Exercise-Associated Hyponatremia: The (Not So) Salty Truth

With this article, my goal is to provide an in-depth understanding of:

  • What exercise-associated hyponatremia (EAH) is and why it occurs with exercise;
  • Why overhydrating during exercise can be so dangerous;
  • How to recognize EAH when it does occur;
  • How EAH is best treated; and
  • How EAH is best prevented (and why salt supplements are not necessarily a good prevention strategy).

As an iRunFar reader, I expect that most of you have some familiarity with the above concepts. I hope this article will not only provide more details about EAH for you, but also that you can teach others about EAH in your roles as coaches, fitness instructors, exercise physiologists, health-care workers, journalists, and more.


Here are a few definitions to get us all speaking the same language.

Exercise-associated hyponatremia (EAH): A low blood plasma sodium level that develops during exercise. In most labs, this is defined as and Na+ (sodium) of less than 135 mEq/L. The normal Na+ range either during or outside of exercise is 135-145 mEq/L.

Arginine vasopressin (AVP)/antidiuretic hormone (ADH): Two names for the same hormone which is released from the pituitary gland in response to dehydration and increased sympathetic drive (the ‘fight-or-flight response,’ which occurs during exercise, stress, pain, and more). As examples, this hormone is known to be released in heart failure, respiratory failure, various cancers, and in muscle breakdown.

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): When the hormone ADH is not released in response to dehydration, but instead in response to one of the stressors listed above. SIADH is believed to be the major physiologic occurrence, when coupled with drinking fluids, that predisposes humans to EAH.


I was recently taking a class at our local gym and the instructor said numerous times, “Remember to keep drinking and finish your bottle by the end of class.” It was a 45-minute class. The notion that unlimited hydration is what all of us should strive for during exercise is so ingrained in the fitness world that I sometimes wonder if it can be unlearned. Maybe you, too, have been running a trail race and an aid-station volunteer offered you the seemingly helpful advice to “stay hydrated.” Maybe you are thirsty and that is what you need, but I hope when you have finished reading this article that you will see why this advice to “keep hydrating” can be so dangerous. Specifically, not only can athletes become ill from EAH, but deaths have occurred due to EAH in numerous sporting activities including but not limited to marathon running, military drills, hiking, and American football.

Figure 1. Activities where exercise-associated hyponatremia has occurred, including known deaths (Hew-Butler, 2017).

Figure 2. A water stop during 2014 Toulouse Marathon. Photo: Pierre-Selim Huard

Historical Background

Figure 3. Cynthia Lucero. Image from https://www.williamjames.edu/giving/lucero-run/index.cfm.

Cynthia Lucero, a previously healthy 28-year-old female, was running her second marathon, the 2002 Boston Marathon. She was the type of person who thoughtfully planned ahead. She had just completed her doctoral dissertation entitled “Effects of a Marathon Training Program on Family Members and Friends of Cancer Patients.” And that day, she was running to raise money for the Massachusetts Chapter of the Leukemia and Lymphoma Society.

Her race was going as planned. She had numerous friends watching her run and they reported that she drank copious amounts of Gatorade at every aid station, which were one mile apart. She looked strong at mile 20’s Heartbreak Hill, but then, just before mile 22, she started to lose her footing. She looked to be struggling so much that a friend jumped into the race to run alongside her. Cynthia said she felt “rubber legged” and then collapsed to the pavement (Smith, 2002).

An ambulance took her to Brigham and Women’s Hospital where she was found to be in a coma. A breathing tube was placed and she was given intravenous (IV) fluids (normal 0.9% saline, or a fluid-salt solution that is isotonic with human blood–in other words, it will not cause ‘pickling’ or swelling of human tissues) and her sodium level was found to be 113 mEq/L, far below the normal 135-145. She was found to have diffuse cerebral edema, or brain swelling, and elevated arginine vasopressin (AVP), consistent with EAH. Shortly thereafter, she was found to be braindead (Siegel, 2007). This was only the second death in the race’s long history.

And then, just six months later, in October of 2002, it happened again, in an eerily similar way. Hillary Bellamy was running the Marine Corps Marathon and, at mile 21, she felt so sick that she left the race course (Orton, 2006). She was transported by ambulance to the nearest hospital, still coherent, and was given IV fluids (again 0.9% saline). She then proceeded to go into a coma. Her sodium level was 123 and her AVP was elevated, consistent again with EAH, but a milder case. However, she too would go on to die of cerebral edema two days later (Siegel, 2007).

Numerous similar cases occurred in the 2004 and 2005 Boston and Marine Corps Marathons, where runners became comatose, developed seizures, or experienced other neurologic complications from EAH (Seigel, 2007).

However, now the treating physicians had figured something important out: they needed to treat these runners with a more concentrated sodium solution, in other words hypertonic (3% saline) IV fluids. Hypertonic fluid is a salt-fluid solution with higher tonicity/concentration than normal blood—it will cause pickling of human cells. Importantly, in this case, it will promptly reduce the brain swelling. By doing so, they stopped a potential scourge of deaths at these races (Siegel, 2007).

