Exercise-Associated Hyponatremia: A Clinical Review for the Internal Medicine Physician

Marathon Runner's Hyponatremia - Understanding the Mechanism and Prevention

A Comprehensive Review for Postgraduate Medical Education

Dr Neeraj Manikath , claude.ai

Abstract

Exercise-associated hyponatremia (EAH) represents a potentially life-threatening complication of endurance athletic events that is frequently mismanaged due to misconceptions about its underlying pathophysiology. Unlike classic hyponatremia syndromes encountered in hospitalized patients, EAH occurs in otherwise healthy individuals and results primarily from excessive free water intake rather than sodium depletion. This review explores the unique pathophysiological mechanisms of EAH, emphasizes critical diagnostic pearls, and provides evidence-based management strategies to prevent iatrogenic complications including osmotic demyelination syndrome.

Keywords: Exercise-associated hyponatremia, endurance athletes, water intoxication, non-osmotic ADH release, osmotic demyelination syndrome

Introduction

The marathon finish line represents triumph for most athletes, but for a subset of participants, it marks the beginning of a medical emergency. Exercise-associated hyponatremia (EAH), defined as a serum sodium concentration below 135 mmol/L during or up to 24 hours after physical activity, affects 10-15% of endurance athletes, with severe cases (sodium <120 mmol/L) occurring in 1-3% of participants.[1,2] The condition gained widespread medical attention following several high-profile fatalities in the early 2000s, prompting a fundamental reassessment of hydration recommendations for athletes.

What makes EAH particularly treacherous for the internist is its counterintuitive pathophysiology. These patients present with hyponatremia but are not dehydrated—they are water-intoxicated. Administering the reflexive "normal saline bolus" can prove fatal. Understanding this paradox requires abandoning assumptions derived from hospital-based hyponatremia and embracing the unique physiology of the exercising human.

The Fundamental Misconception: It's Water Intoxication, Not Salt Loss

The Historical Context of "Drink More"

For decades, athletic communities operated under the paradigm that dehydration posed the primary threat to endurance performance and health. Sports medicine organizations and race directors promoted aggressive hydration strategies, with some recommending athletes drink "as much as tolerable" or follow rigid schedules of 200-300 mL every 15-20 minutes regardless of thirst.[3] Elite marathoners completed races with 2-3 kg weight loss from sweat, yet recreational athletes increasingly finished with weight gain.

This well-intentioned advice created an iatrogenic epidemic. Studies of marathon finishers reveal that athletes who gain weight during a race have a 50-fold increased risk of developing symptomatic EAH compared to those who lose weight.[4]

The Pathophysiology: A Two-Hit Mechanism

Hit One: Excessive Free Water Intake

The primary driver of EAH is consumption of hypotonic fluids (plain water or dilute sports drinks) in excess of obligate losses. During prolonged exercise, athletes can consume 500-1000 mL per hour. Even with generous sweat rates of 1-1.5 L/hour, slower athletes completing marathons in 4-6 hours may drink 4-6 liters while sweating only 4-5 liters—creating positive free water balance.

The sodium concentration of sweat ranges from 20-80 mmol/L (average 40-50 mmol/L)[5]—markedly hypotonic compared to plasma at 140 mmol/L. While sodium is lost in sweat, the relative loss of free water is proportionally greater, meaning that dehydration from pure sweating would actually increase serum sodium (hypernatremia), not decrease it. The athlete who develops hyponatremia has therefore consumed hypotonic fluid in excess of all losses combined.

Pearl #1: If an athlete sweats, drinks nothing, and loses 3 kg during a marathon, their serum sodium will rise. If they drink 3 liters of water while sweating 3 liters, they will become hyponatremic. EAH is a dilutional phenomenon.

Hit Two: Impaired Free Water Excretion

A healthy kidney can excrete 15-20 L of free water daily under optimal conditions. Why doesn't the exercising athlete simply urinate away the excess water? The answer lies in non-osmotic arginine vasopressin (AVP, also known as antidiuretic hormone or ADH) release.

