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Drinking Too Much
Understanding and defeating the too-much-water part of hyponatremia.
by Lulu Weschler
Weschler attended the First International Exercise-Associated Hyponatremia Consensus Development Conference in Cape Town, South Africa in 2005 and is a coauthor of the Consensus Statement. She is a Contributing Editor to UltraCycling, a physical therapist and ultra cyclist.
Overhydration does not equal good hydration. On the contrary it is dangerous and should be avoided as carefully as underhydration.
During a training ride or event, an athlete may add to the body's total water. The phenomenon "too-much-water" has been a feature of almost every case of
symptomatic exercise-associated
hyponatremia or EAH (Hew-Butler 2005). We will use this term rather than
"overhydration" because it happens not just to athletes who grossly overdrink, but also to athletes who are drinking
moderately more than they need and retaining the overload that they would otherwise readily excrete (urinate) at rest. Regardless of how it happens, by gross overdrinking or by inappropriate
retention, too-much-water puts an athlete at high risk for EAH (Almond 2005), a potentially life-threatening condition. Fortunately, the first, and often by itself sufficient, remedy is quite simple: stop drinking. Also, weight gain is a certain sign: if you weigh more than you did at the start of the ride or race, then you have too-much-water. Finally, we are beginning to understand why it can be so insidious, attacking very quickly even those who are only modestly overdrinking
(Hew-Butler 2005). Understanding how and realizing that this can happen will help you to believe your body when it signals that you have too-much-water.
How too much water can kill
Osmotic Equilibrium
Body water is both inside and
outside of cells, but it can move in or out of most cells as though the cell membrane were no barrier
whatsoever. What drives water to move (or for that matter, to stay where it is) are the relative
osmolalities, or concentrations of effective osmotic solutes inside versus outside the cell. An effective osmotic solute is any discrete ion (e.g., sodium, potassium, chloride) or molecule (e.g., glucose) that is
compartmentalized to the extracellular or the intracellular compartment. An osmole is a
number (like 'dozen' is a number) of any such solute particles, regardless of their identity. Thus, the number of osmotic entities per kg of water determines osmolality. Osmotic equilibrium means that osmolalities inside and outside the cell are equal. Osmotic equilibrium is maintained with a vengeance: when osmolality is changed inside or outside the cell, water moves rapidly across the membrane to restore equilibrium, in the direction of higher osmolality.
What happens with too-much-water is a consequence of the drive to maintain osmotic equilibrium (see sidebar 'osmotic equilibrium'). Water is quickly absorbed from the gut into blood stream, and when it gets to the capillaries it quickly moves
into the cells' exterior milieu, called the interstitium (interstitial fluid and blood plasma are the two components of extracellular fluid). Interstitial fluid now becomes dilute relative to that inside cells, so water moves into cells until the osmolality in the cell, interstitium and blood plasma are all equal. Water movement into cells causes them to swell, which is particularly problematic in the brain because the skull is almost
completely closed, allowing very little room for expansion. Consequently the symptoms and illness of too-much-water are those of brain dysfunction (hyponatremia
encephalopathy): change in mental status, sensory distortion, confusion, incoordination, bizarre behavior; and ultimately seizures, coma and death. Normally excess water ingestion does not lead to such drastic consequences, because the excess water is very rapidly excreted by the kidneys. Only when fluid ingestion exceeds the ability of the kidneys to excrete it do plasma and interstitial osmolality fall sufficiently to cause
problematic degrees of cell swelling.
Hyponatremia and low osmolality
When excess fluid cannot be ecreted by the kidneys, the retained water dilutes the sodium in the blood leading to hyponatremia. Hyponatremia simply means that the plasma sodium concentration (how much sodium is dissolved in a given volume of plasma) is too low. Although the osmolality difference rather than the low plasma sodium concentration per se produces the pathology of dilutional (that is, water overload) hyponatremia, plasma sodium concentration is a reliable indicator, or surrogate for, body fluid osmolality. In fact, doubling the numerical value for plasma sodium concentration gives a reasonable numerical approximation of body fluid osmolality although units differ for the two entities. For example, a plasma sodium concentration of 140 mEq/liter (see sidebar 'measuring sodium') corresponds with an osmolality of about 290 milliOsmoles/kg water (or mOsmol/kg water).
