Exercise Associated Hyponatremia - the effects of over-hydration

Exercise Associated Hyponatremia (EAH) is a decrease in sodium levels caused by over-hydrating;  this typically means consuming more fluid than the kidneys can excrete, typically during or up to 24 hours after prolonged physical activity.(1)   The outcome can be as serious as dehydration, the problem is that the signs and symptoms of both are very similar which means correct diagnosis and treatment for the condition is essential.

Sodium is required for several functions including blood pressure.  Under normal conditions, sodium and water levels are regulated by the renal and hormonal systems. 

When sodium levels outside the cells decrease  water moves into the cells causing swelling, commonly observed in the extremities.  Sodium is also important in regulating the amount of water which passes through the blood/brain barrier.  Extreme hyponatremia can cause swelling of the brain – hyponatremic encephalopathy - and eventually, death.



As of 2012, 20 deaths have been attributed to EAH (2-4).   Most cases are seen in endurance events such as Iron Man and Ultra Marathons but an increasing number of cases are being reported in shorter distance events.   Military personnel are also at risk from prolonged training and operational roles in in hot environments.    Perhaps one of the most famous deaths associated with hyponatremia was Leah Betts, who in 1992, died shortly after he 18th birthday after consuming 7 litres of water within 90 minutes following advice to stay hydrated while taking Ecstasy.  

The symptoms of EAH are, unfortunately, very similar to heat related illness usually associated with dehydration:  nausea, vomiting, headache, swelling of hands and feet, reduced level of consciousness.  Because of the similar symptoms of dehydration and heatstroke, it is likely that many cases go unreported (5)

There are believed to be several contributory factors which increase the likelihood of EAH (1)

  • Females
  • Non Steroidal Anti Inflammatory Drugs (NSAIDs) such as ibuprofen
  • Low body weight
  • Event inexperience
  • Exercise exceeding 4 hours
  • Hot and extreme cold environments



There are two pathological pathways to EAH

Excessive fluid consumption
Individuals with normal renal function can excrete between 500 and 1000ml/h of water.(6)   With the additional non-renal losses of water (sweating, digestion, respiration etc.) athletes should be able to consume as much as 1000 to 1500ml/h before developing water retention and dilutional hyponatremia.  As such EAH is unlikely when fluid intake exceeds his limit.

Excessive Vasopressin secretion
Vasopressin, also known as antidiuretic hormone (ADH) and arginine vasopressin (AVP).  Its two primary functions are to retain water in the body and to constrict blood vessels.    Vasopressin regulates the body's retention of water by acting to increase water reabsorption.    Alcohol causes the pituitary gland in the brain to block the creation of vasopressin, the kidneys send water directly to the bladder instead of reabsorbing it into the body.   This is why drinking pints of beer, which is largely water, will still cause dehydration (one of the main mechanisms of a hangover) and once you have cracked the seal on a night out you will find yourself visiting the smallest room more frequently than normal!

Under normal circumstances, ingestion of excessive water should suppress vasopressin,  leading to production of dilute, high-volume urine.   If vasopressin is not appropriately suppressed, the ability to excrete excessive water is reduced causing fluid retention and dilutional hyponatremia.   Vasopressin secretion may be triggered by a range of stimuli including intense exercise, nausea,  vomiting, hypoglycaemia and non-specific stresses such as pain and emotion.(7-9)

Sodium loss through sweating
Normal sodium levels in the blood are 135mml/l.   Sodium levels in sweat varies between 15-65mmol/l meaning that sweat is hypotonic – lower levels of electrolytes than serum and cells.   While sweating does account for some sodium loss, it is not in proportion to fluid loss through sweat.  (10, 11)



The key strategy in preventing EAH is to prevent over-hydration.   The best advice is to drink according to thirst.   This simple method is sufficient to prevent both dehydration and hyponatremia. (1, 12-15) 

This is in contrast to the traditional advice that athletes should consume as much fluids as tolerable.

There is little evidence to suggest that supplemental sodium prevents EAH during exercise lasting less than 18 hours or when athletes drink according to thirst.  (16-19).   EAH is a result of over-hydration not inadequate sodium intake.



Given the similarities in signs and symptoms of EAH with dehydration, diagnosis in the field is exceptionally difficult.

 Signs & Symptoms



 Fatigue / Weakness



 Increased thirst



 Raised temperature



 Nausea / Vomiting



 Reduced Level of Response  / Neurological deficit (e.g.  blurred vision)



 Respiratory Distress


 Not present

 Reduced urine output



After Bennet et al(20)


Laboratory testing

EAH is definitively categorised by having a blood serum sodium level of less than 135mmol/L.   This is only obtainable through laboratory testing.

Weight Gain
Given the pathophysiology of EAH is over-hydration combined with an inability to excrete excess water, weigh gain during exercise would be a logical indicator, however EAH is also seen with weight-loss (21-23) so is not, on it’s own, a reliable indicator.  Those who exhibit heat related illness without weight loss are, however, more likely to have developed EAH (24,25).

Understanding the casualty’s history is perhaps the greatest indicator.  Knowing their fluid intake  (>1500ml/h)  and over what time period is essential.



Correct diagnosis is essential; the principle treatment is restriction of fluids – if the casualty is suffering from dehydration, fluid restriction will have as serious consequences as hydrating a casualty with EAH.

In the situation in which the diagnosis of EAH is uncertain, the potential benefits of fluid restriction if the individual has EAH must be weighed against the potential harm that could result when the individual might have dehydration.

When and where body weight can be monitored in organized events, and in the presence of weight gain during exercise, fluid and sodium intake should be reduced until weight returns to 2% to 4% of body weight loss from base line level. (20)  In all other contexts this is likely to be impractical if not impossible. 

Where the suspicion of EAH is high, fluids should be restricted and salt sodium supplementation started.  The definitive treatment is a 100ml bolus of 3% hypertonic saline, which can be repeated twice at 10 minute intervals (up to 3 doses in total) with the aim of acutely increasing serum sodium concentration by about 4 to 5mmol/l and reversing cerebral oedema. (20)

In the field or with a limited skill-set oral sodium supplementation with minimum fluids has seen positive results (26).   This may include:

  • concentrated chicken broth (four bouillon cubes in 125 ml/one-quarter cup of water).  (27)
  • 100 mL of 3% saline flavoured with low-calorie sweetener (28, 29)

Administration of hypotonic (low sodium) fluids are absolutely contraindicated where EAH is confirmed. (26)

Then evacuate the casualty to emergency care.


Related Article:  Heat Stroke & Heat Related Illness



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