The Hyponatremia of Exercise, Part 10

On March 11, 2004 — 19 years after our group published the first description of exercise-associated hyponatremic encephalopathy (EAHE) (1); 13 years after we published definitive proof that EAHE is due to fluid overload with sodium deficit playing no proven role (2); two years after Cynthia Lucero had died because, according to the inquest into her death and as confirmed by our calculations in Waterlogged (3), she had consumed too much fluid, including Gatorade, during the 2002 Boston Marathon; and while I was in the process of helping to organize the First International Exercise-Associated Hyponatremia Consensus Development Conference that gave rise to the First International Exercise-Associated Hyponatremia Consensus Document (4) and the definitive paper on the factors causing EAH and EAHE (5) — I decided to determine whether I could pass a test designed ostensibly to evaluate the knowledge of professionals on the factors causing EAH and EAHE.

The test was provided not by an august scientific body but by an organization, the Gatorade Sports Science Institute (GSSI), funded by Gatorade, the makers of a sports drink that includes sodium. The test included seven questions. The heading for each page of the test said, “Sharing knowledge on sports nutrition and exercise science.” The bottom of the page said, “The information herein is intended for professional audiences, including scientists, coaches, medical professionals, athletic trainers, nutritionists and other sports health professionals who have a fundamental understanding of human physiology.” Thus, as a medical professional, I fell within the target audience the test sought to evaluate.

After I submitted my test answers I was acutely embarrassed to be informed that I had failed the test: “You did not achieve a passing score.” I had failed the test as I had answered only three of the seven questions correctly (for a fail mark of 43%)! Furthermore, I was informed: “You must answer all questions correctly to pass the test and apply for continuing education credits.” Accordingly, I was advised to “please study the course reference articles further.”

I was clearly under the false impression that as the first person ever to describe EAH and EAHE, I must know something about what causes both conditions.

But in truth, since to apply for my educational credits I would have had to provide answers that I knew to be incorrect, it became apparent to me that this test was not designed for “sharing knowledge of sports nutrition and exercise science” as the GSSI claimed.

Rather, the desired outcome was to force a particular dogma upon all “the scientists, coaches, medical professionals, athletic trainers, nutritionists and other sports health professionals” who wished to earn their education credits — a quite different agenda. Clearly the internet was providing a novel and unexpected method to ensure that those interested in furthering their education in sports nutrition should all profess a common opinion, carefully orchestrated by an industry that stands to benefit commercially from it.

Here are the test questions and my responses, with appropriate explanations.

Question 1: The normal range of sodium concentrate in the plasma is 136 – 142 mmol/L. At what point does a reduction in sodium usually lead to severe symptoms?

The following were the optional answers:

1. 135 and below
2. 139 and below
3. 125 and below
4. 120 and below
5. 115 and below

Comment: It is not immediately clear what the educational value of this question is. The first important educational point that needs to be made is that a sports doctor treating an athlete with an altered level of consciousness must always measure the blood sodium concentration before any treatment is initiated. This is absolutely essential if the clinician is considering the use of intravenous fluid therapy.

A much better opening question would have been the following: A female athlete is admitted to a medical facility at the end of the Hawaiian Ironman Triathlon. She is unconscious and reportedly vomited clear fluid repeatedly before losing consciousness. Her heart rate, blood pressure, and blood glucose concentrations are all normal, and there is no other obvious cause for her condition. What is her most likely blood sodium concentration?

Then the selections would include a very high value (155 mmol/L), a slightly elevated value (145 mmol/L), a normal value (140 mmol/L), the most likely value (115-125 mmol/L), and an impossibly low value (100 mmol/L), at which blood sodium concentration the patient would already be dead.

The question would have established that the candidate understands that EAHE causes the described symptoms and signs, none of which is a feature of “dehydration.” Had the athlete been significantly “dehydrated,” her blood sodium concentration probably would have been >150 mmol/L, but she would not have been unconscious (unless there was another unrelated cause for her unconsciousness, since dehydration alone in an Ironman Triathlon will not cause loss of consciousness).

