Too Much Water (Long)

This is a really good article that should be of interest to people doing longer rides/events. This is the most up-to-date research yet on this subject. Here in Florida, we've had several deaths in the last year due to hyponatremia, in otherwise healthy, experienced athletes. I feel strongly that we should all be familiar with this information.

Nanci

Posted with the author's permission

Understanding and defeating the too-much-water part of hyponatremia

(Sidebars follow text)

Overhydration does not equal good, conscientious 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 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, but retaining the overload that they would otherwise readily excrete (urinate) at rest. Regardless of how it happens, by gross overdrinking or by inappropriate water 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

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 the 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 by osmosis until 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 (hyponatremic 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 excreted 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 the 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 a 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. 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 be consumed when there is hyponatremia (Hew-Butler 2005).

Because sports drinks are so dilute, overdrinking a sports drink does very little to prevent a drop in plasma sodium concentration compared even to plain water. Consider the example of adding 3% body weight by plain water versus sports drink. The athlete starts properly hydrated and with normal plasma sodium concentration of 140 mEq/liter. A 3% weight increase achieved with plain water will the 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 could 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 a 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 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.

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 particular 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 yet 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 a secondary sodium loss via pressure natriuresis.

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 accumulate. 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 implications are 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.

[SIDEBAR: 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. Think, “water chases osmoles” to visualize which direction the water flows.

[SIDEBAR: -URESIS]
The word ending –uresis 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 decreases urinary excretion of water.

[SIDEBAR: 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 – 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.

--Louise B. Weschler, October 19, 2005 (Reviewed)

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 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, 899-922, 2005.