But let’s rewind a second, why were runners now getting this previously unknown entity of EAH in scores? Honestly, it should be said that, already in 1985, life-threatening cases of “water intoxication” were starting to crop up at the Comrades Marathon, including runners with seizures and hospitalizations. Fortunately, all survived. Then, in 1986, two physicians running 80- and 100-kilometer races respectively in Chicago, Illinois both developed EAH so severe that they required hospitalization (Frizzell, 1986). They had both been advised to drink 300-360 milliliters/10-12 fluid ounces every mile (at each aid station). They were treated at separate hospitals; one received hypertonic 3% saline and was discharged home the same day and the other received isotonic 0.9% saline and was semi-comatose for 36 hours and developed numerous complications before finally being discharged after five days (Frizzell, 1986).

By the end of 1986, a body of evidence (Noakes, 1985; Frizzell, 1986; Noakes & Speedy, 2006) showed that:

  • EAH in runners was related to excessive fluid consumption;
  • Athletes who drink to excess appear to do so at the well-intended advice of others to keep hydrated; and
  • Recovery is rapid when hypertonic (3–5%) saline is given, but 0.9% saline is ineffective.

Despite growing evidence of the dangers of overhydration, in 1991, the United States Army developed guidelines (Burr, 1991) that mandated recruits drink 1.8 liters/almost 61 fluid ounces of liquid per hour when the temperature was 30 degrees Celsius/86 Fahrenheit or greater. This unfortunate mandate resulted in 125 hospital admissions for EAH and at least six fatalities attributed to it (Gardner, 2002; Garigan, 1999; O’Brien, 2001).

Apparently unaware of the above evidence and the now-six-known fatalities related to overdrinking during exercise, the American College of Sports Medicine published a new position statement in 1996 (Armstrong, 1996; Convertino 1996) that encouraged athletes to drink “as much as tolerable” during exercise. It was these guidelines that were in place at the time of the deaths of Cynthia Lucero and Hillary Bellamy. In 2007, they were revised (Sawka, 2007) to specify that athletes should replace the fluid they lost and not beyond.

From 1998 to 2007, there were four total deaths in marathon runners. And the development of low sodium during long-distance running was found to be anything but uncommon. In one study (Cairns, 2015), 70% of ultramarathoners were found to develop EAH during the course of the 100-mile race, The Great North Walk Ultras. And it is certainly not limited to ultramarathons. Yoga, for example, is one lower-intensity activity where practitioners are encouraged to drink excessive amounts and complications have occurred as a result (Reynolds, 2012; Bailowitz, 2016).


Why does hyponatremia occur, and what is it about exercise that makes it much more likely to occur?

First of all, under normal physiologic circumstances, hyponatremia (low salt, or, better stated, excess fluid) does not occur. The salt-fluid balance in the human body is very tightly regulated. When your salt level begins to rise, you get thirsty, and normally humans have access to fluids, but if you don’t, your body will hold onto the fluid that is already in your body and your urine will become very concentrated. The opposite occurs on the rare occasion that a human is overhydrated: you will urinate a lot of dilute urine to get rid of the extra fluid. This is so rare, though, because it is uncomfortable to drink when you are already excessively hydrated.

This system can go haywire when the body is under extreme stress (respiratory failure, certain cancers, certain drugs, as well as during exercise and rhabdomyolysis) and this is called Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH). Again, SIADH is when the antidiuretic hormone (ADH) is not released in response to dehydration, but in response to stressors in the body.

Figure 4. The current mechanism believed to be behind the development of exercise-associated hyponatremia (Urso, 2014).
Flogosis, or phlogosis: Inflammation.
NT-pro BNP: The N-terminal pro b-type natriuretic peptide is released in the blood when there is stress to the heart.
Hypotonic fluid: Fluid that has lower tonicity/concentration than normal human blood and thus causes swelling of cells and tissues—think reverse pickling.

It should be noted that the relationship between rhabdomyolysis and hyponatremia appears to be that of a vicious cycle where ‘rhabdo’ can lower sodium and low sodium can induce rhabdo. (Ellis, 2009; Bruso, 2010; Hoffman, 2015)

In exercise, again likely due to SIADH, humans tend to inappropriately secrete AVP/ADH, which holds onto the fluid you have, so you concentrate your urine even when you are not dehydrated. In other words, the fluid you drink stays in your body. Perhaps this is truly not something ‘going wrong’ during exercise, but is a strong protective mechanism to help you avoid dehydration.

The SIADH that occurs during exercise is not a problem unless humans start drinking a lot, specifically when they are not thirsty. In this unfortunate circumstance, the body just continues to secrete AVP and, instead of peeing out the extra fluid, the fluid builds up in the blood and tissues, and the sodium level in our blood drops. This drop in sodium in the blood is particularly problematic for the brain because water will be transported (through osmosis; again, think the reverse of pickling) to the brain, causing swelling. This is why weakness, seizures, and brain death can occur.


