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Seven clear symptoms of Exercise-Associated Hyponatremia

This is an excerpt from Waterlogged by Timothy Noakes.


Make sense of the hydration hype with Waterlogged.

Symptoms of Exercise-Associated Hyponatremia

Having established how much and what endurance athletes should drink to optimize health and performance, we now turn to the defining characteristics of EAH and EAHE.

A review of the symptoms reported by real patients with clinically documented EAH or EAHE shows that the symptoms they develop are specific, common, and unmistakable. The order in which these diagnostic symptoms typically appear is usually the following:

1. Impaired exercise performance

This probably occurs at quite low levels of weight gain (>1% BW gain) and is due either to swelling of the brain cells or to an increased pressure within the brain (intracerebral pressure), either or both of which impair brain function.

While an acute weight loss of greater than 2% may impair exercise performance if it is associated with an uncorrected thirst (Sawka and Noakes, 2007), we and others have measured levels of dehydration of 6% or greater in winning athletes in ultramarathon races (Sharwood, Collins, et al., 2002; Sharwood, Collins, et al., 2004), as was typically the case in the 1950s and ’60s when athletes were actively discouraged from drinking during exercise. In contrast, athletes who gain 6% or more of their body weight during exercise are likely to be close to death.

2. Nausea and vomiting

These symptoms result either from an increased intracerebral pressure caused by brain swelling or the presence of a large volume of unabsorbed fluid in the stomach and intestine, or perhaps a combination of both.

Especially the vomiting of large volumes of clear fluid (water) can occur only if the rate of fluid intake has been excessive. Similarly, the presence of excess unabsorbed fluid in the gut will cause a sensation of fluid sloshing around in the intestines. Neither of these symptoms can occur in dehydration, since in dehydration the content of water lying free in the intestine is reduced.

Indeed, one theory, discussed in chapter 9 (see note 20, page 284), is that humans can sustain a substantial (~2 kg) water loss without any noticeable effects. Spare fluid could lie freely in the intestine where it serves little real function except to act as a biological reserve in humans who practice delayed drinking. Delayed drinking, you will recall, is the likely adaptation our ancestors were forced to make once the size of the human gastrointestinal tract was reduced as we became increasingly more successful long-distance hunters. The body may first mobilize this water reserve stored in the gut before it begins to activate its defenses against dehydration.

Thus, by definition, dehydration cannot be the direct cause of the vomiting of large volumes of clear fluid from the gastrointestinal tract since the first consequence of water loss in humans is to reabsorb the fluid that lies freely within the intestine.

3. Headache

This results from the increased intracranial pressure caused by brain swelling in EAHE. Since dehydration reduces the fluid content of the brain, it cannot cause headache by this mechanism. Whereas headache might be an expected feature of EAHE, there is no reason for it to develop in dehydration. Headache is not listed as a common symptom in cholera, the disease causing the most rapid onset of profound and life-threatening dehydration in humans.

4. Altered level of consciousness

Athletes with mild EAHE become sullen, sleepy, and withdrawn; they avoid social interaction, close their eyes, and turn away from the light seemingly because they have photophobia (dislike of light). When addressed, they appear confused and somewhat dull; they are unable to hold a conversation of substance. They have difficulty concentrating and speak only when addressed directly. They have no interest in conversation. They appear to be either intoxicated or to have suffered a head injury causing concussion.

In those with mild EAHE, all these symptoms can be reversed almost miraculously within minutes by the administration of a hypertonic (3-5%) saline solution (Hew-Butler, Anley, et al., 2007; Hew-Butler, Noakes, et al., 2008). Observing the miraculous effects of this form of treatment taught me that EAHE makes clever people appear (temporarily) rather stupid. After questioning one confused patient with EAHE, I concluded that he was definitely not a rocket scientist. Minutes later, after he received 100 ml of 3% saline intravenously, he suddenly became fully alert, recognized me, and introduced himself as a highly qualified businessman. He wanted to know what had possibly caused his problem.