Multiple stimuli during endurance exercise trigger AVP secretion independent of plasma osmolality:[6]

Exercise intensity and duration: Physical stress stimulates hypothalamic AVP release
Pain and muscle damage: Inflammatory mediators promote AVP secretion
Nausea: A potent non-osmotic stimulus for AVP release
Hypovolemia or hypotension: Though often absent in EAH, any degree of circulatory stress triggers baroreceptor-mediated AVP release
Medications: NSAIDs (taken by 50-70% of marathoners) impair free water excretion

This non-osmotic AVP release creates a state functionally similar to SIADH but arising from entirely different mechanisms. The kidney retains water despite falling plasma osmolality, trapping the athlete in a positive free water balance state.

Pearl #2: EAH represents "SIADH of exercise"—but it's physiologically appropriate stress-response AVP release, not a syndrome of inappropriate secretion. The inappropriateness lies in the athlete's excessive water consumption, not the ADH response.

Why EAH is NOT SIADH: Critical Distinctions

While EAH shares features with SIADH (euvolemia, concentrated urine, hyponatremia with low plasma osmolality), understanding the differences prevents management errors:

Feature	EAH	Classic SIADH
Onset	Acute (hours)	Subacute/chronic (days-weeks)
Volume status	Euvolemic to mildly hypervolemic	Euvolemic
Brain adaptation	Minimal (acute presentation)	Often substantial (chronic presentation)
Trigger	Excessive hypotonic fluid intake + exercise stress	Tumor, CNS disease, drugs, lung disease
AVP elevation	Appropriate stress response	Inappropriate/autonomous
Treatment priority	Avoid iatrogenic correction; fluid restriction	Fluid restriction, treat underlying cause
ODS risk	Very high (young, healthy brain, acute)	Lower (often elderly, chronic, adapted)

Oyster #1: The young athlete's brain is remarkably healthy and will rapidly adapt to correct sodium after the exercise stress resolves—making overzealous correction with hypertonic saline particularly dangerous. The 50-year-old cirrhotic with chronic hyponatremia needs careful correction; the 25-year-old marathoner needs protection FROM overcorrection.

Clinical Presentation: Recognizing EAH in the Field and Emergency Department

The Classic Scenario

A 32-year-old female recreational runner completes her first marathon in 5 hours 20 minutes. She followed race organizers' hydration advice, drinking at every water station and consuming 6 liters of fluid total. One hour post-race, she develops severe nausea, headache, and confusion. Race medical staff note she is "well-hydrated" with clear urine. She receives 2 liters of normal saline for "dehydration" and is transferred to the ED with worsening mental status.

Key Historical Clues

Event duration >4 hours: EAH risk correlates with race duration, as slower athletes have more time to over-drink
Weight gain from race start: The single most specific indicator of EAH risk. Weight gain indicates positive fluid balance
Aggressive hydration behavior: Athletes who drink at every station, follow rigid schedules, or drink when not thirsty
Symptom timing: Symptoms during final stages of event or within hours of completion
Female sex: Women have 2-3 times higher EAH incidence, likely due to smaller body mass, lower sweat rates, and greater adherence to hydration recommendations[7]

Pearl #3: Always ask about the athlete's weight change. A runner who weighs 2 kg more at the finish line than the start has consumed 2 kg (2 liters) of excess fluid. This simple data point transforms your diagnostic approach.

Physical Examination Findings

The examination in mild to moderate EAH may be surprisingly benign, creating a false sense of reassurance:

Early (Na 130-135): Nausea, mild headache, bloating, normal mental status
Moderate (Na 125-130): Vomiting, throbbing headache, confusion, lethargy
Severe (Na <125): Altered consciousness, seizures, obtundation, respiratory arrest

Critical examination points:

Volume status: Euvolemic or mildly hypervolemic. Moist mucous membranes, normal skin turgor. May have peripheral edema or puffiness
No signs of dehydration: Absence of tachycardia, orthostatic hypotension, or poor skin turgor argues against volume depletion
Neurological: Ranges from normal to severely altered. Seizures indicate severe hyponatremia and cerebral edema

Oyster #2: A "well-hydrated appearing" marathoner with confusion and nausea has EAH until proven otherwise. Appearance can deceive—these patients look better hydrated than they should, because they are overhydrated.

Diagnostic Approach: Beyond the Serum Sodium

Essential Laboratory Studies

Immediate:

Serum sodium and plasma osmolality
Basic metabolic panel
Urine sodium and osmolality (if obtainable)

Expected findings in EAH:

Serum sodium: <135 mmol/L (severe <125 mmol/L)
Plasma osmolality: Low (<280 mOsm/kg)
Urine osmolality: Inappropriately concentrated (>100 mOsm/kg)
Urine sodium: Variable, often >30 mmol/L

The finding of dilute plasma with concentrated urine confirms water retention despite hypoosmolality—the hallmark of non-osmotic AVP release.

