Exercise-Associated Hyponatremia: Low Sodium in Endurance Athletes

Table of Contents

1. What It Is and How It Differs From Dehydration
2. How Often It Occurs, Study by Study
3. Causes Reported in the Research
4. Symptoms and the Signs Hospitals Treat as Urgent
5. Hospital and Field Treatment Reported
6. What the Published Consensus Statements State
7. What Studies Found About Drinking to Thirst
8. What Sodium Supplements Did and Did Not Do
9. Reported Deaths
10. What Is Not Known
11. Key Research Papers
12. Connections
13. Featured Videos

What It Is and How It Differs From Dehydration

The 2019 Wilderness Medical Society guideline defines exercise-associated hyponatremia as a serum or plasma sodium concentration below the normal reference range of 135 mmol/L, occurring during or up to 24 hours after prolonged physical activity (Bennett 2020). The first description came in 1985 from South Africa, when four athletes developed what the authors called water intoxication during events lasting more than 7 hours. Told to drink less, three of them later finished long events without trouble (Noakes 1985; Knechtle 2019).

Dehydration and exercise-associated hyponatremia are close to opposites. In plain dehydration the body has lost more water than it has taken in, and the blood tends to become more concentrated. In exercise-associated hyponatremia the blood has become too dilute, so water moves into cells, and in the brain that swelling is what causes harm. Reviews describe treatment as pulling in opposite directions as well: fluids given for dehydration or heat illness can make hyponatremia worse (Rosner 2019; Rosner 2024).

The two conditions look alike from the outside. The American Family Physician summary of the Wilderness Medical Society guideline lists these differences and overlaps (Jonas 2021):

• Leaning toward hyponatremia: a bloated feeling, weight gain, no thirst, normal vital signs, no dizziness on standing.
• Leaning toward heat illness and fluid loss: small fluid intake, dry mouth, thirst, raised temperature, dizziness on standing.
• Seen with both: weakness, fatigue, irritability, headache, nausea, vomiting, dizziness, and in severe cases altered mental state, collapse, seizures and coma.

The same summary reports that injury logs from a national park showed one in five nonfatal incidents first labelled as heat-related were in fact exercise-associated hyponatremia. Body weight helps but does not settle the question. In five years of data from 161-km races in northern California, 23.8% of runners with low sodium had gained weight or held steady, 40.6% had lost up to 3%, and 35.6% had lost more than 3% (Hoffman 2013). So a runner who has lost weight can still have low sodium. Dehydration also remains the more common outcome in some events: in a 250-km multistage desert race, the cumulative share with high sodium was 52.3% against 14.8% with low sodium (Krabak 2017). For the high-sodium side of this, see Hypernatremia: Thirst and Confusion.

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How Often It Occurs, Study by Study

Reported rates range from 0% to 51% (Rosner 2019). Much of that spread comes from who was tested. Most figures below come from volunteers who gave blood for research at the finish, and most of those with a low reading had no symptoms. Rates of symptomatic illness are far lower, typically under 1% of marathon runners (Rosner 2019). A reader comparing the numbers is comparing different groups, weather, course rules and cut-off values.

Marathons (42 km)

• Boston, 2002: 13% of 488 runners had 135 mmol/L or less, and 0.6% had 120 mmol/L or less (Almond 2005).
• London: 12.5% of 88 volunteers, all without symptoms, with values of 128–134 mmol/L, in cool conditions (Kipps 2011).
• Zurich, 2006: 3% of 167 recruited runners, all without symptoms, in cool, rainy weather with a 5-hour time limit (Mettler 2008).
• Houston: 21 runners came to the medical area with hyponatremia in 2000, or 0.31% of entrants (Hew 2003). Among 96 runners in research projects at the same race from 2000 to 2004, 22% met the definition (Chorley 2007).
• A marathon and half marathon in Florida, 2008: 8.2% of 195 runners after the race, but also 5.0% of 161 before it started (Mohseni 2011).

