To continue the discussion on exercise related hyponatremia (low concentration of sodium in the blood)....

There are thought to be three potential mechanisms to account for hyponatremia during exercise,


I) salt and water lost in sweat and urine are replaced unequally (i.e. water replacement is greater than sodium). Over a period of time (e.g. an Ironman), the cumulative sodium losses mount up. If an athlete overhydrates with water during an event, this dilutional hyponatremia is more likely to occur.

II)Syndrome of inappropriate ADH release.The hormone that regulates this sodium/water balance is called ADH (anti-diuretic hormone). It is also referred to as vasopressin. It is released by a specific group of cells in the posterior pituitary that monitor blood sodium concentration and blood volume. Normally these cells are more sensitive to small changes in blood sodium. If the sodium level drops, ADH secretion drops, and the kidneys respond by dumping out more free water (the urine becomes more dilute). Thus the blood sodium concentration increases. If the sodium conc. rises, the secretion of ADH increases and the kidneys hold on to more free water; the sodium concentration then falls back to normal.


In the case of changes in blood volume, the pituitary cells are less sensitive to changes in blood volume, but the response is of a much greater magnitude than with osmolality (sodium concentration) changes. A fall in blood volume causes a greater release of ADH -- to try to get the kidneys to hang on to more water to bring the volume back up.


So what happens if the sodium falls and the blood volume falls? The former tells the pituitary to decrease ADH and the latter tells it to increase. The result of these conflicting signals depends upon the magnitude of the changes. Beyond a certain %, the volume pathway predominates and is a much more potent stimulus for ADH release than the sodium pathway. Protecting blood volume is a survival mechanism. Thus, in the case of an athlete who is dehydrated and hyponatremic, the pituitary will continue to release ADH to try to hold on to water, even though this may make the hyponatremia worse.


If ADH is released in an excess, or inappropriate, amount it is referred to as syndrome of inappropriate ADH (SIADH) secretion. In this situation there is a release of ADH from the pituitary in response to certain stimuli (e.g. exercise, pain, stress, narcotic medications). The released ADH then instructs the kidneys to hold on to more free water and less sodium, thus causing hyponatremia. This is seen in a variety of conditions, including post-surgery, head injuries, or in response to certain medications. Under the right conditions, the pain/stress of triathlons or other endurance events may be sufficient to generate SIADH. The hyponatremia would be made worse by drinking water, and corrected by ingesting salt.


Another scenario is, as both sodium and water losses mount during a long race, ADH is released to better protect against dehydration. What may happen as the athlete is slipping towards both dehydration and hyponatremia is that the body must make a tough choice,

a. pee out a lot of dilute urine, thus clearing free water and raising the sodium concentration in the blood. Unfortunately this would be at the expense of dropping the blood pressure and facing potential circulatory collapse (shock).



b. Protect the declining blood volume by holding on to water; Keep the blood pressure up to make sure that vital organs get perfused with blood and to heck with the sodium concentration. (And hope that the idiot stops exercising soon and finds a salt lick someplace.)


The latter is the decision that will best protect survival, but it will cause a lowering of the blood sodium and the consequent hyponatremic symptoms.

III)Excess fluid intake may under certain conditions be sufficient to generate a "third space" effect in the intestine. In this mechanism excess ingested fluid, especially fluids with a high (>10%) carbohydrate content, may pull sodium out of the bloodstream and into the intestine. Thus, sodium is redistributed from the bloodstream into the unabsorbed fluid in the intestinal lumen, and hypontremia occurs.



So Which Mechanism is Responsible?

The exact sequence of events leading to exercise associated hyponatremia is most likely a combination of the three mechanisms. Depending upon race conditions and length of the event, different mechanism may predominate. The first mechanism is the easiest to understand but is too simplistic and does not account for the experimental observations seen in hyponatremic athletes. More than likely it is mechanism #2 (ADH), or a variable combination of mechanism #1,#2 and#3.


Clinical Example

I was recently consulted by a triathlete who had several visits to the emergency room for hyponatremia following short triathlons (1k/30k/5k or shorter). He is a "front of the pack" level triathlete, and consistently finishes in the top 10%. These triathlons lasted less than 1 1/2 hours, so the cumulative sodium loss would not be anywhere near enough to result in hyponatremia. Similarly, the amount of ingested fluid would be insufficient to allow for a "third space" effect. From reviewing the lab data acquired in the emergency rooms, it was quite clear that inappropriate release of ADH was the likely culprit. Each time the data indicated that he was well hydrated but had a low blood sodium concentration.


Unfortunately, an emergency room physician had told him that he was "dehydrated", and that the low blood sodium was the result of vomiting. He was erroneously encouraged to drink more water following his races. He did, but this simply made the hyponatremia develop even faster, resulting in another trip to the ER.


The most likely mechanism in him was that the races were causing an increased, and inappropriate, release of ADH. Drinking more water just made the hyponatremia worse. The hyponatremia *caused* the vomiting, not vice versa. The cure for him was to ingest salt following his race. Any food with a hefty salt content (pizza, salty chips, pretzels, etc.) is acceptable. This simple maneuver completely cured his problem. He is now able to train and race under a wide variety of conditions and has not had a further episode of hyponatremia.



As many physicians are taught, there are two ways to treat SIADH, water restriction, and increased salt ingestion. The former is cruel and, in the case of triathlons or other endurance events, potentially very dangerous. Dr. Doug Hiller's experience and observations on triathletes at the Ironman in Hawaii have shown that most hyponatremic athletes in this hot climate are both dehydrated and hyponatremic. Thus, fluid restriction is really not a practical consideration.

Increased salt ingestion is the most prudent course. As long as there is not a medical reason to restrict sodium intake, then increasing your salt intake is perfectly safe. If you consume more sodium than your body needs, then your kidneys simply dump the excess.

In summary, eating salty foods, is a very safe, effective treatment and preventive strategy for exercise associated hyponatremia.


Selected References,


  1. Renal and Electrolyte Disorders, Third Edition. Edited by RobertW. Schrier, MD. 1986. Little Brown and Company
  2. Fluid replacement during exercise. [Review], Timothy Noakes, MD Source = Exercise & Sport Sciences Reviews. 21:297-330, 1993.,
  3. Fluid replacement during prolonged exercise: effects of water, saline, or no fluid. Authors, Barr SI. Costill DL. Fink WJ. Source = Medicine & Science in Sports & Exercise. 23(7):811-7, 199I Jul.
  4. 4. Dehydration and hyponatremia during triathlons. [Review] Hiller WD. Source = Medicine & Science in Sports & Exercise. 21(5Suppl):S219-21, 1989 Oct.
  5. 5. Symptomatic hyponatremia during prolonged exercise in heat.Armstrong LE. Curtis WC. Hubbard RW. Francesconi RP.Moore R. Askew EW.Source = Medicine & Science in Sports & Exercise. 25(5):543-9, 1993 May.

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