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Hyponatraemia

by Mark Jenkins


There have been two instances this year of the death of female runners in mass-participation marathons in the US, where the death has been attributed to hyponatraemia. This is a serious condition where excessive water intake causes a loss of sodium from the blood, with potentially fatal consequences. The condition is particularly dangerous because the symptoms can be readily mistaken for exhaustion, or even dehydration leading to incorrect first aid treatment. To help participants in endurance events understand the potential for hyponatraemia we present this 2-part article on the subject by Mark Jenkins.

PART 1 Salt and the ultraendurance athlete

Recently, Americans have been urged to pay more attention to their sodium intake. Decades ago, all foods seemed heavily salted. Then, a link between sodium intake and high blood pressure was discovered. Suddenly, "sodium - free" or "low sodium" products began flooding the consumer market. Certainly, to a degree, this is justified. Many diseases are worsened by excess sodium intake, and millions of Americans must closely watch the amount of sodium in their diet.

However, sodium is a required element for normal body functions. It is lost in sweat and urine and is replaced in the diet. The body has a remarkable ability to maintain sodium and water balance throughout a variety of conditions, thus ensuring our survival. Ultraendurance events challenge this survival mechanism.

In hot, humid conditions a large amount of sweat is lost, which can disturb sodium and water balance. Adequate hydration and sodium intake - either via sports drinks or food - becomes vitally important during long races. The goal of this article is to help you determine how to maintain sodium balance during training and racing and during recovery. The information for this article came from a variety of published studies done on healthy, young athletes and may not be appropriate for everyone. Athletes who are under a physician's care or have health problems should check with their doctor about salt and their ability to exercise in the heat.
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Hyponatraemia -- what is it?

Hyponatraemia means a low concentration of sodium in the blood. When it occurs in triathletes, it usually happens during long or ultra-distance races in the heat but may occur anytime. It is estimated that approximately 30% of the finishers of the Hawaii Ironman are both hyponatraemic and dehydrated. The longer the race, the greater the risk of hyponatraemia.

What causes it?

The exact mechanisms are not fully understood and I won't go into the complex physiologic pathways of sodium and water balance. The simplest answer is that lost sweat (salt and water) is replaced by ingested water (no salt). This dilutes the sodium in the bloodstream, and hyponatraemia results. Longer races carry a greater risk of hyponatraemia because of the total amount of sweat lost. During exercise in the heat, more salt is lost in sweat per hour than is usually replaced by food and fluids, including sports drinks. Your body can tolerate a degree of imbalance for a short period of time, but it may decompensate if this continues for too long.

Sweat contains between 2.25 - 3.4 grams of salt per litre, and the rate of perspiration in a long, hot race can easily average 1 litre per hour. So, for a 12 hour race, one could lose approximately 27 to 41 grams of salt. If the athlete replaces only the lost water and has minimal salt intake, hyponatraemia can result.

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Medications and hyponatraemia

Aspirin, ibuprofen, and other non-steroidal anti-inflammatory agents interfere with kidney function and may contribute to the development of hyponatraemia in triathletes. The same applies to acetaminophen (Tylenol). I have seen many athletes taking these drugs during Ironman races, and I strongly recommend against this practice. They won't make you faster and may hurt you. Under tough conditions, your kidneys need to function at 100%. Other drugs that may contribute to hyponatraemia are diuretics, narcotics, and certain psychiatric medications.

What are the symptoms of hyponatraemia?

The spectrum of symptoms can range from mild to severe and can include nausea, muscle cramps, disorientation, slurred speech, confusion, and inappropriate behavior. As it progresses, victims may experience seizures or coma, and death can occur. Severe hyponatraemia is a true medical emergency.

Treatment

Minor symptoms, such as nausea and mild muscle cramps, can be treated by eating salty foods and hydrating with a sodium containing sports drink. More severe symptoms require treatment by qualified medical personnel. If you think you are suffering from hyponatraemia or are unsure, seek medical attention immediately.