Since I could not answer the actual question and as I had failed the test, I decided to share my displeasure with the GSSI. In my email to gssi@gssiweb.com, posted at 9:03 p.m. on Thursday, March 11, 2004, I wrote: “I was quite surprised by the large number of errors in the questions about hyponatremia. As a result of those errors I failed the test. To pass the test, I would have to give incorrect answers. The answer to question 1 can be 3, 4 or 5 depending on what you mean by severe. If you mean a fatal outcome, then 4 and 5 would be more correct. If you mean unconscious, then 3 would also be correct.”

I would have answered 3 to this question. I suspect I scored a correct answer.

Result:                    Noakes 1                    GSSI 0

Question 2: Which of the following is NOT a potential severe effect of hyponatremia?

1. Seizure
2. Coma
3. Breathing failure
4. Brain damage
5. Spleen rupture

Comment: Here the answer was fairly uncontentious. Rupture of the spleen, which occurs only in contact sports and not in endurance activities, is not associated with EAH and EAHE. However, although long-term brain damage could occur in those with EAH and EAHE who are treated incorrectly, brain damage is improbable in those who are treated properly.

I’m fairly sure I answered this one correctly.

Result:                    Noakes 2                    GSSI 0

Question 3: Which of the following conditions characterizes one type of hyponatremia?

1. The hypothalamus secretes too much antidiuretic hormone, resulting in a severe loss of plasma potassium.
2. The kidneys excrete too much water so the plasma sodium concentration is too great.
3. The blood plasma contains more water than normal for the amount of dissolved sodium in the plasma.
4. The blood plasma contains more dissolved sodium than normal for the amount of water in the plasma.
5. The hypothalamus secretes too much aldosterone into the blood, resulting in an excessive retention of sodium in the plasma.

Comment: Here, the most correct answer is option 3, although inappropriate production of antidiuretic hormone (ADH) is also an essential feature of all cases of EAH and EAHE (5). But inappropriate secretion of ADH causes excessive losses of sodium, not potassium, in the urine.

The examiner who formulated this question clearly understands that EAH due to SIADH is a condition of sodium, not potassium wasting. It follows that he or she must also understand that providing salt in hypotonic solutions either for ingestion or infusion will neither prevent nor cure EAH or EAHE (since it will simply be excreted as part of the salt-losing phenomenon induced by SIADH and whole body fluid overload).

But this is not the educational message conveyed by the questions that follow. An alternative message is provided instead. Such logical discrepancies must always occur when the truth is being laundered.

Result:                    Noakes 3                    GSSI 0

So far, so good. But there must be some surprises in store.

Question 4: What is the most typical cause of hyponatremia in athletes?

1. Too great a rate of antidiuretic hormone secretion.
2. Too low a rate of antidiuretic hormone secretion.
3. Use of non-steroidal anti-inflammatory drugs.
4. Retention of water in the gut until it is massively released during recovery from exercise.
5. Excessive drinking of water and excessive loss of sodium in the sweat.

Comment: In my 2004 email I wrote, “There is no correct answer for Question 4. Significant hyponatremia (serum sodium concentrations below 127 mmol/L) can occur in athletes, without large sodium losses as documented in the literature, but cannot occur without overhydration.”

The evidence for this opinion is found in our two key papers (2, 5). What I have learned since I wrote to the GSSI in 2004 would not cause me to change my opinion other than to add that I now appreciate that EAH cannot occur without “too great a rate of antidiuretic hormone secretion” (5). However, it is perhaps obvious that the GSSI wants everyone to believe that option 5 is the only correct option.

I suspect answer 5 was “correct”; thus, my selection of option 1 was incorrect.

But answer 1 is probably the most correct since excessive ADH secretion (or any allied condition that produces the same effect) must be present in all cases of EAH and EAHE or else there will not be fluid retention.

Answer 2 is wrong; answer 3 can be correct in some individuals but does not cause EAH or EAHE in the absence of overdrinking; answer 4 is likely correct in some individuals but is not yet established (because it would be very difficult to study); answer 5 is wrong since there is no published evidence that EAH and EAHE are due to excessive sodium losses in sweat, although all cases have to drink to excess (relative to their requirements).