Differential Diagnosis Considerations

While EAH dominates the differential in the post-race setting, consider:

Exertional heat stroke: Core temperature >40°C, anhidrosis, may have hypernatremia
Exertional hyponatremia with cerebral edema: Severe EAH complication
Hypoglycemia: Rapid glucose check rules out
Traumatic brain injury: History of fall or collision
Substance intoxication: Particularly in recreational runners

Hack #1: Point-of-care sodium testing at race medical tents (using portable i-STAT devices) allows immediate diagnosis and prevents dangerous empiric normal saline administration. Advocate for this technology at major endurance events.

The Danger of Standard Management: Why Normal Saline Kills

The Fatal Reflex

An athlete arrives in your ED with confusion, nausea, and lethargy. Your resident orders "NS bolus 1 liter" before labs return. The sodium comes back at 118 mmol/L. You realize with horror that your standard approach has worsened the patient's condition.

Why isotonic saline is dangerous in EAH:

Normal saline contains 154 mmol/L of sodium. In a patient with serum sodium of 115 mmol/L drinking water, 1 liter of normal saline adds sodium but also adds 1 liter of free water to a patient who already has excess total body water. The net effect can paradoxically lower serum sodium further.[8]

Mathematically, the Adrogue-Madias formula predicts change in serum sodium:

ΔNa = (Infusate Na - Serum Na) / (Total Body Water + 1)

For a 60 kg female with TBW of 30 L and serum Na of 115:

Infusing 1L NS: ΔNa = (154-115)/(30+1) = +1.3 mmol/L
But if she continues to retain water due to ongoing AVP, the actual change may be 0 or negative

Moreover, volume expansion can trigger natriuresis, further lowering sodium concentration.

Pearl #4: In euvolemic hyponatremia, isotonic saline is at best ineffective and at worst harmful. The patient needs either free water restriction (mild cases) or hypertonic saline (severe cases), never isotonic saline.

The Overcorrection Catastrophe: Osmotic Demyelination Syndrome (ODS)

The second danger lurks at the opposite extreme: overzealous correction. Young, healthy marathon runners develop acute hyponatremia—their brains have not adapted through osmolyte regulation. When the exercise stress resolves, AVP levels plummet, and these athletes can undergo rapid spontaneous correction of their sodium.

If clinicians simultaneously administer hypertonic saline without careful monitoring, correction rates can exceed safe limits (8-10 mmol/L in 24 hours), risking osmotic demyelination syndrome. ODS typically manifests 2-6 days post-correction with dysarthria, dysphagia, paraparesis, quadriparesis, and altered consciousness.[9] In young patients, ODS can be devastating and permanent.

Oyster #3: The greatest danger in managing EAH is often not the hyponatremia itself, but our treatment of it. A 25-year-old marathoner with Na of 118 will likely survive with supportive care alone. That same patient may develop permanent neurological disability if we "aggressively correct" to 132 in 8 hours.

Evidence-Based Management: Less is More

Treatment Algorithm

Step 1: Assess Severity

Asymptomatic or Mild Symptoms (Na 130-135):

Treatment: Fluid restriction
Monitoring: Serial sodium every 2-4 hours
Disposition: Can often manage in race medical tent or observe in ED

Moderate Symptoms (Na 125-130):

Treatment: Fluid restriction to <500 mL daily
Monitoring: Admit for observation, sodium every 4-6 hours
Duration: Typically resolves within 24 hours
Avoid: Any IV fluids unless specifically indicated

Severe Symptoms (Seizures, obtundation, Na <125):

Treatment: 100 mL of 3% hypertonic saline IV over 10 minutes
Goal: Increase sodium by 4-6 mmol/L to resolve symptoms
Re-dosing: Can repeat 100 mL bolus once or twice if symptoms persist
Monitoring: Sodium every 2 hours initially, then every 4 hours
Correction limit: Target 4-6 mmol/L increase in first 24 hours, maximum 8-10 mmol/L

Step 2: Prevent Overcorrection

Once symptoms improve (often after only 4-5 mmol/L increase), STOP active treatment. Implement:

Strict I&O monitoring
Hold all IV fluids
Consider desmopressin (DDAVP) 2-4 mcg if correction exceeds 6 mmol/L in 6 hours[10]

Hack #2: Write an explicit order: "Hold all IV fluids. Patient has EAH, not dehydration." This prevents well-meaning nurses from connecting maintenance fluids overnight.