Initially the runner will notice they are no longer thirsty, likely become nauseated and/or experience a headache or become confused. A headache is a very rare symptom for a runner to have and should immediately raise the suspicion of hyponatremia. Unfortunately, oftentimes aid-station volunteers or a runner’s crew mistake this for dehydration and encourage the athlete to drink more, despite the athlete sometimes being adamant about not wanting to drink more. If drinking continues (even if the athlete has taken salt tablets), loss of muscle control and weakness can be seen.

Figure 5. Evidenced-base treatment options for exercise-associated hyponatremia associated with mild (yellow), moderate (orange), or severe clinical signs and symptoms (Hew-Butler, 2017).
Obtundation: Decreased level of alertness.
Dyspnea: Difficulty breathing, in this case it would be due to fluid building up in the lungs.
Decorticate posturing: When an unconscious person curls up into the fetal position.
Mydriasis: Dilated pupils.

We have all seen the videos of athletes stumbling all over the place or crawling to reach a race’s finish line. While most of the world seems to view this as ‘heroic,’ I and likely others familiar with EAH see this as a person with severe hyponatremia who now has swelling of the brain bad enough to lead to incoordination and muscle weakness, and is on the verge of seizures, coma, or death. This is what I think of when I see the images of 29-year-old Hyvon Ngetich crawling to third place at the 2015 Houston Marathon.

Figure 6. Image is a screenshot from a KXAN video of Hyvon Ngetich crawling across the finish line to finish third at the 2015 Houston Marathon. (In full disclosure, I do not know what her post-race sodium level was, but the way she loses muscle control and coordination in her legs and needs to crawl is strikingly similar to that seen in a video of Brian Morrison, who was known to have exercise-associated hyponatremia (EAH) with critically low sodium measured at a nearby hospital after he crossed the finish line at the 2006 Western States 100. Though the symptoms, such as confusion, associated with exertional heat stroke can be similar to that of EAH, an important distinction is that runners with heat stroke should not lose coordination or control of their muscles, as is shown in these videos. That loss of coordination is due to swelling of the brain and would not be expected in heat stroke. If temperatures are hot and heat stroke is suspected, a rectal temperature in excess of 104 degrees Fahrenheit/40 Celsius would confirm heat stroke. Please see Liza Howard’s heat-illness article for more information. If EAH is suspected, this can be confirmed or ruled out with an i-STAT machine, explained later in this article).

Figure 7. Image is a screenshot from a Fleet Feet Seattle video of Brian Morrison on the Placer High School track about to win the 2006 Western States 100. He lost control of his legs to the degree that he was helped across the finish line, disqualifying him from the win. Brian survived this medical incident.

Prevention and Treatment

I have heard people say various iterations of if only ultrarunners ‘kept up’ on their salt tabs, pills, or other means of ingesting supplementary sodium, finishes like that of Brian Morrison would never happen. But I think there is good reason to question this. Sodium supplementation during a 100-mile race has not been found to be related to the prevention of hyponatremia (Hoffman, 2015), or the prevention of cramping for that matter, but low sodium levels in the blood are instead related to fluid retention (Hoffman, 2015). It should truly be viewed as a problem with fluid and not a problem with salt. I think Hew-Butler et al. said it very well in their 2017 EAH review that, “It is the amount of fluid ingested rather than the amount of sodium ingested during exercise that drives the final blood sodium concentrations.”

The sodium level in the blood is exceptionally tightly controlled through innate mechanisms in the human body, which includes the ability to mobilize sodium from internal stores (such as the gut and bone) when needed. Indeed, runners can finish the Western States 100 (WS 100) without sodium supplementation and not develop EAH (Hoffman, 2015). Basically, when people take salt tabs, they tend to keep drinking and, rather than peeing out the fluid, their body bloats up. Sure, one could take salt tabs and drink nothing, but the tabs would be really hard to swallow and likely stimulate nausea (which in itself can lead to low sodium levels).

Based on available research (Hew-Butler, 2017; Hew-Butler, 2015; Hoffman, 2013; Hoffman, 2015) and my personal experience with salt tabs, if I were to run the WS 100, I would plan to drink and eat according to thirst and hunger and then go for salty foods if I felt like it. At this time, there is insufficient evidence to suggest that salt tablets are necessary to prevent EAH, even in an ultramarathon, and, in fact, they may come with risks.

That being said, there have also been many runners who have had record-setting ultramarathon finishes who did take salt tabs. Andy Jones-Wilkins, a seven-time consecutive WS 100 top-10 finisher reports having good success with sodium supplements, taking “600-800 milligrams of sodium per liter of fluid and increasing to 1,000 milligrams per liter of fluid in very hot (over 110 degrees Fahrenheit) conditions.” He continues to use this strategy today.