Ultramarathons

• 161 km in northern California, five years combined: 15.1% of 669 finishers overall, ranging from 4.6% to 51.0% by year, higher in hotter weather (Hoffman 2013). Later years gave 5.8% of 207 tested finishers (Winger 2013) and 6.6% of finishers tested (Hoffman and Stuempfle 2015).
• 161 km at high altitude, Colorado: 20% of 84 runners tested after the race, all without symptoms; 40% of women against 16% of men (Khodaee 2021).
• 100 km in Switzerland: 4.8% of 145 men, all without symptoms (Knechtle 2011).
• 44-km mountain trail, Greece: 8% of 62 runners, all without symptoms, under rules allowing fluids only at set checkpoints (Arnaoutis 2020).
• 104 km and 174 km in Australia: 4 of 15 runners after the race, but 10 of 15 at some point during it (Cairns 2015). This suggests a finish-line reading can miss cases that come and go.
• 250-km multistage desert races: 1.6%, 4.8% and 10.1% after successive stages, with a cumulative 14.8% of 128 runners (Krabak 2017).

Full-distance triathlons (3.8-km swim, 180-km cycle, 42.2-km run)

• New Zealand, 1990s: 18% of 330 finishers; 18 of those 58 sought medical care for symptoms, and 11 of the 58 had below 130 mmol/L (Speedy 1999).
• New Zealand, 2004: 1.8% of 330 athletes, after changes to fluid guidance and drink stations (Wharam 2006).
• South Africa, 2000: 0.6%, three readings below 135 mmol/L (Sharwood 2002).

Swimming and cycling

• 26.4-km open-water swim: 8% of 25 men and 36% of 11 women (Wagner 2012).
• 720-km road cycling event: none of 65 cyclists (Rüst 2012).
• Five Swiss ultra-endurance events pooled: 12 of 200 male athletes (6%) (Knechtle, Gnädinger 2011).

Beyond organized races, a 2019 review gives 16% of Grand Canyon hikers seeking care for collapse or exhaustion over one summer in 1993, and 6.7 cases per 100,000 person-years in the United States military from 1999 to 2012 (Rosner 2019). A 2025 review of 56 field studies found that running and hiking produced far more cases and published studies than cycling, swimming and triathlon (Armstrong 2025).

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Causes Reported in the Research

Drinking more than the body loses

This is the finding reported most consistently. In Boston, weight gain during the race carried an odds ratio of 4.2 on multivariate analysis, and drinking more than 3 liters or drinking at every mile were associated on simpler analysis (Almond 2005). In Houston, runners with hyponatremia drank more water and more sports drink, and the lower the sodium, the more they had drunk (Hew 2003). In a pooled analysis of 2,135 athletes, sodium after the race fell in a straight line as body weight rose (Noakes 2005). In the New Zealand triathlon, 8 of the 11 athletes with the lowest sodium had held or gained weight (Speedy 1999). A 2019 review states there is no evidence that sports drinks lower the rate, and notes their sodium content sits around 20 to 30 mmol/L, well below that of blood (Rosner 2019).

A 2019 review gives a sense of the volumes. A person with healthy kidneys eating a regular diet can clear 500 to 1,000 mL of water an hour, and with sweat and breath losses as much as 1,000 to 1,500 mL an hour may be handled before water builds up (Rosner 2019). Many people who develop the condition did not drink that much, which is why the research looks for a second factor.

Vasopressin that stays high

Vasopressin (also called antidiuretic hormone) tells the kidney to hold water. It normally falls when blood becomes dilute, so the extra water leaves as urine. During long exercise it can stay up for other reasons. How this works is animated on the Thirst, ADH and How Your Body Guards Its Water page. Numbers from the field:

• Among 82 runners in a 56-km race, vasopressin rose 3.9-fold even though sodium barely changed, from 139.3 to 138.1 mmol/L (Hew-Butler, Jordaan 2008).
• Runners with hyponatremic collapse met the diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion, and 43% of 22 had measurable vasopressin (Siegel 2007).
• In 25 soldiers on a 40-km march, vasopressin went from 2 to 11 pg/mL (Nolte 2019).
• In two saline trials at a 161-km race, vasopressin did not change significantly after either treatment, and in the first it was raised at the finish in both groups (Rogers 2011; Owen 2014).

