaver BJ, Finlay SE. Exercise associated hyponatraemia leading to tonic-clonic seizure. BMJ Case Rep. 2012;2012.
  24. Morton A. An unusual cause of exercise-induced hyponatremia. Emerg Med Australas. 2007;19:377–378.
  25. Elsaesser TF, Pang PS, Malik S, et al.. Large-volume hypertonic saline therapy in endurance athlete with exercise-associated hyponatremic encephalopathy. J Emerg Med. 2013;44:1132–1135.
  26. lsaesser TF, Pang PS, Malik S, et al.. Large-volume hypertonic saline therapy in endurance athlete with exercise-associated hyponatremic encephalopathy. J Emerg Med. 2013;44:1132–1135.
  27. 139. Owen BE, Rogers IR, Hoffman MD, et al.. Efficacy of oral versus intravenous hypertonic saline in runners with hyponatremia. J Sci Med Sport. 2014;17:457–462.
  28. Sawka MN, Burke LM, Eichner ER, et al.. American College of Sports Medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc. 2007;39:377–390.
  29. Cheuvront SN, Carter R III, Montain SJ, et al.. Daily body mass variability and stability in active men undergoing exercise-heat stress. Int J Sport Nutr Exerc Metab. 2004;14:532–540.
  30. Armstrong LE, Maresh CM, Gabaree CV, et al.. Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and water intake. J Appl Physiol. 1997;82:2028–2035.
  31. Cheuvront SN, Haymes EM. Ad libitum fluid intakes and thermoregulatory responses of female distance runners in three environments. J Sports Sci. 2001;19:845–854.
  32. Brown MB, McCarty NA, Millard-Stafford M. High-sweat Na+ in cystic fibrosis and healthy individuals does not diminish thirst during exercise in the heat. Am J Physiol Regul Integr Comp Physiol.
  33. Stricker EM, Verbalis JG. Hormones and behavior. Am Sci. 1988;76:261–267.
  34. Vrijens DM, Rehrer NJ. Sodium-free fluid ingestion decreases plasma sodium during exercise in the heat. J Appl Physiol. 1999;86:1847–1851.
  35. Weschler LB. Exercise-associated hyponatremia: a mathematical review. Sports Med. 2005;35:899–922.
  36. Sharwood K, Collins M, Goedecke J, et al.. Weight changes, medical complications and performance during an Ironman triathlon. Br J Sports Med. 2004;38:718–724.
  37. Hew-Butler T, Sharwood K, Boulter J, et al.. Dysnatremia predicts a delayed recovery in collapsed ultramarathon runners. Clin J Sport Med. 2007;17:289–296.
  38. Speedy DB, Rogers IR, Noakes TD, et al.. Diagnosis and prevention of hyponatremia at an ultradistance triathlon. Clin J Sport Med. 2000;10:52–58.
Created by:
John Kiel on 25 January 2020 16:03:41
Last edited:
27 January 2020 00:58:53