Camille Herron, the 2017 winner of Comrades Marathon and current holder of the women’s 100-mile world record, reports using a different strategy: “I tried taking salt tablets during long runs for a while, and it made me feel weird and crash and burn… What works for me is to use the salt shaker on foods and sip sports drink and water leading up to races. Then, during the race I carry a water bottle and a sports-drink bottle. I sip on both as needed. My gels have salt in them too—I take a gel with water every 30 minutes, and then sip on the sports drink in between. One thing I’ve learned is I feel the best taking a drink or supplement with potassium/magnesium/calcium in it—I think it helps to keep me peeing and the muscles firing!”

With these two examples, one can easily see that runners can have success with or without salt tablets. However, my review of the literature leads me to believe that taking salt tabs for sodium is more likely to cause problems than using a mixture of electrolyte drink and (potentially salty) food.

One incredible published example of sodium-tab supplementation gone wrong is this is that of a man who had previously developed EAH and was advised by his physician to take upward of 6 grams of supplemental sodium during a 72k run. At the finish line, emergency services were called because of this gentleman’s condition, and despite having taken in excess of 6,500 milligrams of supplemental sodium, his blood sodium level was critically low at 122 mEq/L (Hoffman & Meyers, 2017). This case elegantly demonstrated that EAH absolutely can develop despite ingesting large quantities of sodium.

One should also consider the potential side effects of sodium supplementation which are not limited to bloating and swelling but may include high blood pressure. I am personally aware of one runner who started taking salt supplements prior to his race and, in the pre-race medical screening, was found to have a blood pressure so high that he was not allowed to start the race. Granted his blood-pressure elevation may have been related to other factors, but ‘preloading’ with salt tabs could easily have raised it above the acceptable limit. This is truly something to keep in mind if you have an underlying diagnosis of high blood pressure.

Fortunately, prevention of EAH is very simple: drink when you are thirsty. And I advise drinking (and eating) whatever you are craving: water, sports drink, food, salt or not. Go for it, and let your body be the guide. Though there has been some recent debate about whether or not ‘thirst’ is as reliable during exercise as it is at rest. After reviewing the literature presented in Keneflik’s 2018 review, the argument that drinking to thirst does not do well to prevent dehydration during exercise is based on the fact that subjects who drink to thirst tend to lose weight. As discussed below, weight loss is an expected consequence of endurance exercise and suggests to me that thirst does indeed work correctly during exercise to prevent both hyponatremia and hypernatremia. Further, blood sodium level should be used as an indicator of whether or not drinking to thirst works rather than weight change during exercise.

Figure 8: Recommended strategy for avoidance of hyponatremia and dehydration (Hew-Butler, 2015).
Osmolality: The concentration of a solution, or the number of soluble particles per unit kilogram. Sodium and potassium, paired with chloride, are examples of soluble particles in the blood.

As discussed above, the treatment of EAH with brain dysfunction is with IV hypertonic (3%) saline. The treatment algorithm is shown in Figure 5.

Of note, physicians have historically been hesitant to give hypertonic 3% saline because it has been found to cause brain damage. (This occurs via central pontine myelinolysis, which is when the center of the part of the brain stem called the pons is severely damaged due to rapid movement of particles across the neurons’ protective cells, which is due to rapid correction of sodium levels in a person who has chronically low blood sodium. In these people, their brain has adjusted to being in something of a chronically swollen state.) For this reason, most doctors are taught to not use hypertonic 3% saline in anyone with low sodium. However, it takes the brain over 48 hours to reach the same sodium concentration as the blood. So for runners with EAH, the brain still has a close-to-normal sodium concentration, and you can correct the blood sodium as quickly as possible. So, please, especially those of you in health care, spread the word about hypertonic 3% saline (Hew-Butler, 2017; Noakes & Speedy, 2006). As you can see in Figure 5, it is the recommended treatment of EAH for athletes with the most severe symptoms (Hew-Butler, 2017).

Finally, physicians have been hesitant to give hypertonic 3% saline when a runner has elevated creatine-phosphokinase (CPK) consistent with rhabdomyolysis, but a CPK rise is expected after a long-distance running event (learn more in our rhabdo article) and should not delay or prevent administration of hypertonic 3% saline in cases of EAH. To reiterate, 0.9% saline treatment has been found to prolong recovery and may fail, and has likely failed, to save lives.

Figure 9. An intravenous-fluids bag of hypertonic 3% saline. Image from www.empem.org.

What We Have Learned at the Western States 100

I started working on research and in the finish-line medical tent of the WS 100 in 2013 and, that year, we were prepared to see EAH thanks to the research efforts of Marty Hoffman and Tamara Hew-Butler, both of whom are well known California-based physician researchers in ultra-endurance sports with extensive research experience at the WS 100. Marty even had a teaching session with me, where he showed me the video of Brian Morrison.