The sole “evidence” that EAH and EAHE are caused by large sweat sodium losses is the simplistic model promoted by the GSSI, Gatorade, and their favored scientists (6-8). As I will show in a subsequent column (9), these same scientists (10, 11) have provided experimental evidence that absolutely disproves this false explanation.

Result:                    Noakes 3                    GSSI 1

Question 5: Which of the following is the best characterization of how gender affects the incidence or outcome of hyponatremia?

1. Men over age 30 suffer a much greater incidence than do women, but outcomes are similar.
2. Men under age 30 suffer a much greater incidence than do women, but outcomes are similar.
3. Women of all ages suffer a much greater incidence than do men, but outcomes are similar.
4. There is no gender effect on incidence or outcome.
5. Women probably suffer a somewhat greater incidence than do men, but even if they do not, women afflicted with hyponatremia are more likely to have serious outcomes compared to men.

Comment: The clear evidence is that, in proportion to the number of men and women who run marathons or ultramarathons or who compete in the Ironman Triathlon, women are considerably more likely to develop EAH or EAHE. But the reason for this anomaly was completely unknown since it had not been studied at the time this test was devised. Thus, the GSSI, like everyone else, did not know what the correct answer to this question was in 2004.

However, one of the authors of the 2007 ACSM Position Stand on Exercise and Fluid Replacement (12), Dr. Nina Stachenfeld, herself a Gatorade-funded scientists, would subsequently show in a 2009 publication that women with a previous history of hyponatremia developed EAH during an experimental study because they retained more fluid during exercise, not because they lost more sodium than did a control group (11). Her finding disproves the gist of that ACSM Position Stand (12) and the GSSI publications (7, 8), which invoke high rates of sweat sodium losses as the cause of EAH and EAHE in both men and women.

At the time I wrote, “The only correct answer for question 5 is option 4. More women do develop the condition but only because they are more likely to run slowly and to overdrink when told to ‘drink as much as possible during exercise.’ They are also smaller and so require less fluid overload to cause hyponatremia.”

Now I would argue that perhaps women are at greater risk because they are more likely to develop SIADH or store circulating sodium in the osmotically inactive exchangeable sodium store, as I postulated had occurred in the case of Lucero in the Boston Marathon (3, pp. 6-9).

If true, this biological difference might explain the prevalence of this condition among female athletes—in which case, answer 4 is not the most correct answer.

Perhaps I must now acknowledge that either answer 3 or 5 could also be the correct option since the incidence of the condition is certainly higher in women than in men, but the outcomes might also show a gender difference. In an experimental model, male rats were more likely to survive experimental hyponatremia (13). In addition, administration of testosterone also improves outcomes in both male and female rats with hyponatremia.

In addition, four of 12 EAHE deaths reported by the time I originally wrote this had occurred in women. This might be because women are more likely either to receive inappropriate treatment (intravenous hypotonic or isotonic solutions) or to respond differently to that treatment than do men.

Once again, it is unclear what the educational value of this question is.

A better question would raise awareness of the fact that, because they are smaller (with a lower total body sodium content), women are more likely to develop EAH and EAHE if they overdrink to the same extent as heavier men.

But perhaps this is not an educational point the GSSI would want to make.

I suspect the answer the GSSI was seeking was either 3 or 5. As I answered 4, the score alters to:

Result:                    Noakes 3                    GSSI 2

Question 6: Which of the following scenarios best explains how it is possible for a marathon runner to be both dehydrated and hyponatremic?

1. She could have lost 10 L of salty sweat and consumed 8 L of water.
2. She could have lost 10 L of dilute sweat and consumed 8 L of a sports drink that contained lots of sodium.
3. She could have lost 8 L of salty sweat and consumed 8 L of a sports drink that contained lots of sodium.
4. She could have lost 8 L of dilute sweat and consumed 8 L of a sports drink that contained a moderate amount of sodium.
5. She could have lost 4 L of dilute sweat and consumed 4 L of a sports drink that contained a moderate amount of sodium.

Comment: This question is troubling for a number of reasons.

First, it promotes the incorrect concept that EAH is caused by “dehydration,” whereas the clear evidence (6, Figure 1) is that EAH and EAHE cannot occur without overdrinking and related fluid retention. This point is not emphasized in a single question in this entire test, which indicates the true focus of the GSSI and its marketing team.