The Role of Hypertonic Saline: When and How

Indications for 3% saline:

Seizure activity
Glasgow Coma Scale <8
Respiratory compromise
Profound confusion with inability to protect airway

Administration:

Use 100 mL boluses of 3% saline (513 mmol/L Na)
Each 100 mL bolus increases serum Na by approximately 2-3 mmol/L
Give over 10 minutes via peripheral or central line
Recheck sodium 2 hours after each bolus
Stop when symptoms resolve, not when sodium normalizes

Pearl #5: Small boluses of 3% saline (100 mL) allow precise, controlled correction while minimizing overcorrection risk. Avoid continuous infusions of 3% saline in EAH—they're too easy to overshoot.

What About Diuretics?

Loop diuretics promote free water excretion and can theoretically hasten EAH resolution. However, use cautiously:

Potential role for furosemide:

Reserved for confirmed hypervolemic EAH with evidence of volume overload
Dose: 20-40 mg IV once
Monitor for excessive correction

Cautions:

Most EAH patients are euvolemic, not hypervolemic
Diuresis may trigger rapid overcorrection
Theoretical benefit exceeds proven clinical utility

Current consensus: Fluid restriction alone suffices for most cases; reserve diuretics for exceptional circumstances.[1]

Prevention: The Best Treatment

Revolutionizing Hydration Recommendations

The cornerstone of EAH prevention is abandoning scheduled hydration in favor of thirst-guided drinking. Large-scale studies demonstrate that "drink to thirst" prevents both EAH and dehydration in >99% of athletes.[11]

Evidence-based hydration advice for athletes:

Drink when thirsty, stop when not thirsty
Trust physiological cues. Thirst mechanism is exquisitely sensitive and maintains plasma osmolality within 2% of normal
Do not drink to a schedule
Recommendations like "drink 200 mL every 15 minutes" ignore individual variation in sweat rates, body size, and pace
Target zero weight change
Weigh athletes pre- and post-race. Weight gain indicates overhydration; >2% weight loss indicates underhydration
Use sodium-containing fluids for events >2 hours
Sports drinks containing 20-30 mmol/L sodium are safer than plain water, though they don't prevent EAH if consumed excessively
Salty snacks during prolonged events
Pretzels, salted nuts, or electrolyte capsules provide concentrated sodium without adding fluid volume

Hack #3: Teach athletes the "hand test": if you can make a fist and squeeze hard without cramping, you don't need to drink right now. If you're genuinely thirsty, you'll know—and that's when you drink.

Education for Athletes and Race Organizers

Pre-race athlete education should emphasize:

More athletes are harmed by overdrinking than underdrinking
Performance does not improve with prophylactic hydration beyond thirst
Water stations are available if needed—using them all is dangerous
Warning signs of EAH: nausea, headache, confusion, swelling, weight gain

Race organizer responsibilities:

Post "drink to thirst" signage at water stations
Train medical staff to recognize EAH and avoid routine saline administration
Provide weighing stations pre- and post-race
Stock 3% saline in medical tents for severe cases
Have point-of-care sodium testing capability

Special Populations and Scenarios

Women: The Highest Risk Group

Women develop EAH 2-3 times more frequently than men, likely due to:

Lower body weight (smaller distribution volume for excess fluid)
Lower sweat rates (less obligate fluid loss)
Higher adherence to hydration recommendations
Possible hormonal influences on AVP secretivity[7]

Implications: Female athletes require particularly strong emphasis on thirst-guided drinking and may benefit from additional education about EAH risk.

Ultra-Endurance Events (>4 hours)

Ironman triathlons, 100-mile ultramarathons, and multi-day adventure races pose unique challenges:

Prolonged AVP elevation
Cumulative fluid intake over many hours
Sodium loss in sweat becomes more significant

Management adjustments:

Encourage sodium supplementation (electrolyte capsules)
Monitor for both EAH and true dehydration
Weigh athletes at checkpoints when feasible

NSAIDs and EAH Risk

Nonsteroidal anti-inflammatory drugs impair renal free water clearance and increase EAH risk. An estimated 50-70% of marathon runners take NSAIDs before or during races.[12]

Recommendation: Advise athletes to avoid NSAIDs during endurance events. The modest analgesic benefit is outweighed by EAH risk, plus additional concerns for acute kidney injury and gastrointestinal bleeding.