Suggested triggers include pain, nausea, low blood sugar, heat and stress (Hew-Butler 2017). One proposal, described by its reviewers as speculative, is that the inflammatory signal interleukin-6 drives the release: in 15 ultramarathon runners the two were correlated at r = 0.31 (Cairns 2015).

Sex and body size

The picture here is less tidy than it is often presented. Women in New Zealand finished with lower sodium than men, 133.7 against 137.4 mmol/L (Speedy 1999), and two later races found higher rates in women (Wagner 2012; Khodaee 2021). But in Boston, the link to female sex was present on simple analysis and disappeared once body-mass index and racing time were accounted for; extremes of body-mass index remained (Almond 2005). In Houston, lighter and slower runners had the most positive fluid balance (Chorley 2007). The 2025 review of 220 cases found that a greater percentage of women were affected, not a greater absolute number (Armstrong 2025). A 2017 review describes a hypothesis that estrogen limits the brain's ability to adapt to swelling, and stresses that men have also died (Hew-Butler 2017).

Long event time

In Boston, finishing in over 4 hours carried an odds ratio of 7.4 compared with finishing under 3 hours 30 minutes (Almond 2005). In Houston, finish time and sodium were inversely related, with an r² of 0.51 (Hew 2003). One exception: in the 2004 New Zealand triathlon, race time was not associated with sodium (Wharam 2006). Rates also rose with heat in California (Hoffman 2013), and a 2019 narrative review lists duration, discipline, sex, temperature and race location as factors (Knechtle 2019).

Anti-inflammatory drugs

Nonsteroidal anti-inflammatory drugs are a suggested contributor, but the studies disagree:

• Link found: in a triathlon of 330 athletes, 30% used these drugs and their use was related to hyponatremia (P = 0.0002), although estimated fluid intake was no different (Wharam 2006). In a small ultramarathon study, 7 of 10 runners with low sodium had taken them against 0 of 5 without (Cairns 2015). All seven runners in one hospital case series had a history of use (Ayus 2000), and users were overrepresented in five Western States cases who also had muscle breakdown (Bruso 2010).
• No link found: Boston (Almond 2005), Houston (Hew 2003) and a Colorado 161-km race (Khodaee 2021).
• Mixed within one report: the abstract of a New Zealand 60-km study says users were more likely to become hyponatremic, and also that sodium did not differ between users and nonusers (Page 2007).

A 2022 review places these drugs among the risk factors but to a smaller extent than the others (Seal 2022).

Other mechanisms proposed

Most athletes who gain weight do not develop low sodium. In the pooled analysis, 70% of the 231 who gained weight had normal or high sodium, and its authors proposed that some sodium is drawn from internal stores that do not normally count toward the blood level, with failure to mobilize it adding to risk (Noakes 2005). A 2017 review adds water released as stored muscle sugar is used, rapid absorption of fluid from the gut at the end of an event, and sweat sodium losses, which it calls controversial. A cluster of cases also links this condition to rhabdomyolysis, or muscle breakdown: five of 400 starters at one 161-km race were hospitalized with both, and three progressed to acute kidney failure (Bruso 2010).

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Symptoms and the Signs Hospitals Treat as Urgent

Many people have no symptoms at all. In the New Zealand triathlon only 31% of those with low sodium sought care for symptoms (Speedy 1999). For the mild end, a 2025 review of 220 reported cases across seven kinds of outdoor activity lists nausea, weakness or lethargy, dizziness, headache and swelling of the hands and feet as most common (Armstrong 2025). The Confusion and Headache and Muscle Cramps pages explain these symptoms in general. A review from 2019 attributes all of the symptoms to the central nervous system, through swelling of cells raising pressure inside the skull (Rosner 2019).

