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Aetiology and pathophysiology

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

exercise associated hyponatraemia
- is predominantly a dilutional hyponatremia caused by an increase in total body water relative to the amount of total body exchangeable
- primary aetiologic factor appears to be
  - consumption of fluids (water or sports drinks) in excess of total body fluid losses: insensible (transcutaneous, respiratory and gastrointestinal), sweat and renal (urine) fluid losses
    - fluid consumption in excess of fluid loss (Primarly dilutional hyponatremia)

In resting state the maximal urinary excretion is in the region of 800- 1000ml/hr.

During exercise sweating becomes primary mode of water and sodium loss.

Exercise stimulates secretion of antiduretic hormone (ADH, arginine vasopression (AVP)).

During exercise body weight loss is to be expected (so dilutional hyponatraemia may occur if weight stays stable or increases

No strong evidence exists for loss of sodium as primary cause

Notes:

in most reported cases of symptomatic EAH
- there is body weight gain suggestive of an absolute increase in total body water
  - however, it should be recognized that some loss of body weight is expected with prolonged physical activity due to substrate oxidation without a net loss of total body water
    - for example, during a typical 42 km marathon a 1-2% decrease in body weight typically occurs without a change in total body water as inferred by the maintenance of plasma osmolality from pre to post race
    - therefore dilutional hyponatraemia may therefore occur despite no change or even a fall in body weight
antidiuretic hormone (ADH) secretion has been shown to be exacerbating factor in most cases
- during exercise, plasma ADH levels are not maximally suppressed implicating non-osmotically stimulated ADH secretion
  - in the presence of hyponatraemia and/or hypervolaemia, plasma ADH levels within 'normal ranges' are physiologically inappropriate because ADH should be maximally suppressed under these two conditions
    - this pathophysiology characterises the syndrome of inappropriate anti-diuretic hormone secretion (SIADH)
    - small increases in circulating ADH markedly reduce maximal kidney excretory capacity, thus increasing the propensity to retain ingested fluids even if rates of drinking do not exceed 800-1,000 mL/h
      - thus, the risk of developing fluid overload with previously 'normal' or excessive fluid intakes is enhanced when ADH is secreted inappropriately during prolonged exercise, resulting in increased urine osmolality and decreased urine volume
      - multiple potential stimuli to ADH secretion, such as nausea/vomiting, hypoglycemia, hypotension or hypovolemia can exacerbate fluid retention at any time during prolonged exercise.

Contributors (September 2010):

Dr Volker Scheer (GP Locum), Dr Andrew Murray (Marathon Medical Services)

Reference:

1) 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 Mar;18(2):111-21

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