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Exercise-Associated Hyponatremia

Editor: Jeremy D. Schroeder Updated: 6/12/2023 7:59:38 PM


Exercise-associated hyponatremia (EAH) is defined as a serum sodium level below 135 mmol/L that develops during or up to 24 hours after physical activity.[1][2] EAH was previously thought to occur only in extreme endurance athletes; however, its incidence is increasing among various athletes presenting with a wide spectrum of symptoms.[3] 

Prompt differentiation of EAH from other exertional illnesses is critical, as isotonic fluid administration that may be given for other exertional diagnoses can worsen EAH, resulting in life-threatening sequelae of hyponatremia. EAH is treated with fluid restriction or sodium replacement, depending upon severity. Avoiding overhydration can prevent EAH. Athletes, coaches, healthcare providers, and athletic event staff must be educated on EAH prevention strategies and presenting symptoms to decrease athletes’ risk of development and progression to hyponatremic encephalopathy, coma, or death.


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EAH develops due to increased total body free water relative to total body sodium via two major mechanisms.[1] Firstly, before and during strenuous physical activity, athletes often increase their intake of hypotonic fluids such as water and sports drinks due to conditioned behaviors, leading to increased total body water. Secondly, physical exertion itself may result in inappropriate non-osmotic antidiuretic hormone (ADH) secretion, leading to free water retention.[1][4]


EAH occurs in a wide variety of athletes in activities of various intensities, including ultramarathon and marathon running, triathlon, shorter distance running, military training operations, team ball sports, recreational hiking, and yoga.[2][1][3]  The greatest risk factors for EAH are excessive hypotonic fluid consumption beyond the capacity for normal renal free water excretion, high ambient temperature, and longer exercise time, usually exceeding 2 hours. Several studies demonstrate a linear relationship between temperature and incidence of EAH.[5] 

Men and women are at equal risk for EAH when adjusted for body mass index and exercise duration.[4] Low oral intake, specifically of high sodium foods, may also contribute. Non-steroid anti-inflammatory drug use may exacerbate or propagate EAH by potentiating the water retention effects of ADH by the kidney.[2]

EAH is commonly an incidental finding in asymptomatic athletes. Incidences of 5-51% are reported following endurance events where athletes are screened, or their serum is analyzed for another reason.[2][3] It is estimated that 0.1% to 1.0% of endurance athletes experience symptomatic EAH, with marathon runners, ultramarathon runners, Ironman athletes, long-distance backpackers, and military service members most commonly affected.[5][2][3] The incidence in military service members is 6.9 cases per 100,000 person-years.[6]


EAH stems from both increased consumption of hypotonic fluids and inappropriate water retention. Before and throughout strenuous physical activity, athletes often over hydrate with hypotonic fluids (water, sports drinks). When intake exceeds that of water lost via urine, sweat, and insensible respiratory and gastrointestinal losses (often greater than 1.5 liters), athletes may retain free water, resulting in dilutional hyponatremia.[2][4] The contribution of sodium loss from excessive sweat is controversial and not well characterized, as sweat loss varies greatly between individual athletes.[1][2]

It is postulated that stimuli related to physical exertion may result in sympathetic activation of the hypothalamus, which stimulates ADH secretion from the posterior pituitary inappropriately during low osmolar states. These stimuli include pain, emotional stress, nausea, emesis, hypoglycemia, heat exposure, and medication use (particularly NSAIDs).[2][4] Elevated ADH leads to stimulation of renal V2 receptors, causing water reabsorption rather than excretion. The retained free water is returned to the extracellular fluid resulting in a net lowering of serum sodium concentration.[2]

Subsequent hyponatremia results in an osmotic gradient that favors free water movement from the vascular space to the extravascular and intracellular spaces, leading to tissue edema (particularly brain and lung), which drives the most severe symptoms of EAH.