Brain cells (and many other cells, including red blood cells) do mount a defense against water influx from a low osmolality environment: they extrude (or "dump") osmotic
material out of the cell. Cells won't swell if they can match pace with the decreasing osmolality of the interstitial fluid. When a water excess accumulates over several days, cell osmolyte extrusion can successfully prevent cell swelling and hence dire illness. However, it cannot keep pace with the rapidly changing osmolality in
exercise-associated hyponatremia. For this reason, athletes have symptoms from too-much-water (that is, are ill) at relatively higher plasma sodium concentrations than patients with chronic hyponatremia (Verbalis 2003).
Taking in sodium does NOT make it OK to overdrink
It is a common misconception that EAH can be prevented by use of sports drinks formulated with sodium and potassium. However, sports drinks will not keep you from developing hyponatremia if you overdrink. This follows logically from the fact that sports drinks are dilute. The sodium concentration in sports drinks is typically 18-25 mEq sodium per liter, whereas normal plasma sodium concentration is 135-145 mEq/liter (see sidebar 'measuring sodium'). Even in dire cases of EAH, plasma sodium
concentrations are typically in the range of 120-125 mEq/liter, still 5 to 6 times as concentrated as the sports drink. Keep in mind a useful common sense check: mixing two solutions of differing concentrations must yield a solution with an in-between concentration. Using this simple analogy, it is obvious that ingestion of a sports drink
will further reduce plasma sodium concentration in even the most dire hyponatremia. Think, "water chases osmoles" to visualize which direction the water flows.
Consequently Sports drinks can also cause too much water, and in light of these considerations, it should be clear that sports drinks are absolutely not to consumed when there is hyponatremia (Hew-Butler 2005).
Overhydration does not equal good hydration.
On the contrary it is dangerous and should be avoided as carefully as underhydration. Because sports drinks are so dilute, overdrinking a sports drink does very little to
prevent a drop in plasma sodium concentration compared to even plain water. Consider the example of adding 3% body weight by plain water versus sport drink. The athlete starts properly hydrated with normal plasma sodium concentration of 140 mEq/liter. A 3% weight increase achieved with plain water will lower plasma sodium concentration to 132.2 whereas the same weight increase achieved with sports drink at 20 mEq
sodium/liter will lower it to 133.2 mEq/liter (Weschler 2005). In either case, the athlete will be hyponatremic to nearly the same degree. For a 150 lb athlete, a 3% weight gain is 4.5 lb, or about 2.1 liters of either water or sports drink.
Even if you match the sodium
concentration of your drink concoction to the sodium concentration of blood
plasma, it still would not make sense to overdrink. First, fluid overload causes a disproportionately large "dumping" of sodium into urine, because various natriuretic hormones (see sidebar '-uresis') are released in response to increased blood pressure or volume. Secondly, volume overload even with normal plasma sodium concentration can impair aerobic capacity (Robertson 2004). Consequently, it does not make physiological sense to overdrink anything during exercise, even a drink whose
sodium concentration equals that of blood plasma.
Water retention caused by inappropriately high concentrations of AVP
Normal kidneys can excrete about 0.8 to 1.0 liters of water per hour in urine at rest (Noakes 2001). It is therefore easy to understand the development of EAH when hourly rates of fluid ingestion far exceed these limits. However it is not clear why some athletes accumulate a fluid overload while consuming fluid at rates equal to or considerably lower than this. An emerging culprit is the hormone arginine vasopressin (AVP). AVP is the only human antidiuretic hormone (ADH), so when you see 'ADH', think 'AVP', at least for humans. About a week's worth of AVP is stored in the brain (posterior pituitary) and is ready to be released in time of need (Verbalis 2003). As an antidiuretic, AVP's job is to protect against dehydration by stimulating water reabsorption by the kidneys. Thus, it is appropriately released into the blood stream in response to an increase in plasma osmolality (to which it is very sensitive) or a decrease in body water volume (to which it is considerably less sensitive) both situations in which the body needs to conserve fluid. There are, however, 'non-need' and hence inappropriate triggers for AVP's release. The most potent of all is nausea; other stimuli include various drugs, too little oxygen or too much carbon dioxide in blood, pain, and hypoglycemia (Verbalis 2003). Any of these conditions can be present during exercise. Some drugs, such as NSAIDs, do not stimulate release of AVP, but they increase the antidiuretic response to any AVP that is already circulating.