It was a hot year in 2013 and, even in the early morning, it was too warm to stand out in the rising sun. We received report of a runner at who was down at Brown’s Bar (at about mile 90), shaking and possibly having a seizure. He was transported by ambulance to the finish-line medical tent where he now clearly had developed seizures and (without knowing his blood sodium level) 100 milliliters of IV hypertonic 3% saline was administered. The runner stopped seizing and his mental status returned to normal. When he was admitted to the hospital, his sodium was still critically low at 122. We calculated that he likely had been as low as 119 before the hypertonic 3% saline. This was such a vivid example to me of how such a simple intervention can save a life. He did survive and ran again the next year (Thornley, 2014). However, unfortunately, his 2013 hospital stay was prolonged, apparently due to the refusal of the treating hospital to continue to use hypertonic 3% saline to normalize his sodium. (They used 0.9% instead.) This was due to concern for rhabdomyolysis, which was likely unfounded, again due to what we know about CPK levels in ultrarunners. As a side note, this runner reported that he had taken one salt tablet every 30-45 minutes during the race, but rather than preventing hyponatremia, it promoted weight gain. (He was up four pounds from his pre-race weight at the Rucky Chucky aid station, at mile 78.)

Historically, runners were weighed at the WS 100 aid stations and forced to drink if they were losing weight. Reportedly, runners put rocks in their pockets to avoid being pulled or stopped and told to drink more. This was purportedly begun to avoid dehydration in runners. By 2013, we did not use weight as a diagnostic tool at the WS 100. This was because of knowledge of the dangers of EAH and fluid retention as well as the research that had shown that weight does not always correspond to sodium levels (Hoffman, 2013). However, a couple good rules of thumb are:

  • Runners are expected to lose weight over the course of a 100-mile race, and a runner who has not lost weight is likely overhydrating; and
  • There is actually a significant correlation between faster finishing time and more weight loss. The fastest runners can lose up to 5-7% body weight over the course of 100 miles without developing medical issues (Hoffman & Hew-Butler, 2013; Hoffman, 2013). That being said, as shown in Figure 10, a number of slower runners lost weight in excess of this, which was likely not beneficial. Additionally, we do not know the weights of runners who did not finish, though it stands to reason that excessive weight loss or gain would likely be associated with an increased risk of not finishing. However, mild weight loss was seen in the best performers.

Figure 10. Change in body weight relative to performance at the 2009 Western States 100 (Hoffman, 2013).

A similar trend was also reported in marathon running, with the fastest finishers losing the highest percent body mass (Cheuvrant, 2007).

Figure 11. Percent body-mass change versus marathon finish time (Cheuvront, 2007).

By 2014, we ditched the scales entirely at the WS 100 (in 2013 they were only used for research purposes) and instead told the runners to drink if they were thirsty, but not according to a schedule or at the encouragement of others.

Figure 12. A 2013 Western States 100 runner feeling light and free at Robinson Flat, mile 30, knowing he would not be pulled from the race or told to hydrate because of his weight. Photo: Tracy Beth Høeg

Figure 13. The 2017 Western States 100 research team including Brian Toedebusch, Ali Warrick, Tracy Høeg, and Sarabeth Maciey in the finish-line medical tent getting ready to draw blood from participating finishers. Photo: Tracy Beth Høeg

At the 2017 WS 100 (Figure 13), post-race blood sodium levels were checked as part of the metabolomics of performance study (Høeg, 2018). What we found was surprising and encouraging: only 1/30 (3.3%) of runners participating in our study had hyponatremia post-race, and the one who did had a borderline low sodium of 134 mEq/L. This was in stark contrast to the 30% (14/47) found at the 2009 race (Hoffman, 2013). Though it is difficult to draw conclusions based on these results, it suggests that WS 100 runners are currently using more effective hydration strategies than in the past.

The i-STAT

Figure 14. i-STAT handheld blood analyzer. Image from www.pointofcare.abbott.

A helpful tool called the i-STAT allows for immediate laboratory analysis on site at a race. This is something we have used the last couple of years at the WS 100 and it has eliminated doubt about whether or not a participant has EAH. This is something all major races could consider purchasing especially if there is a concern for frequent EAH.


  • Overdrinking (water, sports drink, or other hypotonic fluid) can be deadly during exercise.
  • Hyponatremia presents initially as headache, nausea, vomiting, and an aversion to fluids, and it progresses to muscle weakness and incoordination, seizures, and brain death due to brain swelling.
  • Severe hyponatremia should be treated with cessation of exercise and hypertonic 3% saline IV fluids. Mild hyponatremia can be treated with oral hypertonic fluids.
  • Runners should drink to thirst and not beyond, and their supporters should support and recognize this.

Now, go enjoy a cold beverage on me! It’s hot out there.

Call for Comments

  • Do you have a personal experience with exercise-associated hyponatremia that you would like to share?
  • If yes, what lessons did you learn and how did you adjust your hydration strategy?


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Tracy Beth Høeg MD, PhD

is currently a Sports and Spine Medicine physician at Mountain View Rehabilitation in Grass Valley, California, and an assistant professor at UC Davis. She completed residency in Physical Medicine and Rehabilitation at UC Davis and a PhD in Ophthalmology at The University of Copenhagen. She is a Danish-American double citizen who ran for the United States at the 2013 IAU Trail World Championships and for Denmark at the 2018 WMRA Long Distance Mountain Running Championships. She is married to Dr. Rasmus Høeg and they have two sons.