Signs that the research associates with hyponatremic encephalopathy, the severe form with brain swelling, and that hospitals and race medical teams treat as urgent (Armstrong 2025; Jonas 2021):

• Altered mental state or confusion
• Vomiting
• Seizure
• Agitation or restlessness
• Collapse or loss of consciousness
• Shortness of breath or frothy sputum, the signs of fluid in the lungs

Fluid in the lungs was the feature that defined one report: seven marathon runners collapsed and were hospitalized with lung swelling, a normal heart and brain swelling, with oxygen saturation under 70% and an average sodium of 121 mmol/L (Ayus 2000).

Three reported features catch people out:

• Timing. Symptoms can arrive after the finish line. Fourteen runners came to one London hospital several hours after the 2003 marathon (Kipps 2011). A 2019 review describes a clear-headed period followed by symptoms within about 30 minutes, possibly as water left in the gut is absorbed (Rosner 2019).
• The number does not tell the whole story. The 2025 review concluded that the absolute sodium value is not a reliable guide to severity, and that none of its 220 cases below 130 mmol/L were free of symptoms (Armstrong 2025). Individual studies differ on that second point: 4 of 11 New Zealand triathletes below 130 mmol/L had no symptoms (Speedy 1999), and all those with low sodium in the Colorado race were symptom-free, including one below 130 (Khodaee 2021).
• Telling it from other collapse. In Houston, vomiting was the only clinical sign that separated it from other causes of collapse (Hew 2003). The same symptoms can occur with high sodium, which is why reviewers say a blood sodium measurement is what settles it (Hew-Butler, Noakes 2008). The guideline summary adds that rectal temperature is key when mental state is altered, since exertional heat stroke presents similarly, with a core temperature above 40°C (Jonas 2021).

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Hospital and Field Treatment Reported

Hypertonic saline is salt water stronger than blood. Case series and reviews describe it as the treatment that reverses brain swelling in this condition.

• Early hospital series. Seven collapsed marathon runners were all placed on ventilators. Six were treated with intravenous sodium chloride at 514 mmol/L, which raised sodium by 10 mmol/L over 12 hours; their lung and brain swelling resolved and all were well a year later. The seventh, whose low sodium went unsuspected, died (Ayus 2000).
• Marathon medical teams. Runners with encephalopathy at later races were given intravenous 3% saline, reported as producing rapid improvement without adverse effects (Siegel 2007).
• Size of the rise. Reviewers report that 100 mL of 3% saline raises sodium by 3 to 5 mmol/L and lowers pressure in the skull (Rosner 2019). The guideline summary gives up to 2 mmol/L per dose, and records larger totals used without harm: 600 mL over one hour and 950 mL over seven hours (Jonas 2021).
• Why correction limits differ here. The parent page describes limits on how fast sodium is raised in longer-standing low sodium, because of a brain injury called osmotic demyelination. Reviewers state that because this form develops quickly, no such case has been reported and that the bolus is safe in this setting (Rosner 2024; Hew-Butler 2017).
• Plain saline. Isotonic (0.9%) saline has been used, but recovery is reported as far slower, days instead of hours, and reviewers raise the concern that it can add to water retention when vasopressin is high. They describe an exception when an athlete is clearly short of fluid and sodium, and state that fluids weaker than blood are contraindicated once the diagnosis is confirmed (Hew-Butler 2017).

Trials of oral versus intravenous saline

Only two small randomized trials turned up, both at the same 161-km race, and both in runners with mild or no symptoms. Neither tested severe illness.

• Of 47 finishers screened, 14 (30%) had low sodium and 8 agreed to be randomized to a 100-mL dose of 3% saline by mouth or vein. Only the intravenous group changed significantly, from 130.8 to 134.6 mmol/L over 60 minutes (Rogers 2011).
• A larger follow-up randomized 26 runners, 11 by mouth and 15 by vein. Both rose by 2 mmol/L at 60 minutes, with no significant difference between them (Owen 2014).