-Uresis
The word ending ñuresis means that something is being excreted in urine, usually, but not always, in
abnormally large amounts. Diuresis
means the excretion of water;
natriuresis the excretion of sodium. A
diuretic (for example, caffeine) increases urinary excretion of water; a natriuretic increases sodium in urine excretion. An antidiuretic
AVP acts primarily in the kidney (and does not appear to have an effect on sweat glands). Kidneys filter a certain fraction of blood (the filtrate), which is destined to be urine unless it is
re-absorbed. AVP facilitates re-absorption of the water part of the filtrate. AVP does not, however, directly stimulate sodium re-absorption, with the result that sodium continues on into what will be a
decreased volume of urine. Under conditions of volume expansion, an inappropriately high level of AVP can cause a dumping of sodium and re-absorption of water so extreme that an infusion of Isotonic Saline (NS, 0.9% or 154 mEq sodium/liter) ultimately has the same effect as infusing an extremely dilute, hypotonic fluid. This particlar phenomenon was key to elucidating the Syndrome of Inappropriate AntiDiuretic Hormone Secretion (SIADH), or in more modern terminology, Syndrome of Inappropriate Antidiuresis (SIAD) (Schwartz 1957 with Schwartz and Verbalis commentaries).
To date, only a few cases of
inappropriately high levels of AVP have been documented in EAH (Verbalis 2005). There are two problems with assaying AVP levels during exercise. First, AVP has a half-life of just 6 to 10 minutes, and is rapidly degraded if samples are not handled correctly. Secondly, in EAH, the basal levels from which AVP increases can be very low, and the increases can also be relatively small. AVP operates in a 'leveraged' range where relatively small increases from low baseline values have a large effect on water reabsorption of urine water. Nonetheless, it should be noted
that the original diagnostic criteria for SIAD, established before AVP assay techniques were available, remain valid. Thus, it has been possible to implicate inappropriately high levels of AVP as the culprit in EAH where sufficient data (e.g.,plasma osmolality, urine osmolality and urine sodium concentration) are available (Verbalis 2005).
Sodium Loss
To what extent sodium loss is part of the etiology of EAH has not been ascertained. Too-much-water can all by itself, without sodium loss, cause hyponatremia because mathematically, plasma sodium concentration is highly sensitive to changes in body water (Weschler 2005). Note also that too-much-water can induce sodium loss via pressure natriuresis.
Measuring Sodium
Labeling on US foods (but not supplements) requires that sodium content be expressed as "mg sodium." However, "mg" are
unwieldy for describing blood plasma concentration, so "milliequivalent," or "mEq" is used instead.
Milliequivalent is a number, like 'dozen.' Twenty three mg of sodium is equivalent to one mEq of sodium. Normal plasma sodium
concentration is 135-145 mEq/liter (or 3105 ñ 3335 mg/liter!). One teaspoon of table salt contains about 100 mEq sodium, 2400 mg sodium, and 6000 mg sodium chloride. The average daily intake of sodium in the US is 150 mEq, corresponding to about 1.5 teaspoons of table salt. The sodium concentration in sweat varies considerably across
individuals, but a reasonable
average is 50 mEq/liter. Happily, 50 mEq is about 1000 mg or 1g sodium. Thus, you can easily use "mg" to track your sodium intake. When you get to 1000 mg, you're at about 50 mEq. Among supplements marketed as sodium and/or electrolyte
supplements, Succeed® has 15 mEq sodium/capsule, Thermotabs® have 8 mEq sodium/tablet, and
Endurolytes® have 2 mEq
sodium/capsule. Thus, 3 Succeed®, 6 Thermotabs® or 25 Endurolytes® capsules have the approximate sodium equivalent of an average liter of sweat.
Implications for endurance athletes
Water retention leading to too-much-water can 'set in' at any time, and you can be completely mystified as to an exact reason. Why has your meticulous feeding and drinking schedule, which has worked 'like a charm' up until the present, suddenly gotten you water-overloaded?
Weight gain is a sure sign of too much water (Hew-Butler 2005), but there are other clues: feeling bloated, feeling as though you are morphing into the Michelin Man, puffiness at sock line, shorts line, ring band, headache accentuated by riding on a bumpy road, tight and/or shiny skin.