There are 28 comments

  1. Mario Hahnel

    Excellent article highlighting the causes and dangers of EAH. The author is correct to outline that in ‘fitness’ circles’ you still constantly get to hear ‘Hydrate often, hydrate plenty, hydrate before you are thirsty’. You also see a lot of casual or short-distance runners doing a couple of miles dragging huge water bottles around with them.
    Its so important to spread the word and create awareness so that EAH can be avoided.
    I was particularly interested to read about the analysis of additional salt intake and that during long work outs and ultra -runs on its own it does not prevent EAH.
    For my Ultra’s I’m still trying to find the sweet spot when it comes to effective hydration and have in the past over-hydrated in combination with salt supplements and felt bloated as a result.
    Thank you for publishing this article!

  2. Pete

    Very interesting post Tracy, thanks or putting all of that together.
    There is strong support for salt supplementation amongst ultrarunners and aid station staff in the UK. Many times I’ve been advised to ‘take some salt’, whether it’s for mild cramping or hitting a low point. I stopped supplementing salt a few years ago following severe cramping during a run in hot weather, during which I was taking a slat replacement solution. Rarely have I had an episode since.
    Do you think it is just that runners are drinking to a schedule, or are they over drinking in the hope of reducing the heat effects of exertion?

    1. Tracy Beth Høeg

      Pete, great question. I think newer/novice long-distance runners tend to overdrink in the hopes of preventing dehydration – especially in the heat. They may go out an a moderate effort and way overestimate the amount of fluid they lose through sweat and then overhydrate. I think it is the more experienced runners that get into trouble with a drinking schedule.

  3. Amy

    This was very interesting to read, albeit a bit alarming. I am always thirsty, but especially so when exercising, and feel that I drink much more than those around me. I have had lab work done and nothing seems to be causing that thirst (blood sugar fine, electrolytes fine, lab panel all normal). I will probably heed the advice to focus more on electrolyte drinks and salty food in the absence of just salt tabs. Any tips for those of us who are always thirsty but also don’t want to accidentally overhydrate?

    1. Tracy Beth Høeg

      I don’t know if this applies to you, Amy. But some people do have psychogenic polydipsia where they way overdrink fluids because they find it comforting (a stress reliever/tic). They can develop severe hyponatremia even outside of exercise. The thing you should be aware of is you are MORE likely to develop hyponatremia when exercising than not because of the secretion of ADH. I would focus on hydrating before and after your workout and then only taking very small sips when working out, if needed at all. Of course longer, more intense workout will require a bit more fluid. But yes, I admit, for some people it is particularly tricky to go by feel. So if you start feeling the symptoms listed above of mild hyponatremia, start backing off the fluid!

  4. Jim

    “Do you think it is just that runners are drinking to a schedule, or are they over drinking in the hope of reducing the heat effects of exertion?”

    I’m really curious about that angle, too!

  5. Paul

    My understanding of the WS research is that runners self-selected their sodium protocol and then the investigators compared their results. A finding of no difference in performance between runners with high and low sodium intake could mean that the runners have optimized their sodium intake for their particular need. We don’t know if the high sodium users would have done worse or better if they were forced to consume less sodium. Of course, nobody is likely to volunteer for such research.

  6. solarweasel

    Thought-provoking article (and geeky science, which I love!)

    I stand by the notion that every runner is unique with varying needs. I also believe that the salt/hydration puzzle, while already complex, is further complicated for many of us who haven’t figured out how to calibrate our brains to what’s actually going on inside us. For example, I always *feel* like I’m getting enough fluid and salts, but I’ve got no objective data (or an “i-STAT” device) to tell me otherwise.

    Personally, I grow nauseous at about the 11-12 hour mark of any 100-miler. Food/fluids stop absorbing and things just kind of slosh around until I throw it all up. Unfortunately I rarely reach 12 hours in training, so it’s been tough to try different strategies and analyze the effects, save for a handful of races.

    It would be much easier to make more educated, data-driven adjustments to one’s nutrition strategy based on actual data rather than gut feeling (pun intended).

    1. Sean

      I completely agree that every runner is unique with varying needs. And to further complicate that, every different situation that every runner is faced with is unique and requires different strategies. Just because x works for ten 100-milers in a row doesn’t mean that x will work for #11. There are SO many variables that come into play for each individual in each situation. One of the frustratingly unique aspects of our sport is that we all are truly an experiment of one, almost each and every time we go for a run, and the longer duration each run is, the more variables come into play and the more unique each run becomes.

      Specifically, where we live, on the border of the desert and mountains in the desert southwest, hydrating and electrolyting properly can be particularly tough. I see this to be true generally in training, and even more so while racing because we’re pushing harder and therefore, sweating a lot more. As we have seen while running in the desert, and even in the arid high mountains, dehydration is a real thing, and it’s dangerous. I’ve run in the Grand Canyon dozens of times and the only times I haven’t seen severely dehydrated people are when I’ve kept to the very-seldom used trails in non-peak times of the year.