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Recommendations

There are no clear cut guidelines, and recommendations need to be individualized for each triathlete. Some authorities recommend drinking less water to rebalance sodium and water intake. However, given the risk of dehydration and heat injury, this is not a practical recommendation. To reiterate, all of the hyponatraemic athletes in the Hawaii Ironman were also dehydrated. Others recommend increasing salt intake, and this seems more prudent. By ingesting more sodium, hydration with water is balanced and dilution of blood sodium does not occur.

Relative importance for different length races
 length of race
 less than 1 hr1 - 3 hrs>3 hrs
Water-/+++
Carbohydrate-++
Salt--/++

It cannot be stressed enough that you have got to know what your needs are prior to race day. Rehearse your hydration, feeding, and salt strategy during your training sessions. There are so many variations between individuals that there is no single right answer. Know what your body's' needs are.

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Salt vs. Sodium?

Undoubtedly, some of you have noticed that FDA food labels list grams (or milligrams) of sodium, and at times in this article, I have referred to grams of salt. What is the difference? Salt is made up of sodium and chloride. The FDA labels lists only the sodium content. This is because there are usually other sodium containing salts (eg. sodium citrate) in these products. To avoid confusion, the easiest way to ensure that you have enough sodium intake is to get used to reading the FDA labels. For example to get 1 gram (1000mg) of sodium into your body, you would need to drink more than half a gallon (2.18 litres) of Gatorade - certainly impractical every hour! To get 1 gram of sodium from table salt, you would need to ingest 2.5 grams (1 gram from sodium, 1.5 grams from chloride). A teaspoon of salt weighs approximately 6.6 grams.

What about salt tablets?

It is best if you strive to get your sodium from both sports drinks and salty foods - as opposed to salt tablets - for two reasons. Salty foods stimulate thirst, and it is possible to ingest too much salt with tablets but very difficult with food. If you don't think that your food and sports drink is providing enough sodium, then consider salt tablets. Make sure you know how much you are taking!

What foods are best?

Ideally, foods consumed during a long race should be low fat, low protein, high carbohydrate, and provide a source of sodium. You need water, carbohydrates, and salt to survive a long race. For convenience, I have listed a few foods and sports drinks and their respective sodium content. You'll need to experiment and find the combination that is best for you. Get used to reading the FDA labels.

 mg sodiumservingfat(g)carbo(g)protein(g)
Gatorade1108 fl.oz0140
Exceed508 fl. oz0170
Baked Tostitos1401 oz.(13 chips)1243
SnackWell's Wheat crackers1705 crackers0122
Sunshine Bavarian Sourdough pretzels4902 pretzels0233
Baked Rold Gold pretzels50010 pretzels1223
Baked Rold Gold Hard Sourdough pretzels2201 pretzel0192
Premium Fat-free Saltines1305 crackers0111
Mr. Salty pretzel twists5509 pretzels0.524333

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PART 2 - MECHANISMS

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

Mechanism 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 hyponatraemia is more likely to occur.

Mechanism 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 hyponatraemic, the pituitary will continue to release ADH to try to hold on to water, even though this may make the hyponatraemia 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 hyponatraemia. 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 hyponatraemia 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 hyponatraemia is that the body must make a tough choice,

  1. 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). or
  2. 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 hyponatraemic symptoms.

Mechanism 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.

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So Which Mechanism is Responsible?

The exact sequence of events leading to exercise associated hyponatraemia 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 hyponatraemic 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 hyponatraemia 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 1½ hours, so the cumulative sodium loss would not be anywhere near enough to result in hyponatraemia. 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 hyponatraemia 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 hyponatraemia worse. The hyponatraemia 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 hyponatraemia.

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Conclusion

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 hyponatraemic athletes in this hot climate are both dehydrated and hyponatraemic. 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 hyponatraemia.

Selected References

  1. Renal and Electrolyte Disorders, Third Edition. Edited by Robert W. 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, 1991 Jul.
  4. Dehydration and hyponatremia during triathlons. [Review] Hiller WD. Source = Medicine & Science in Sports & Exercise. 21(5Suppl):S219-21, 1989 Oct.
  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.


Cool Running 13.11.02. Mark Jenkins MD is director of the student health center and the Associate Team physician for Rice University (NCAA Sports). He may be reached by email at jenky@rice.edu. This article first appeared on the SportsMedWeb web site and is reproduced here with the permission of the author.



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