Furthermore, it is important to realize that urination frequency and volume do not always give reliable information about hydration status. For example, if AVP has increased, urination can stop while a fluid overload continues to accumulates. In this case a rider or crew will come to the erroneous and dangerous conclusion that the rider "needs to hydrate more.' Furthermore, the advice to drink until urine runs clear is erroneous. The implication is clear: slavish following of a fixed drinking schedule makes less sense, and listening to your body more sense, than ever. If these symptoms and signs occur, stop drinking until you urinate the excess: water restriction remains the mainstay of treating hyponatremia resulting from SIAD.
Prevention should always be the first line of defense. Since one cannot become fluid overloaded unless fluid consumption exceeds fluid losses, it may be time to re-examine the dogma that thirst is an inadequate guide to need and that therefore we should drink before we are thirsty. Thirst is, in fact, an excellent indicator of dehydration even though it is not activated until plasma osmolality has increased by 1-3% above basal levels (Robertson, 1982). These levels of dehydration have never been implicated in pathological processes.
For more information
For further reading, the Exercise-Associated Hyponatremia (EAH) consensus panel statement (Hew-Butler et al., 2005) is available for free at www.cjsportmed.com. It is the second article in the July, 2005 issue. (Lulu is a co-author on this paper.) Lulu gratefully acknowledges those who have contacted her with comments, questions, and descriptions of their experiences.
References:
Almond CS, Shin AY, Fortescue EB, Mannix RC, Wypij D, Binstadt BA, Duncan CN, Olson DP, Salerno AE,
Newburger JW and Greenes DS. Hyponatremia among runners in the Boston Marathon. N Engl J Med 352: 1550-1556, 2005.
Hew-Butler T, Almond C, Ayus JC, Dugas J, Meeuwisse W, Noakes T, Reid S, Siegel A, Speedy D, Stuempfle K, Verbalis J and Weschler L. Consensus Statement of the 1st International Exercise-Associated Hyponatremia Consensus Development Conference, Cape Town, South Africa 2005. Clin J Sport Med 15: 208-213, 2005.
Noakes TD, Wilson G, Gray DA, Lambert MI and Dennis SC. Peak rates of diuresis in healthy humans during oral
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fluid overload. S Afr Med J 91: 852-857, 2001.
Robertson GL, Aycinena P, and Zerbe RL. Neurogenic disorders of osmoregulation. AM J Med 72: 339-353, 1982. Robertson HT, Pellegrino R, Pini D, Oreglia J, DeVita S, Brusasco V and Agostoni P. Exercise response after rapid intravenous infusion of saline in healthy humans. J Appl Physiol 97: 697-703, 2004.
Schwartz WB, Bennett W, Curelop S and Bartter FC. A syndrome of renal sodium loss and hyponatremia probably
resulting from inappropriate secretion of antidiuretic hormone. 1957. J Am Soc Nephrol
12: 2860-2870, 2001. (Re-issued, with Commentary by Schwartz WB and Verbalis JG.) Verbalis JG. Disorders of body water homeostasis. Best Pract Res Clin Endocrinol Metab 17: 471-503, 2003.
Verbalis JG. Exercise-associated hyponatremia. In: American College of Sports Medicine 52nd Annual Meeting. Nashville: Mobiltape, 2005.
Weschler LB. Exercise-associated hyponatremia: a mathematical review. Sports Med
35, 2005 (in press).
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1. WEEKLY DISPATCH
Hot enough for you? Most of the northern hemisphere is baking right now and the heat is putting extra demands on daily rides.
Hydration is a key concern in high temperatures. A roadie can easily sweat off several pounds of water weight on a three-hour ride, making it imperative to keep chugging down liquids.
Right? Maybe not. When it comes to hydration there can definitely be too much of a good thing.
That caution comes from Lulu Weschler, a physical therapist and long-distance cyclist. In 2005 she authored the summary of the first International Exercise-Associated Hyponatremia
Consensus Development Conference in Cape Town, South Africa. In October she'll fly to New Zealand for the next session.
The key word: hyponatremia. It describes a dangerous condition caused by over-hydration -- drinking to the point where sodium levels in the blood become so low a medical crisis is at hand (see below).
Dehydration is bad, but hydrating to the point of hyponatremia can be deadly.
