The Danger of Drinking Too Much Water
Hyponatremia is a major health concern of marathon and ultramarathon runners, as well as some other athletes. A group of worldwide experts recently held a conference with the purpose of revising the Consensus Statement on Exercise-Associated Hyponatremia. The following summary of the Third International Exercise-Associated Hyponatremia Consensus Development conference was written by the lead author of the Consensus Statement, Tamara Hew-Butler, DPM, PhD, from Oakland University in Rochester, Michigan, and published in the Nov/Dec 2015 issue of Marathon & Beyond.
Hew-Butler T., et al. 2015. “Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference. Clinical Journal of Sport Medicine 25(4): 303-320, and British Journal of Sports Medicine (2015) doi:10.1136/bjsports-2015-095004.
The 2015 International exercise-associated hyponatremia (EAH) consensus conference served to update the 2008 (second) EAH Consensus Statement. Key changes were made based upon new evidence that evolved our understanding of how EAH develops (etiology), how to diagnose EAH, how to treat EAH, and strategies to prevent EAH. A synthesis of the latest EAH Consensus guidelines, highlighting the key 2015 updates, is summarized below:
Definition and Epidemiology
EAH is defined as any blood-sodium concentration that is below the normal range for the laboratory (or instrument) analyzing the blood sample. For most labs, this cutoff value is 135 mmol/L. Therefore, any runner with a blood-sodium concentration below 135 mmol/L is, by definition, hyponatremic.
First reported in the 1980s, EAH was once a rare sodium imbalance seen in desert hikers, ultramarathon runners, and Ironman triathletes. By the year 2000, EAH was reported in clusters of marathon runners, with five deaths confirmed from EAH-associated brain swelling (encephalopathy). Since publication of the second EAH Consensus Statement, symptomatic EAH has been reported after half-marathons, cycling, trekking, canoeing, swimming, yoga, weightlifting, and American football practice sessions. Additionally, multiple blood samples taken from ultramarathon runners, rugby players, and elite junior rowers (all for research purposes) revealed that more than half of the athletes tested were hyponatremic at one point during races or training. Thus, over the past decade, EAH has been detected with increasing frequency and across a wider variety of sports.
The main cause of both symptomatic and asymptomatic EAH is drinking too much fluid during exercise combined with an inability to “pee out” any excess water to keep blood-sodium levels within the normal range. Dilutional hyponatremia has also been called “water intoxication” because all drinks—including sodium containing sports drinks—have far less sodium (10-38 mmol/L) compared with blood-sodium concentrations (135-145 mmol/L). It is important to note that exercise above the intensity of a brisk walk will stimulate secretion of the body’s natural antidiuretic hormone (arginine vasopressin, or AVP). That means that the stress of exercise causes one oe pee less. Exercise-induced AVP secretion makes evolutionary sense, because moderate to vigorous physical activity induces sweating, which is necessary for evaporative cooling. In order to preserve total body water, the body instinctively “shuts off” urinary water losses to compensate for sweat water losses. More practically speaking, if we drink too much fluid at rest, we promptly pee off the excess to maintain blood-sodium levels. However, if we drink too much during exercise (above sweat water losses), urinary free-water excretion is impaired due to exercise-associated antidiuretic hormone secretion. Thus, sustained fluid intake above sweat water losses, combined with the inability to pee out any fluid excess during exercise, is the main cause of dilutional EAH in runners.
Of note, recent evidence suggests that runners who are not heat acclimatized and participate in longer (>18 hours), hotter races will lower their individual threshold for the amount of (extra) fluid necessary to dilute body-sodium levels. From a training standpoint, a fluid-intake plan that may have worked well in the past may cause hyponatremia when both environmental temperature and AVP secretion are abnormally high. In these rare instances, sustained sweat-sodium losses do not actually cause hyponatremia but reduce the amount of circulating plasma water (because blood sodium attracts water into the vascular space). This decrease in circulating plasma volume (hypovolemia) is a strong stimulus for antidiuretic hormone secretion. The presence of sustained hypovolemia would then explain why runners may not voluntarily drink as much fluid as they typically would (or plan to) during long, hot races: to prevent further dilution of blood-sodium levels. This unusual variant of hyponatremia is associated with body-weight loss. Thus, hypovolemic hyponatremia can also be attributed to a relative overdrinking with respect to sustained, underreplaced, sweat-sodium and water losses.