A single case report adds field use: a runner with 122 mmol/L improved with 800 mg of sodium in 200 mL of water by mouth, then improved further in hospital as he passed large volumes of urine, and went home about 5 hours after admission (Hoffman and Myers 2015).

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What the Published Consensus Statements State

International panels met in Cape Town in 2005 (Hew-Butler 2005), New Zealand in 2007 (Hew-Butler 2008) and Carlsbad, California in 2015 (Hew-Butler 2015). The PubMed records of these three statements carry no abstract, and their full text could not be read for this page. What follows is how panel members and later authors report them. The Wilderness Medical Society published its own guideline in 2014 and updated it in 2019 (Bennett 2020).

• Main cause (2015 conference, as reported): overconsumption of fluids weaker than blood, likely combined with vasopressin release not driven by blood concentration (Hew-Butler 2017).
• On-site testing (2007 conference, as reported): concluded that medical directors need on-site sodium testing available. A 2019 review notes this is still not widely available or feasible (Rosner 2019).
• Severe illness (2015 conference, as reported): a 100-mL bolus of 3% saline every 10 minutes until signs of brain swelling resolve (Hew-Butler 2017).
• Severe illness (Wilderness Medical Society, as summarized): mental state changes with a normal or slightly raised rectal temperature are taken as severe hyponatremia; 100-mL intravenous boluses of hypertonic saline repeated every 10 minutes for three doses; rapid cooling added if heat illness is also suspected or the diagnosis is uncertain (Jonas 2021).
• Mild illness (Wilderness Medical Society, as summarized): fluid restriction until urine flows freely, with salt replaced by mouth through a concentrated broth of three to four bouillon cubes in 125 mL of water or salty foods, and observation for at least an hour (Jonas 2021).
• Prevention (both, as reported): no fixed fluid volume has been shown to prevent hyponatremia, and the statements describe drinking in response to thirst as the guide. Limiting fluid availability along a course lowered rates (Jonas 2021; Hew-Butler 2017).
• Sodium (2015 conference, as reported): sodium taken during a race may slow the fall in blood sodium but cannot prevent the condition when fluid intake is excessive (Hew-Butler 2017).
• Weight: a 2017 review calls weight gain during exercise a sign that fluid intake has run ahead of losses, while the guideline summary states that basing fluid replacement on weight loss during prolonged exercise does not prevent the condition (Hew-Butler 2017; Jonas 2021).

Consensus statements are expert opinion built on the evidence available, and much of that evidence here is observational. The authors of the 2024 Grand Canyon paper state that case reports suggest this approach works, while acknowledging that accurate outcome data do not exist (Rosner 2024).

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What Studies Found About Drinking to Thirst

"Ad libitum" drinking means drinking as desired. No randomized trial comparing drink-to-thirst with a fixed schedule on hyponatremia turned up in the records read for this page. The evidence is observational:

• 56-km ultramarathon: 82 runners drinking as desired kept sodium steady, 139.3 to 138.1 mmol/L, with vasopressin still rising (Hew-Butler, Jordaan 2008).
• 720-km cycling event: 65 riders drinking as desired, with no cases (Rüst 2012).
• 40-km military march: 25 soldiers drank water as desired at 736 mL an hour, lost 4.0% of body mass, and sodium ranged from 134 to 143 mmol/L afterward. None had high sodium. The authors state that no single hydration strategy likely prevents the condition, even though the paper's title says this one did (Nolte 2019).
• 161-km race beliefs: the most common plan among finishers, used by 43.1%, was drinking on a schedule. The pre-race plan was not associated with sodium at the finish (Winger 2013).
• Mountain races of 69 km and 121 km: the authors conclude that drinking to thirst seems an adequate approach, on a small sample (Schenk 2021).