      From what I’ve personally witnessed, there now seems to be too big of a shift away from adequately hydrating. As discussed in this article, the pendulum previously swung towards over-hydration, and once WS got rid of their scales (which I was very happy to see, as a scale doesn’t tell us how a person is actually doing internally), I’ve noticed that the pendulum now has swung too much toward under-hydration for fear of hyponatremia. When it’s hot and you’re running in the heat, you need to hydrate (and keep your core temperature cool, but that’s another topic for another article).

      I’m not so sure that citing elite marathoners losing 7% of their body weight during a marathon is very relevant to the masses. Elite marathoners have a very different physiological makeup than most of us, they’re very highly trained athletes whose bodies have adapted to deal with high stress better than most, and they’re out on the course for roughly half the amount of time than the average marathoner is.

      The best teacher for me regarding heat and proper hydration/electrolyting was crewing at Badwater in 2009 and 2010 for Jamie Donaldson. Before then, I wasn’t very good at proper hydration while running, especially in the heat. Since then, I feel like racing in the heat is one of my relative strengths (as long as I properly execute what I know I need to do). I’ve raced in hot conditions, including Desert RATS stage race (5 stages, 148 miles), where temperatures reached nearly 110F. Both years I ran RATS, I typically drank 40 oz/hr and consumed 1400 ml of sodium/hr using a mixture of electrolyte tablets in my water and salt pills. Those were two of my best performances in races, and I’ve since successfully used that same fluid/electrolyte strategy in other hot races (>100F). I don’t say this because I think everyone needs to, or should, use that same strategy, but that’s what I learned to work best for me, and I encourage others to find out what their own n=1 is.

      As weasel says, geeky science, which I love, and there’s also some art to it all.

  7. Keith Straw

    Loved this one Tracy. A running buddy forwarded this to me after seeing Figure 12. I’m glad they did. I’ll be looking for more of your stuff. Thank you.

  8. Alex

    Great article. Keep hammering on the point that your body knows what it wants. Evolution has had countless millions of years to perfect the hunger and thirst cues that allow us to maintain homeostasis. These mechanisms don’t stop working just because you’re running a trail race…

  9. Markus

    People eat and drink too much these days in training runs and races. I frequently join a little running group once a week for a 3 mile run. Some of them take a bottle with them. Seriously? You can’t survive 30 minutes without water?
    In the last 10-15 years athletes got told that they have to hydrate and now they drown in their own fluids.

    Some runners need to use their own senses more: Hunger and thirst.

  10. John K

    For years I have actually listened to the “drink to thirst” mantra. And here I am with my first kidney stone, for which chronic dehydration is considered by my doc to be the likely cause. A couple of years ago, I did a sweat test and found that I lost 13lbs during a 3-hour summer run. I simply can’t carry enough water on a run to replace that kind of weight. And yet, I am also never quite that thirsty on these runs either. In winter I can easily run for 3-4 hours and not drink even one drop.

    You write “As discussed below, weight loss is an expected consequence of endurance exercise and suggests to me that thirst does indeed work correctly during exercise to prevent both hyponatremia and hypernatremia.”

    If I am not thirsty, *and* yet I lose significant amounts of weight (which to me, indicates dehydration, and now I have a doctor telling me that my condition is caused by chronic dehydration) I don’t think I can “drink to thirst” any more — not in either exercise, or outside of exercise.

    At the one end, you have hyponaetremia, and at the other end, you have dehydration (which may be chronic rather than acute). I think it is better to advise people to “know themselves” by doing things like a sweat test than to give the same advice to all. “Drink to thirst” may be OK for many, but it might not be OK for “me”.

    1. Brad M

      I believe that when the author states that losing weight is a consequence of endurance exercise and that it proves that the thirst mechanism is working, she is speaking about the importance of blood plasma ion concentrations, not water balance. If your blood plasma is at the proper levels and yet you have lost 13 lbs, replacing that 13 lbs of water will result in EAH. Which is obviously very bad. I’m not a medical professional, but perhaps there is testing you could have done to check whether or not your plasma levels are in balance and go from there.

  11. David

    Interesting read. Does sweat loss rate come into the argument, or should I say, how does it affect the findings? Is there an accurate method of calculating sweat loss? Do you recommend drinking to thirst and eating (salty possibly) foods regardless of sweat loss? I’m still trying to find that sweet/sweat spot!