There is a saying that what is left out often reveals more than that which is included.

Second, no female marathon runner could ever lose 8–10 L of sweat during a 42-km marathon. The sweat rate is determined by the metabolic rate, which is a function of how fast the athlete runs. Because she runs slower than the world’s fastest male runner and is likely to be a few kilograms lighter, even the world’s fastest female marathon runner is unlikely to sweat at a rate faster than about 2 L/hr, which would result in a maximum sweat loss during a 2:15 marathon of about 4.5 L.

But we also know that no athlete finishing in 2:20, male or female, could ever develop EAH or EAHE, since he or she could not possibly drink enough during that time to become “waterlogged.”

To develop EAH, the athlete would need to gain at least 2 L, meaning he or she would have to drink at a rate of 3 L/hr, which even the GSSI would need to admit is impossible.

In contrast, a female runner who took six hours to finish the race would sweat at a rate of ~400 mL/hr, losing a total of about 2.4 L during the race. These are the athletes who are at risk of developing EAH and EAHE.

Yet none of the options in this question describes this type of athlete. Thus, the question has been constructed on false grounds by someone with no appreciation of real human exercise physiology in order to advance a clear commercial agenda; it was not designed to educate health professionals seeking knowledge.

Second, since sports drinks contain relatively homeopathic amounts of sodium compared to that required to prevent EAH and EAHE, there is no sports drink that contains “lots of sodium.” Nor is there even one that contains “moderate” amounts of sodium (that can reverse the development of EAH in an athlete who is unable to retain sodium because of SIADH and the hormonal effects of fluid overload). Instead, as I show very clearly in Waterlogged (3), the amount of sodium present in a sports drink such as Gatorade does not produce a greater effect on the blood sodium concentrations during exercise than does drinking just pure water.

At the time I wrote: “There is no correct answer for Question 6 since clinically significant hyponatremia (serum sodium concentration below 127 mmol/L) does not occur without fluid overload. An athlete who lost 10 L of salty sweat would lose a total of about 400 mmol of sodium. This is the amount of sodium contained in less than 3 liters of extracellular fluid. By reducing the ECF volume by 2 liters and which corresponds to a ‘gain’ of sodium of 280 mmol – she would finish with a sodium deficit of only 120 mmols if she had not ingested any sodium in any form during the race. Distributed through an ECF volume of 15 liters this would mean that the ECF sodium concentration would fall by only 8 mmol/L, not sufficient to produce significant hyponatremia. You do not mention that this athlete would need to run for about 10 hours to generate this sweat loss and during that time would be unlikely not to eat anything containing salt. The normal salt intake during 10 hours of the day is about 5 grams which is about 220 mmols. So the probability is that the athlete running for 10 hours would have finished the race without any sodium deficit even if she only drank water.”

In fact, my comments were in error since the volume in which the sodium loss is distributed must account for the volume that includes the osmotically inactive exchangeable sodium store, which is greater than just the extracellular fluid (ECF) volume (of 15 liters).

The calculation of the effect of this degree of sodium loss on blood sodium concentration must be made as if that loss comes not just from the ECF (including blood) but from the total body water of 42 liters.

Thus the 120-mmol deficit distributed in 42 liters would drop the blood sodium concentration by only 120/40 mmol/L (i.e., by ~3 mmol/L), a negligible effect.

The “scientists” from the GSSI who compiled this question had to ignore:

(i) all the historical evidence showing that before 1981, when runners in the Comrades Marathon and other events lasting up to 10 hours drank exactly as this example suggested so that they became dehydrated by about 2 liters, their post-race blood sodium concentrations always increased rather than decreased; and

(ii) the studies from South Africa (2) and New Zealand (14) showing that athletes with EAHE are suffering from fluid overload without any evidence of a sodium deficit larger than that present in control athletes who do not develop EAHE during the same races.

Instead, this question is based on the simplistic model the Gatorade-favored scientists had developed, a model that says sodium deficiency causes EAH and EAHE (6, 7, 8, 10). Significantly, the question writers also had to ignore the series of studies funded by Gatorade and the GSSI showing that the blood sodium concentrations of athletes who drink little or nothing during exercise increase, they do not fall (15-18).