History and Physical

Prompt identification and differentiation from other common exertional injuries are essential to caring for an athlete with EAH. Healthcare providers should suspect EAH when athletes present during or within 24 hours following intense physical exertion, such as marathon running, cycling, triathlon, hiking, backpacking, or prolonged military field training or combat operations. The likelihood of EAH is increased if the exertional event occurred over a period greater than 2 hours or in hot weather.[2][3][1][4]

Presenting symptoms range from asymptomatic, to mild, to severe. Mild symptoms include lightheadedness, malaise, fatigue, irritability, generalized weakness, headache, nausea, and sluggish urine output.[2] Severe symptoms include vomiting, oliguria or anuria, altered mental status, collapse, seizure, coma, and death during sport or soon after.

Diagnosis of EAH is further supported by the absence of signs of symptomatic heat illness or dehydration, such as thirst, postural dizziness, dry mucous membranes, orthostatic hypotension, and elevated core temperature. Differentiating EAH from exercise heat illness and dehydration is critical, as isotonic fluid administration that would be given for the empiric treatment of either heat illness or dehydration could be life-threatening if the true diagnosis is EAH.[2][3][7]

On physical examination, patients with mild EAH may demonstrate mild hyperthermia, tachycardia, flushing, diaphoresis, and lethargy. Patients with severe EAH may demonstrate altered sensorium ranging from inattentiveness to complete obtundation, loss of sweating, hypotension, and abnormal limb movements.


Initial evaluation of suspected EAH includes vital signs, determination of mental status via the Glasgow coma scale, and assessment of airway patency, adequate respiration, and intact circulation. Accurate core temperature is key and should be taken rectally if possible to differentiate from heat illness. Exertional heat illness such as heat stroke or heat exhaustion can occur concurrently with EAH, given the similarities in precipitating events and risk factors.[6]

The serum sodium should be determined if point-of-care (POC) serum sodium testing is available (though this is not often practical due to cost and limited functional temperature range of POC testing devices).[1][2] A history supporting excessive hypotonic fluid intake and prolonged exertion should be taken if the patient can participate in an interview or a coach, teammate, partner, or another witness is available. A serum sodium level of less than 135 mmol/L with accompanying excessive fluid intake history is diagnostic for EAH.[1][2] The serum glucose should also be determined if POC glucose testing is available, as hypoglycemia can present similarly.

Treatment / Management


Prior to treatment, EAH must be correctly differentiated from other exertional illnesses such as heat exhaustion, heatstroke, and exercise collapse associated with sickle cell trait (ECAST), as their treatments are often contradictory. Treatment is dictated by the presence or absence of neurologic symptoms. The goal of treatment is the correction of serum sodium and improvement in symptoms.

If a patient does not demonstrate neurologic symptoms, EAH is considered mild, and the patient is eligible for oral fluid restriction. Patients restrict their total fluid intake to induce osmotic ADH suppression and, therefore, free water excretion.[2] Patients may also be given concentrated oral sodium repletion, though this may be poorly tolerated due to taste or nausea and vomiting. Proposed regimens include 100 ml of hypertonic saline, 3 or 4 broth bouillon cubes in 125 ml of water, or a serving of salted pretzels.[2] Oral hypertonic saline is as effective as IV hypertonic saline in mild EAH. One study demonstrated faster time to recovery and shorter duration of hospital stay for athletes who receive oral treatment.[5] IV isotonic fluids of any type or volume are not recommended in mild EAH.(A1)

EAH is considered severe if a patient demonstrates neurologic symptoms (altered mental status, seizure, coma). The patient should receive a bolus of 100 ml of IV hypertonic saline.[2] This can be repeated every 10 minutes for a total of 3 doses. Up to 600-1000 ml over 1 hour of hypertonic saline has been given without complication in case studies, though larger volumes of sodium repletion increase the risk for rapid sodium correction and osmotic demyelination.[8][2](A1)


On transfer to the hospital for advanced care, patients with suspected EAH should have immediate measurement of serum sodium and other electrolytes. Treatment in the hospital is similar to that in the field. Athletes with severe hyponatremia or evidence of cerebral edema with neurologic symptoms should be treated with a bolus of hypertonic saline as described above, with a goal serum sodium increase of 4-5 mmol/L and reversal of neurologic symptoms.[2] Patients with EAH encephalopathy may require ICU admission depending upon institutional criteria.(A1)

Differential Diagnosis

EAH falls on the spectrum of exertional injuries. The differential diagnosis for exertional injuries includes heat exhaustion, heatstroke, exercise-associated collapse, and exertional collapse associated with sickle cell trait (ECAST). Providers caring for athletes must also consider hypovolemia, hypoglycemia, sudden cardiac arrhythmia (Wolff-Parkinson-White syndrome, prolonged QT syndrome, channelopathy), hypertrophic cardiomyopathy, sudden cardiac death of unknown cause, seizure, vasovagal syncope, and malingering.