Changing what races do has been studied too. A New Zealand triathlon combined education on fluid intake, fewer support stations and a compulsory weigh-in. Athletes treated for hyponatremia fell from 25 (3.8% of starters) in 1997 to 4 (0.6%) in 1998 (Speedy 2000). The study had no control group, so other factors cannot be ruled out. A later report at the same race, with a 1.8% rate, attributes the low figure to these same changes (Wharam 2006).

The usual concern with thirst-based drinking is dehydration and heat. A 2017 review states that fluid replacement beyond thirst has not been shown to reduce fatigue, cramping or exertional heat stroke, and that deficits up to about 3% of body mass are well tolerated in healthy people (Hew-Butler 2017). In a South African triathlon, greater weight loss was not related to higher rectal temperature or poorer marathon time (Sharwood 2002). These are findings in fit athletes, and they do not speak to people who are unwell or unacclimatized. The same review describes persistent misconceptions about heavy drinking: in one survey only 7.3% of 110 websites discussed basing fluid intake on thirst (Hew-Butler 2017). For more on how sweat and water balance work, see Sweat: How Your Body Cools Itself and Hydration Beyond Water.

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What Sodium Supplements Did and Did Not Do

Salt tablets and sports drinks are common: 93.9% of runners surveyed in one 161-km race used sodium supplements (Hoffman and Stuempfle 2015). The results depend on the setup. When researchers set fluid intake high, sodium often slows the fall. In real races, where people drink as they choose, the amount of sodium taken has shown little link to the outcome.

Controlled trials with high, set fluid intake

• 13 women, 4-hour runs, 1 liter an hour: sodium fell 2.5 mmol/L with the higher-sodium drink (680 mg/L) against 6.2 mmol/L with water. Mild hyponatremia occurred in 46% with the higher-sodium drink, 69% with the lower (410 mg/L) and 92% with water, and two women on water went under 130 mmol/L. Performance did not differ (Twerenbold 2003).
• 13 men, about 4 hours in 30°C heat, fluids matched to weight loss: sodium ended at 137.3 and 136.7 mmol/L with sodium drinks (36.2 and 19.9 mmol/L) against 134.5 and 134.4 with mineral and distilled water (Anastasiou 2009). None had cramps on any drink.
• 8 people, 6-hour cycling at 30°C, fluids matched to losses: saline at 25 mmol/L gave no significantly higher sodium than water, 137.3 against 135.5 mmol/L, and nobody reached the 130 mmol/L stopping point (Barr 1991).

Observational findings in real events

• Full-distance triathlon: 38 athletes given salt tablets of about 700 mg of sodium an hour were matched to others. Sodium did not change significantly more than with fluid alone, and none finished below 135 mmol/L. The study reported less weight loss in the salt group, 4.3% against 5.1% (Speedy 2002).
• 161-km race: sodium intake from supplements did not differ between those with low and normal sodium. A weak relation to finish sodium appeared, r = 0.24, and weight change also tracked, r = −0.19. The authors conclude low supplement intake has minimal responsibility, and name overhydration as the primary characteristic (Hoffman and Stuempfle 2015).
• 161-km race at up to 39°C: in 20 finishers, with total sodium ranging from 2,541 to 38,338 mg, intake rates were similar across those with and without low sodium, cramping and nausea (Hoffman, Stuempfle and Valentino 2015).
• A single case: a runner with a prior episode, advised to take plenty of sodium, took more than 6,500 mg with 9.2–10.6 liters of water over a 17-hour, 72-km outing and still reached 122 mmol/L with symptoms (Hoffman and Myers 2015).
• Performance: in a study of 266 ultramarathon runners, no association appeared between sodium supplement intake and race pace or finish rank (Lipman 2021).

Reviews sit in different places. One calls sodium an ineffective preventive strategy when heavy drinking and vasopressin release are present, while an intravenous concentrated dose is an effective treatment, and names this the sodium paradox (Hew-Butler, Noakes 2008). A 2022 review says sodium supplementation may help soften the decline (Seal 2022). The guideline summary reports the position that sodium-rich foods and fluids be available during lengthy exertion in high heat, and states that they will not prevent the condition when overdrinking occurs (Jonas 2021). A trial finding that salt slowed the fall is not the same as a finding that it prevents illness, and the trials above did not measure severe illness.