Here's the scary thing: Hyponatremia can occur even when drinking seemingly reasonable amounts. To explain, we're turning this over to Ms. Weschler, who has written extensively about the malady. At the end we'll provide the link to a more detailed article she wrote for the
UltraMarathon Cycling Association website.
LESSONS FROM LULU
Every serious case (including deaths) of hyponatremia thus far reported during or after exercise has involved over-hydration. Sodium is lost during exercise and that's a concern, but by far the dominant factor in exercise-related hyponatremia is excessive fluid intake.
Some cyclists assume they're safe because they're drinking sports drinks with electrolytes. However, a sports drink has a much lower concentration of sodium than blood. Thus, drinking too much sports drink can dilute blood sodium to a dangerous level, just like drinking too much water.
Salty snacks and/or salt capsules do not necessarily protect you from hyponatremia if you are overdrinking.
Hyponatremia means that when you divide the amount of sodium by the volume of blood plasma, the number you get is too small. This number is called plasma sodium concentration. (Hypo
means too small; natremia means sodium status.)
Theoretically, there are two ways to make the number too small: (a) by decreasing the amount of sodium, or (b) by increasing the volume of fluid. Thus far, in exercise-related hyponatremia cases studied, there has always been increased volume of water. (We do not know to what extent sodium loss was a contributor to the illness.)
Fatal Brain Swelling
Over-hydration all by itself (regardless of whether or not sodium is "washed out") can cause hyponatremia simply by diluting sodium. When the dilute blood gets to the brain, water seeps into brain cells and causes swelling. In hyponatremia deaths, brain swelling is the killer.
you are moderately over-drinking and retaining the overload that you would urinate at rest.
Take seriously any sign that you are putting on water weight during a ride.
Weighing yourself before and after a ride is a good way to sort out hydration needs. You should never finish with a weight higher than when you started.
Other signs of over-hydration include bloating -- puffiness in the hands or feet (at the sock line, watch, rings) or at the shorts line; "boggy" feeling flesh; headache (especially noticeable when you ride on a bumpy road); and looking like or feeling like the Michelin Man.
Early Signs
Nausea and vomiting are often seen early in the development of hyponatremia.
Since it's the brain swelling that kills, signs of weight gain plus any change in mental status (confusion, memory loss, disorientation) or any neurological symptom (uncoordination, slurred speech) are a clear indication of hyponatremia and represent a dire medical emergency.
What to do? Stop drinking.
You want urination to dump the fluid overload. A strong dose of salt could help get urination started. The medical staff at the Boston Marathon uses concentrated bouillon, one bouillon cube per ounce of water. This is the one exception to the no-drinking rule -- you need a delivery vehicle for salt. Other remedies include V-8 or tomato juice to which salt is added. Find a way to get salt in. Then wait eagerly to start urinating.
Do not drink sports drink (unless a significant amount of salt is added). The concentration of sodium is way too low and the additional fluid will make the situation worse. Do not resume drinking until you are certain that you have gotten rid of the fluid overload.
Not What It Seems
Sometimes over-hydration is counterintuitive. For example:
---"I'm drinking a reasonable amount, not a huge amount. Why am I going bloaty?" (You can retain a water overload during exercise that you would normally urinate at rest.)
---"I haven't urinated for a long time. Doesn't that mean I am dehydrated and need to drink more?" (No! not if you are retaining water.)
---"Isn't this just an issue of sodium intake? Won't I be okay if make sure to keep up my salt intake?" (No! not if you over-drink.)
To prevent hyponatremia, think first about not drinking too much. A distant second is increasing salt intake.
These are two misconceptions I often hear:
---"I'm hot and sweaty and I feel crappy. It must be because I'm not drinking enough."
Not necessarily. You can be perfectly well hydrated and be generating more heat than your body can dump, so it warns you by making you feel bad. In other words, when it's hot and you feel poorly, it may well be because it is hot.
take in more salt."
We have seen people who are way over-salted and have, as a result, stored fluid. Secondly, some people think that if they chug a sports drink instead of water they will be fine. But again, if you over-drink a sports drink you will go hyponatremic almost as fast as if you over-drink water.
The best hydration strategy: "Drink to thirst, salt to taste."
In other words, don't force anything. Listen to your body.
(For more information on hyponatremia, sodium and hydration, see Lulu Weschler's article at http://tinyurl.com/ensuc)