Result: I could not answer this question since there is no correct answer. However, the only “correct” answer acceptable to the GSSI would have to be one in which the word “sports drink” was linked to the prevention and not to the causation of EAH and EAHE. Despite the death of Lucero, the GSSI clearly could not endorse options 2-5 as correct. Thus, option 1 has to be the only “correct” answer the GSSI would allow.

But we also know from the historical record that athletes who develop a 2-kg water deficit during exercise while drinking only water finished marathon and ultramarathon races with elevated blood sodium concentrations (Table 4.2 in reference 3, pp. 129-130).

Answers 1-4 cannot be correct since it is impossible for a female marathon runner to lose 8-10 L of sweat during a 42-km race. But we also know from the Gatorade-funded experiments (16) that a fast female marathon runner able to drink 4 L of fluid during a two- to three-hour marathon so that she matched her sweat losses would not drop her blood sodium concentrations to any extent.

Thus, there is clearly no scientifically correct answer to this question. There is, however, a commercially correct answer.

Result:                    Noakes 3                    GSSI 3

Question 7: To minimize the risk of hyponatremia, what is the best advice for fluid replacement during prolonged exercise in the heat?

1. Drink as much fluid as possible during exercise.
2. Drink to quench thirst.
3. Begin exercise in a well-hydrated condition and consume sports drinks or other lightly salted beverages every 10 – 20 minutes during exercise such that body weight after exercise is the same as or slightly less than that before exercise.
4. Drink one pint (i.e. 470 ml) of cool water with two salt tablets every 15 – 20 minutes during exercise (1.4-1.9L/hr).
5. Drink 300–400ml (1.8-2.4L/hr) of cold water every 10 minutes during exercise.

Comment: I wrote, “Answer 2 is the only correct answer for question 7. Many case studies show that athletes who do not lose weight during exercise are over-hydrated at the finish and consequently have reduced serum sodium concentrations.”

Today, I would add the following:

First, the ACSM guidelines of 1996 encouraged athletes to drink “as much as tolerable.” It is not immediately clear how this is different from drinking “as much as possible,” which is the terminology used here.

Second, answer 3 promotes incorrect physiology since the body protects its osmolality and serum sodium concentration during exercise, not its weight. Drinking according to this plan will cause the blood sodium concentration to fall. Furthermore, we do not know of any receptors the body uses to measure its weight, but the location and function of the osmoreceptors that regulate the blood osmolality, and hence the blood sodium concentration, are well known.

Third, answer 4 is wrong because the rates of intake of both fluid and sodium (up to 3-4 grams per hour) are far too high. All that will happen is that sodium will be excreted during exercise as described previously (6).

Fourth, the rate of fluid intake of 300–400 mL every 10 minutes (1.8 – 2.4 L/hr) proposed in option 5 is not greatly different from the volumes advised by GSSI competitors in the 1989 Hawaiian Ironman Triathlon. It is probable that such high rates of fluid ingestion explain the very high incidence of EAH and EAHE in that race (9).

Adopting the advice advanced in options 1, 3, 4, and 5 will all produce EAH in small slow-running men and women who also have SIADH and abnormal regulation of the osmotically inactive exchangeable sodium stores. An athlete who maintained body weight during a 10- to 17-hour Ironman would, because of weight losses of up to 3 kg caused by fuel (carbohydrate and fat) use and other fluid changes, finish the race with a fluid excess (overhydration) of as much as 3 L.

Indeed, our calculations suggest that to maintain a normal blood sodium concentration, a 70-kg male triathlete would need to lose at least 2% of his starting body weight, or 1.4 kg.

The correct answer for this question is option 2. But of course drinking according to thirst is not an option for the GSSI since this violates the Zero-Percent Dehydration Doctrine.

Accordingly, option 3 is the only correct answer that the GSSI would sanction.

Final Result:                    Noakes 3                    GSSI 4

Thus, I failed to secure even 50% on a test of a subject about which I really thought I was an expert!

I concluded my letter with the following: “I can provide references to support these statements should you so wish. I trust you will correct these questions and answers so that they accurately reflect what is in the published literature.”