Salt excess carries its own hazards, set out on the Sodium overview.

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Reported Deaths

A 2019 review counts at least 12 confirmed deaths of public record directly attributed to complications of hyponatremic encephalopathy, and states that this likely understates the true figure (Rosner 2019). Examples in the literature:

• Marathons. Two runners with fatal brain swelling are described in one series (Siegel 2007), and a 2017 review states that the deaths of two female charity marathon runners in 2003 brought wide attention to the problem (Hew-Butler 2017). A young male runner died after the finish line of the London Marathon (Kipps 2011). In the seven-runner series, one died of cardiopulmonary arrest from brainstem herniation with the low sodium unsuspected (Ayus 2000).
• Other activities. The 2017 review lists deaths, confirmed in the lay press, in high school football players after practice, a soldier on the first day of Ranger training, a policeman on a 19-km bike ride, a college student doing calisthenics for a fraternity, a bushwalker, a triathlete and a canoeist in an ultradistance race. A fit soldier also died on a 50-km training march with both this condition and heat stroke (Hew-Butler 2017).
• Grand Canyon, 2023. A healthy 36-year-old woman on a 17-mile day hike, drinking 6 liters or more of water, developed headache, nausea and vomiting, then confusion after about 12 hours, then lost consciousness and stopped breathing. Her field sodium reading was 123, and 150 mL of 3% saline did not revive her. The cause of death was brain herniation from swelling related to acute hyponatremia (Rosner 2024).

Who dies: a 2015 paper describes marathon deaths from brain swelling as occurring mainly in young women, separate from cardiac deaths in middle-aged men (Siegel 2015). A 2019 review reports several deaths in women (Knechtle 2019). The 2017 review stresses that men are not spared, and lists several (Hew-Butler 2017).

The 2024 paper calls mistaking this condition for heat exhaustion a common error among hikers, since continued heavy drinking then makes it worse (Rosner 2024). The 2017 review states that all of the deaths attributed to it would likely have been prevented by better understanding of hydration needs and rapid recognition of the signs (Hew-Butler 2017). That is the authors' judgement from case reports, not a finding from comparative studies.

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What Is Not Known

• The true rate of illness and death. Authors of the 2024 paper state that accurate data on the exact incidence and outcomes are not available (Rosner 2024). Asymptomatic cases are found only if someone draws blood (Rosner 2019).
• The meaning of a low reading with no symptoms. Low sodium was found before the race in 5.0% of one group of runners, and the authors say the clinical meaning of these findings is unknown (Mohseni 2011).
• Why only some people who overdrink are affected. Most athletes who gained weight kept normal sodium (Noakes 2005). The mechanisms controlling internal sodium stores are unknown, and the idea remains speculative (Hew-Butler 2017).
• What keeps vasopressin high. Several triggers are proposed; interleukin-6 has been studied with modest correlations in a small sample (Cairns 2015).
• How much low sodium comes from sodium lost, not water gained. Sweat's role is called controversial (Hew-Butler 2017). Studies disagree on how often affected athletes are short of fluid: the guideline summary calls this uncommon (Jonas 2021), while a large triathlon series reports it as a significant share of cases (Johnson 2023).
• The sex difference. Whether it reflects hormones, body size, slower times, or drinking habits is unsettled; Boston's analysis removed it after adjustment (Almond 2005), and clinical pictures differ by sex (Johnson 2023).
• Whether anti-inflammatory drugs truly contribute. Studies conflict, as listed above.
• Treatment evidence in severe cases. The randomized data cover 34 runners with mild or no symptoms (Rogers 2011; Owen 2014). The evidence for severe illness is case reports and series. The usefulness of urea, mannitol and vasopressin-blocking drugs has not been tested for this condition (Hew-Butler 2017).
• Whether repeated exercise allows the brain to adapt. Whether multistage races or frequent training produce the slower-onset chronic pattern is unclear (Hew-Butler 2017).
• How to space fluid stations. Further study is needed on the number and spacing for different environments (Hew-Butler 2017).