Mild dehydration of the type found in modern athletes causes none of these symptoms. This is readily confirmed by interviewing the hordes of “dehydrated” runners treated in the medical facilities at any endurance event anywhere in the world. While mentally fatigued, none show these classic features of being dull, sleepy, confused, withdrawn, and disinterested in their surroundings. These characteristic mental features always indicate that the athlete has either EAHE or another real medical condition, such as heatstroke or diabetic precoma.

The fact that dehydration does not cause any of these mental symptoms and especially the altered state of consciousness diagnostic of EAHE was noted already in 1947 in the famous U.S. military studies in the Nevada Desert (Adolph, 1947). Brown wrote, “In general, men cannot continue to walk in the desert heat unless they replace the water lost in the form of sweat. In some way dehydration augments the signs of physical fatigue until merely standing erect is an intolerable strain. Men dehydrated to this extent retain their mental faculties; they are not crazed by thirst. . . . Contrary to the popular legend . . . when the unfortunate victim of water shortage is first incapacitated he is neither delirious nor in agony from ‘mouth thirst’; he simply is incapable of even mild physical effort” (p. 143).

Those who had not read Brown’s work promoted the fatally erroneous idea that dehydration also causes the altered level of consciousness found in those with EAHE. As a result, many athletes with EAHE received intravenous fluids for the treatment of altered states of consciousness supposedly caused by dehydration. And some died.

5. Seizure (convulsion)

This is caused by a marked increase in intracerebral pressure. Since dehydration reduces the intracerebral pressure, it cannot cause a convulsion by this mechanism. People who are lost in the desert without water do not develop seizures. Instead, they become confused and lapse into coma, most likely because of a progressive reduction in blood flow to the brain associated with the accumulation of toxic substances in the blood secondary to kidney and liver failure. Since the mild levels of dehydration (3-8%) encountered in ultramarathon runners and Ironman triathletes do not cause kidney and liver failure, so coma and convulsions in endurance athletes are not caused by dehydration.

6. Bloating and swollen hands, legs, and feet

These are usually first noted by the athlete’s spouse or other relative or friend. Athletes may notice that their watch straps or race number bracelets become tighter as they become progressively overhydrated. In contrast, dehydration will cause the opposite—athletes will look as if they have become thinner, and their watches and race number bracelets will become less tight.

7. Muscle cell breakdown (rhabdomyolysis) with the development of acute kidney failure

Although there have been isolated reports of rhabdomyolysis and EAH occurring at the same time, the study of Bruso, Hoffman, and colleagues (2010) is the first to define this relationship in five competitors in the 2009 Western States 24-Hour/100-Mile Endurance Run. Blood sodium concentrations ranged from 127 to 134 mmol/L and all had blood creatine kinase activities in excess of 40,000 U/L (normal postrace values are up to ~2,000 U/L), indicating the presence of severe muscle cell breakdown; the highest value was >95,000 U/L. Three developed acute kidney failure; the most severely affected athlete required 12 days of hospital care.

Thus, far from protecting against acute kidney failure, aggressive drinking sufficient to produce EAH can, by mechanisms that are currently unknown, induce muscle cell damage that is sufficient to cause kidney failure. It is reasonable to assume that any level of overhydration will impair muscle cell function and hence athletic performance, and in some this effect will be sufficient to produce significant muscle cell damage.

Following are symptoms that are not a feature of either EAHE or dehydration:

1. Dizziness and fainting

Dizziness and fainting are caused by inadequate blood flow to the brain as the result of reduced blood pressure. An altered blood flow to the brain does not occur in EAHE or in dehydration at the mild levels measured in endurance athletes. Postexercise dizziness is due to EAPH, which is unrelated to the level of dehydration in athletes but is caused by an impaired regulation of the circulation when exercise terminates suddenly.

2. Muscle cramping

This is a separate condition that is caused by an altered nervous control of the muscles and is not due to overhydration, dehydration, or sodium deficiency in salty sweaters (chapter 4).

3. Wheezy breathing

This is a feature of asthma or similar respiratory conditions and is unrelated to EAHE or dehydration. Athletes with pulmonary edema due to EAHE may complain of shortness of breath and cough up a blood-stained sputum. Dehydration does not cause pulmonary edema.


Read more from Waterlogged by Timothy Noakes.



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