Clinical Pearls Summary

Pearl #1: EAH is dilutional hyponatremia from excess free water intake, not sodium depletion. Dehydration alone raises serum sodium.

Pearl #2: EAH represents physiologically appropriate stress-response AVP release during exercise, functionally similar to SIADH but mechanistically distinct.

Pearl #3: Always obtain the athlete's weight change from race start to finish. Weight gain is the single best predictor of EAH.

Pearl #4: Never give isotonic saline to euvolemic hyponatremic patients. It adds free water without sufficient osmotic gradient to correct sodium.

Pearl #5: Use small boluses (100 mL) of 3% saline to precisely control correction in severe symptomatic EAH. Stop when symptoms resolve, not when sodium normalizes.

Pearl #6: The young athlete's healthy brain rapidly adapts once exercise stress resolves—making overcorrection far more dangerous than in chronic hyponatremia syndromes.

Pearl #7: "Drink to thirst" prevents both EAH and dehydration in >99% of athletes. Scheduled hydration causes more problems than it solves.

Oysters (Unexpected Insights)

Oyster #1: The chronic hyponatremic needs careful, slow correction; the acute EAH patient needs protection FROM overcorrection. Age and chronicity reverse usual concerns.

Oyster #2: A "well-hydrated appearing" post-marathon runner with neurological symptoms has EAH until proven otherwise—good hydration status is the problem, not the solution.

Oyster #3: Our greatest danger in EAH management is often iatrogenic—either from isotonic saline worsening hyponatremia or overzealous correction causing ODS.

Oyster #4: Thirst is not a late sign of dehydration—it's an exquisitely sensitive early warning system that maintains homeostasis when we trust it.

Hacks (Practical Shortcuts)

Hack #1: Advocate for point-of-care sodium testing (i-STAT) at marathon medical tents. Immediate diagnosis prevents dangerous empiric fluid administration.

Hack #2: Write explicit orders: "Hold all IV fluids. Patient has EAH, not dehydration." This prevents overnight nursing staff from connecting maintenance fluids.

Hack #3: Teach athletes the "hand test": if you can make a tight fist without cramping, you don't need fluids right now. Genuine thirst is unmistakable.

Hack #4: For EAH management, set a smartphone timer to recheck sodium every 2 hours initially. Frequent monitoring catches overcorrection before it becomes dangerous.

Hack #5: Save "100 mL of 3% saline" as a SmartPhrase or order set. In emergencies, you want one-click access to the correct dose—not time wasted calculating infusion rates.

Conclusion

Exercise-associated hyponatremia represents a preventable condition with potentially devastating consequences when mismanaged. The internist must recognize that EAH differs fundamentally from hospital-acquired hyponatremia in its pathophysiology, patient population, and treatment approach. These are healthy young individuals with acute water intoxication, not chronic disease patients with adapted compensatory mechanisms.

The key principles bear repeating:

EAH is water intoxication, not salt depletion
Isotonic saline worsens the condition
Young brains correct rapidly once stress resolves—beware overcorrection
Fluid restriction is first-line treatment for mild-moderate cases
Small doses of 3% saline for severe symptoms only, stopping when symptoms improve
Prevention through "drink to thirst" education remains the ultimate solution

As endurance sports participation continues to grow globally, internists and emergency physicians must maintain vigilance for EAH while resisting reflexive hydration practices that cause harm. By understanding the unique pathophysiology of exercise-associated hyponatremia and applying evidence-based management strategies, we can reduce both morbidity and mortality from this increasingly common condition.

The marathon runner collapsing at the finish line deserves care as sophisticated as our sickest ICU patients—but sophistication here means knowing when to do less, not more. In EAH management, restraint is wisdom, and patience is therapeutic.

References

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Author's Note: This review is intended for educational purposes for postgraduate medical students and practicing internists. Management recommendations should be individualized based on clinical context and institutional protocols. When in doubt regarding hypertonic saline administration or correction rates, consult nephrology.

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