Decisions about medicines and supplements belong with a clinician.

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Key Research Papers

1. Jonas CE, Arnold MJ. Exercise-Associated Hyponatremia: Updated Guidelines from the Wilderness Medical Society. Am Fam Physician. 2021;103(4):252-253. PubMed PMID: 33587580
2. Rosner MH, Myers T, Bennett B, Lipman G, Hew-Butler T. Exercise-Associated Hyponatremia in the Grand Canyon: Preventing Fatalities through Early Recognition, Timely Therapy, and Education. Clin J Am Soc Nephrol. 2024;19(5):660-663. PubMed PMID: 38110223
3. Armstrong LE, McDermott BP, Young SL, Casa DJ. Exercise-Associated Hyponatremia: Serum Sodium, Symptomatology, Severity, and Sport Specificity. Open Access J Sports Med. 2025;16:159-177. PubMed PMID: 41280657
4. Rosner MH. EXERCISE-ASSOCIATED HYPONATREMIA. Trans Am Clin Climatol Assoc. 2019;130:76-87. PubMed PMID: 31516170
5. Bennett BL, Hew-Butler T, Rosner MH, Myers T, Lipman GS. Wilderness Medical Society Clinical Practice Guidelines for the Management of Exercise-Associated Hyponatremia: 2019 Update. Wilderness Environ Med. 2020;31(1):50-62. PubMed PMID: 32044213
6. Hew-Butler T, Rosner MH, Fowkes-Godek S, Dugas JP, Hoffman MD, Lewis DP, Maughan RJ, Miller KC, Montain SJ, Rehrer NJ, Roberts WO, Rogers IR, Siegel AJ, Stuempfle KJ, Winger JM, Verbalis JG. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clin J Sport Med. 2015;25(4):303-20. PubMed PMID: 26102445
7. Hew-Butler T, Ayus JC, Kipps C, Maughan RJ, Mettler S, Meeuwisse WH, Page AJ, Reid SA, Rehrer NJ, Roberts WO, Rogers IR, Rosner MH, Siegel AJ, Speedy DB, Stuempfle KJ, Verbalis JG, Weschler LB, Wharam P. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clin J Sport Med. 2008;18(2):111-21. PubMed PMID: 18332684
8. Hew-Butler T, Almond C, Ayus JC, Dugas J, Meeuwisse W, Noakes T, Reid S, Siegel A, Speedy D, Stuempfle K, Verbalis J, Weschler L, Exercise-Associated Hyponatremia (EAH) Consensus Panel. Consensus statement of the 1st International Exercise-Associated Hyponatremia Consensus Development Conference, Cape Town, South Africa 2005. Clin J Sport Med. 2005;15(4):208-13. PubMed PMID: 16003032
9. Hew-Butler T, Loi V, Pani A, Rosner MH. Exercise-Associated Hyponatremia: 2017 Update. Front Med (Lausanne). 2017;4:21. PubMed PMID: 28316971
10. Almond CS, Shin AY, Fortescue EB, Mannix RC, Wypij D, Binstadt BA, Duncan CN, Olson DP, Salerno AE, Newburger JW, Greenes DS. Hyponatremia among runners in the Boston Marathon. N Engl J Med. 2005;352(15):1550-6. PubMed PMID: 15829535
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Connections

• Hyponatremia (Low Sodium)
• Sodium
• Hyponatremia: Confusion and Headache
• Hyponatremia: Muscle Cramps
• Hypernatremia: Thirst and Confusion
• Rhabdomyolysis
• Thirst, ADH and How Your Body Guards Its Water
• Hydration Beyond Water for Cramp Prevention
• Sweat: How Your Body Cools Itself

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