    1. Tracy Beth Høeg

      Great question. I am not aware of an accurate method of calculating sweat loss. Most people just use weight loss, add fluids in and subtract fluids out. That will not tell you how much salt is in your sweat, though, and that is apparently very variable. I still maintain that the best and most practical strategy is to go by thirst. See this from the 2017 EAH position statement:
      “The issue as to the contribution of sweat sodium loss to the development of EAH remains controversial. Sodium loss from sweat is highly variable between individuals, and compared with the general population, endurance athletes have lower sweat sodium levels (62, 63). The loss of hypotonic sweat would be expected to raise the serum sodium. However, sweat loss could contribute to the development of hyponatremia in two manners: (1) if the degree of fluid loss was sufficient to produce significant volume depletion and provides a stimulus to AVP release, thereby impairing excretion of water and/or (2) through ingestion of fluids that were more hypotonic than the fluid losses. This scenario may contribute to the finding of EAH developing in some athletes with net weight loss.” (Hew Butler, 2017)

  12. Brian

    Is there anything we can do or avoid pre-race? I’m wondering if lower sodium levels pre-race could have an effect, yes they will likely pee it out, but what if their bodies are used to the state. Runners like myself usually avoid drinking much within 60-90 minutes to avoid the long porta potty lines. What about the minority of runners who continue to drink leading up to the race, whom also tend to be high water drinkers throughout a normal day, could they have a higher chance of problems? Or the effects of diuretics pre-exercise, such as strong coffee or caffeine pills, or the overuse of them? And could a pre-race meal with extra sodium be helpful?

    1. Tracy Beth Høeg

      Brian, great questions. Normally drinking pre-race should not give someone low sodium. You would really have to go overboard to accomplish that in non-exercising conditions (think fraternity hazing). If for a medical reason or due to medications one has low sodium before the race, yes, I could see that as a potentially dangerous situation, though I am not aware of that happening to anyone. As far as coffee is concerned, I don’t think that is a big cause, but does lower blood potassium levels. Also, as far as I know people who drink a lot of fluid on a regular basis are probably NOT at increased risk of hyponatremia because in non-exercising conditions you just pee out all of that extra fluid. I don’t think a pre-race meal with lots of sodium will prevent hyponatremia either because basically your body has a set point for sodium and high salt meals usually just result in water retention (high blood pressure, swelling).

  13. Elizabeth A

    I had always avoided adding salt to food, knowing it affected my blood pressure and caused puffiness in my hands and feet. During heat training for Western States, I had a day where all I wanted to do was lie down, as I had no energy to do ANYTHING. At dinner, family complained that the food was too salty — but it tasted fine to me. My energy came back right away with eating, and I made the connection between how I felt and low sodium.

    Later, after an extended running break and near the end of a 50 miler I had done a couple of times before, I went for the chicken soup. It tasted like it had no salt at all. The third cup finally started tasting salty. That’s when I had the “a-HA” moment regarding a severe lack of energy during the race, which I finished 3 hrs slower than my best time. The difference between the 50 miler and Western States years before was that I had started a BP med a few months before the 50 miler. The medication — HCTZ — can lower sodium levels. When one has a low sodium, one usually doesn’t feel thirst, as the body knows more water will make the hyponatremia worse. On this medication, my sodium is in the low normal range, so extended exercise tips me below normal range, and supplementation is important.

    So, I would add to this wonderful article that certain medications can contribute to low sodium levels.

  14. Alex

    Another quick thought – given the potential you describe for exercise-stress-induced secretion of ADH, is the current tendency to put caffeine in every sort of endurance food/gel actually a good thing? I have been kind of annoyed by this trend, as I prefer NOT to over-caffeinate during races for fear of GI consequences, but caffeine certainly acts antagonistically to ADH. Perhaps modest caffeine consumption is a way to take out a little insurance against EAH?

  15. Cary

    I have struggled to find an answer for severe nausea while training and racing for ultras or long triathlons, changing every variable I can think of in training (and racing) to figure it out–more water, less water, more salt, less salt, more calories, far less calories, gels, no gels, more carbs, less carbs, more real food etc…. I am rarely thirsty on runs. For the longest time, since my symptoms would generally appear only after multiple hours and were more severe in the hot conditions, I looked at dehydration as the cause (or major contributor) due to possible low blood volume that would result, but could it be EAH? In some races and training runs I am down 8% of body weight and have stopped sweating altogether. This would be consistent with dehydration, but I recently ran 50+ miles on a hot day just as a test, keeping track of everything per hour (weight/hr, Kcal/hr, Na/hr H2O/hr etc.). I tried to take more salt than normal (600 to 800 mg/Liter water consumed), and I maintained body weight better (only down 5%). But I still got sick. I am always interested in this topic. Thanks for the easy to understand analysis.

  16. Di

    I’m glad to see the scales dropped and hope this will happen across the board.
    I weighted myself before and immediately after my first two 24-hour just out of interest, and then at random intervals.
    I dropped 4kg during the first race, which equated to 5.7% of my bodyweight at the time. After 3 days, I had put 1kg back on. The remaining 3kg stayed off long-term and my weight remained stable at that for several months.
    Half a year later, I did the next 24-hour.
    I dropped 3kg during the second race, equating to 4.4% of the new bodyweight. After 3 days, I had put 1kg back on.
    The remaining 2kg stayed off long-term and my weight is again stable for several months.
    If all this weight loss were water loss, then it would have returned at some point.
    The fact that this weight did not return even months later tells me that it’s something else.
    In the same period (shortly before race 1 until a month after race 2), my body fat percentage dropped from 27% to 22%. This seems to be the obvious correlation.
    To think that I might have been pulled for that at some events is quite troubling.

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