Fifteen years later, I am still awaiting a response from the GSSI.

The questions that I answered incorrectly were 4, 5, 6, and 7—the four questions that were designed to entrench in the minds of all those professionals targeted by the GSSI the dogma that EAH and EAHE are caused by sodium losses in those who either drink too much or too little during exercise (questions 4 and 6), drink water instead of Gatorade (question 6), or drink according to the dictates of thirst and not to ensure that the “body weight after exercise is the same or slightly less than that before exercise” (question 7). In addition, women are at increased risk (question 5), but the reason for this is not revealed.

The reference to the real cause of EAH and EAHE, overdrinking, is obtuse and hidden.

When I originally wrote this rebuttal while preparing material for Waterlogged six years later (3), I found that the GSSI website had done nothing to address the errors in the dogma. Instead CME material available on the website at that time preferred to teach professionals how to diagnose and prevent “dehydration.”

For example, under the heading “Preventing Dehydration: Sports Drinks or Water,” it is stated that after reading the material on the site, clinicians and scientists would:

• Be able to describe the negative effects of dehydration on the physiology of the body.
• Be able to list the symptoms of dehydration.
• Be able to explain why consuming well-formulated sports drinks is usually better than drinking plain water for preventing dehydration.
• Be able to explain why carbonated drinks and drinks with high concentrations of carbohydrate are not optimal rehydrating beverages.
• Be able to explain why sodium is a critical electrolyte in sports drinks.
• Be able to explain the necessity for carbohydrate as a component of sports drinks.

This material is designed to characterize “dehydration” as a medical disease, which, as I describe in detail in Waterlogged (3), it simply is not.

The authenticity of this information is certified by the ACSM, NATA, and the USA Cycling Association, the first two of which receive funding from Gatorade (19, p. 221). One must assume that the USA Cycling Association is also party to the financial support and other forms of largess of Gatorade and the GSSI.

Summary

The goal of education, as I understand it, is to provide the facts and then invite the learner to draw his or her own conclusions. Telling the learner what she will be expected to believe even before she begins the activity is the opposite of the learning process. But it is an excellent indoctrination technique if the desired outcome is not truly education but the pursuit of a commercial objective and the abolishment of thought. The result is that described by George Orwell in his epic work 1984:

As he watched the eyeless face with the jaw moving rapidly up and down, Winston had the curious feeling that this was not a real human being but some kind of dummy. It was not the man’s brain that was speaking, it was his larynx. The stuff that was coming out of him consisted of words but it was not speech in the true sense. It was a noise uttered in the unconsciousness, like the quacking of a duck. (20, p. 57)

Duckspeak became the name applied to this form of communication.

My conclusion is that this GSSI publication is an exceptional example of this form of communication. It is Duckspeak, pure and simple.

The remaining question is: How and why has this indoctrination been allowed to develop in 2020?

---

Additional Reading

• The Hyponatremia of Exercise, Part 1
• The Hyponatremia of Exercise, Part 2
• The Hyponatremia of Exercise, Part 3
• The Hyponatremia of Exercise, Part 4
• The Hyponatremia of Exercise, Part 5
• The Hyponatremia of Exercise, Part 6
• The Hyponatremia of Exercise, Part 7
• The Hyponatremia of Exercise, Part 8
• The Hyponatremia of Exercise, Part 9
• The Hyponatremia of Exercise, Part 11
• The Hyponatremia of Exercise, Part 12

---

Professor T.D. Noakes (OMS, MBChB, MD, D.Sc., Ph.D.[hc], FACSM, [hon] FFSEM UK, [hon] FFSEM Ire) studied at the University of Cape Town (UCT), obtaining a MBChB degree and an MD and DSc (Med) in Exercise Science. He is now an Emeritus Professor at UCT, following his retirement from the Research Unit of Exercise Science and Sports Medicine. In 1995, he was a co-founder of the now-prestigious Sports Science Institute of South Africa (SSISA). He has been rated an A1 scientist by the National Research Foundation of SA (NRF) for a second five-year term. In 2008, he received the Order of Mapungubwe, Silver, from the President of South Africa for his “excellent contribution in the field of sports and the science of physical exercise.”