The majority of athletes recover from acute mild EAH within hours in the emergency care setting and do not require hospital admission. The duration of the emergency room stay after treatment with either oral or IV hypertonic saline solution has been reported between 50 and 79 minutes.[5] Severe EAH requires ward or ICU admission depending upon institutional criteria. Patients who develop exercise-associated hyponatremia encephalopathy risk significant morbidity and mortality secondary to cerebral damage from cerebral edema; the exact mortality rate is unknown.[4][7] It is unknown whether patients with prior EAH injury are at higher risk for repeat development in the future.


The major complications of EAH and its treatment include exercise-associated hyponatremic encephalopathy (EAHE), noncardiogenic pulmonary edema, central pontine myelinolysis, and improper treatment resulting from an alternate diagnosis.

If left untreated, mild EAH can progress to severe EAH with profoundly altered mental status, seizure, and coma—an end-stage finding due to cerebral edema termed EAHE. EAHE is often fatal, though the exact mortality rate is not defined.[3][7] The treatment for EAHE is a prompt correction of serum sodium with hypertonic saline and supportive care for its sequelae (respiratory support, seizure management). 

Noncardiogenic pulmonary edema may also develop secondary to osmotic dysregulation in EAH, leading to respiratory distress and the need for respiratory support.

Rapid correction of hyponatremia may result in central pontine demyelination, a catastrophic and permanent demyelinating event that presents with neurologic deficits despite correction of the serum sodium.

If EAH is diagnosed mistakenly in the presence of true dehydration or heat stroke, treatment with hypertonic fluids, fluid restriction, and lack of cooling may cause further harm to the patient.[3]


Emergency medical providers and athletic event staff should consult a tertiary care center for recommendations on appropriate care and ultimate transfer of patients with suspected or confirmed EAH. Acute care providers in the hospital setting should consider a consultation with a critical care specialist in the event of significant hyponatremia below the institutional cutoff for care on a regular medical ward or for the development of EAHE noncardiogenic pulmonary edema or central pontine demyelination.

Deterrence and Patient Education

EAH can be prevented by avoiding overhydration, ensuring adequate oral sodium intake, and educating athletes, event staff, and healthcare providers on the prevention strategies and presenting symptoms. 

EAH occurs when hypotonic fluid intake exceeds total body fluid losses. Therefore the safest strategy for fluid repletion is a thirst-driven replacement to avoid overhydration. Estimates of individual athlete replacement needs by monitoring weight changes during training activities may also be used, though this may not be practical. Forced hydration, particularly at large volumes, should be discouraged.[3][7]

Salty foods may be consumed in conjunction with oral fluids as desired by the athlete to support osmotic balance during endurance events. Supplementing the serum sodium with salt tablets or packets at any particular rate or total dose during activity has not been shown to decrease rates of EAH.[3][9]

Athletes participating in organized endurance events should be educated on the risks of overhydration, the importance of concurrent food intake, and the signs and symptoms of EAH and other heat injuries. Event staff, EMS and frontline healthcare providers, and military members should also be educated on recognizing EAH in the field and prevention measures via avoiding overhydration and adequate oral intake.[3][7]

Pearls and Other Issues

The Defence Health Agency released a Practice Recommendation on the management of EAH in December 2020 to improve military-wide awareness of EAH and care for service members who develop it. 

The views expressed are those of the authors and do not reflect the official policy of the Department of the Army, the Department of Defense, or the U.S. Government.

Enhancing Healthcare Team Outcomes

Prompt recognition of EAH over other exertional injuries is imperative. Patients with confirmed or suspected EAH should be transferred to a tertiary care center for advanced care. EAH diagnoses must be clearly communicated at transfers of care to ensure appropriate fluid management.



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