Classification and Diagnosis
Hyponatremia that is detected through routine blood testing (as for research) but without symptoms is referred to as “asymptomatic” hyponatremia. Conversely, “symptomatic” hyponatremia is associated with clinical signs and symptoms and classified according to the severity of these signs and symptoms, rather than the actual numerical value of blood-sodium concentration. This is an important update from the previous Consensus Statement and is designed to more properly align diagnosis with treatment. The authors thereby classified symptomatic EAH into two categories: mild and severe, depending on the presence or absence of neurological signs and symptoms. Accordingly, mild EAH is characterized by vague signs and symptoms such as dizziness, lightheadedness, bloating, and nausea. These symptoms overlap with many other causes of exercise-associated collapse, which makes the diagnosis of EAH difficult without a blood test. Severe EAH is diagnosed when neurological signs and symptoms of acute brain swelling are present, which include vomiting, respiratory symptoms associated with fluid in the lungs (pulmonary edema) are present and include signs and symptoms such as wheezing and pink frothy sputum. Severe EAH is an urgent, life-threatening emergency. Thus, if any of the above-mentioned symptoms are present in the runner, especially when associated with body-weight gain and/or a history of high fluid intake, a blood-sodium test is highly recommended to rule out hyponatremia.
Once EAH is diagnosed, the most appropriate treatment is guided by the severity of symptoms, as detailed above. When asymptomatic EAH is encountered, fluid should be restricted until the runner starts to urinate freely. Alternatively, highly concentrated saline solutions can be given, making sure that the sodium concentration of these broths is well above normal blood sodium concentrations (>140 mmol/L; or a “hypertonic” saline solution). One study showed that four bouillon cubes dissolved in 4 ounces (half a cup) of water improved blood-sodium levels within 30 minutes of ingestion. When mild EAH is diagnosed, runners should stop running and be given small amounts of hypertonic salty broth until their symptoms resolve. If athletes with mild EAH cannot tolerate oral fluids, then a small amount (100 ml., or less than half a cup) of hypertonic saline should be administered through an arm vein (intravenously) until they feel better and/or start to urinate freely. Since athletes diagnosed with asymptomatic or mild EAH can deteriorate within a few hours of race finish, either fluid restriction or hypertonic salty broths are encouraged despite somewhat vague symptomatology. Last but not least, severe EAH is a life-threatening medical emergency. Runners with signs and symptoms of severe EAH should be promptly treated with intravenous hypertonic saline until their condition improves, or at least stabilizes, before immediate transport to a hospital. The aim of this life-saving hypertonic saline treatment is to reduce fatal brain swelling (the sodium will attract water out of the brain cells and into the vascular space) rather than restore blood-sodium levels back into the normal range. Thus, brain swelling from water intoxication can be quickly reversed with prompt administration of hypertonic (3%) saline. If EAH-associated brain swelling exceeds 5-8 percent, a runner will likely die from brain-stem herniation.
Drinking fluids only when thirsty will prevent virtually all cases of EAH. Overzealous fluid consumption before, during, or immediately following exercise will not prevent heat stroke or muscle cramps nor enhance performance. Hyponatremia—or water intoxication—is both deadly and preventable.
As such, a wide variety of fluids should be available during races, at refueling stations spaced five kilometers apart, with instructions to drink whatever beverage is most appealing and only when thirsty. For athletes who desire a rough estimate of fluid-replacement needs (to match losses), weighing before and after 60 minutes of running—at expected race pace and ambient temperature—is a good starting guide. Thus, THE best hydration, fueling, and racing strategy is to start with a plan and then adjust accordingly.
For safe and optional training and racing: drink to thirst and salt to taste.