Noakes has published more than 750 scientific books and articles. He has been cited more than 16,000 times in scientific literature and has an H-index of 71. He has won numerous awards over the years and made himself available on many editorial boards. He has authored many books, including Lore of Running (4th Edition), considered to be the “bible” for runners; his autobiography, Challenging Beliefs: Memoirs of a Career; Waterlogged: The Serious Problem of Overhydration in Endurance Sports (in 2012); and The Real Meal Revolution (in 2013).

Following the publication of the best-selling The Real Meal Revolution, he founded The Noakes Foundation, the focus of which is to support high quality research of the low-carbohydrate, high-fat diet, especially for those with insulin resistance.

He is highly acclaimed in his field and, at age 67, still is physically active, taking part in races up to 21 km as well as regular CrossFit training.

---

References

1. Noakes TD, Goodwin N, Rayner BL, et al. Water intoxication: a possible complication during endurance exercise. Med Sci Sports Exerc. 17(1985): 370–375.
2. Irving RA, Noakes TD, Buck R, et al.  Evaluation of renal function and fluid homeostasis during recovery from exercise-induced hyponatremia. J Appl Physiol. 70(1991): 342-348.
3. Noakes TD. Waterlogged: The serious problem of overhydration in endurance sports. Champaign, IL: Human Kinetics, 2012.
4. Hew-Butler TD, Almond CS, Ayus JC, et al. Consensus Statement of the 1st International Exercise- Associated Hyponatremia Consensus Development Conference, Cape Town, South Africa 2005. Clin J Sport Med. 15(2005): 208–13.
5. Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: Evidence from 2,135 weighed competitive athletic performances. PNAS 102(2005): 18550-18555.
6. Noakes TD. The hyponatremia of exercise, part 9. CrossFit.com. 12 May 2019. Available. here.
7. Murray R, Kenney L. Sodium balance and exercise. Curr Sports Med Rep. 7(2008): S1-S2.
8. Murray R, Stofan J, Eichner ER. Hyponatremia in athletes. Sports Sci Exchange 88(2003): 16(1). Available here.
9. Noakes TD. The hyponatremia of exercise, part 11. CrossFit.com (forthcoming).
10. Baker LB, Lang JA, Kenney WL. Quantitative analysis of serum sodium concentration after prolonged running in the heat. J Appl Physiol. 105(2008): 91-99.
11. Stachenfeld NS, Taylor HS. Sex hormone effects on body fluid and sodium regulation in women with and without exercise-associated hyponatremia. J Appl Physiol. 107(2009): 864-872.
12. Sawka 2007 ACSM Sawka MN, Burke LM, Eichner ER, et al. American College of Sports Medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc. 39(2007): 377–90.
13. Arieff AI, Kozniewska E, Roberts TP, et al. Age, gender, and vasopressin affect survival and brain adaptation in rats with metabolic encephalopathy. Am J Physiol. 268(1995): R1143-R1152.
14. Speedy DB, Rogers IR, Noakes TD, et al. Exercise-Induced Hyponatremia in Ultradistance Triathletes Is Caused By Inappropriate Fluid Retention. Clin J Sports Med. 10(2000): 272-278.
15. Gonzalez-Alonso J, Mora-Rodriguez R, Below PR, et al. Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise. J Appl Physiol. 79(1995): 1487-1496.
16. Gonzalez-Alonso J, Mora-Rodriguez R, Below PR, et al.  Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise. J Appl Physiol. 82(1997): 1229-1236.
17. Gonzalez-Alonso J, Mora-Rodriguez R, Coyle EF. Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia. Am J Physiol. 277(1999): H576-H583.
18. Gonzalez-Alonso J, Mora-Rodriguez R, Coyle EF. Stroke volume during exercise: interaction of environment and hydration. Am J Physiol Heart Circ Physiol. 278(2000): H321-H330.
19. Rovell D. First in thirst – How Gatorade turned the science of sweat into a cultural phenomenon. New York: Amacom, 2005. pp. 1-243.
20. Orwell G. Nineteen Eighty-Four. London: The Folio Society, 2001. pp.1-326.