Hyponatraemia in Marathon Runners: When Drinking Too Much Is Dangerous

Oct 16, 2026 · 9 min · hyponatremia marathon runners

Dr Cath

Chemistry PhD · evidence-based supplementation

Hyponatraemia in Marathon Runners: When Drinking Too Much Is Dangerous

Hyponatraemia in a marathon means the sodium in your blood has been diluted, almost always because you drank more fluid than your body lost. At the severe end it is a medical emergency: water moves into cells and the brain swells. The practical difficulty is that its early symptoms resemble dehydration, so the instinctive response of another cup of water can make it worse. Symptoms alone cannot tell you which of the two you have. Only a blood sodium measurement can.

No marathon-specific trial answers this question directly. The evidence below is a systematic review of ultra-endurance racing, two case reports and established physiology, and the text says which is which at each step.

What does hyponatraemia mean for a marathon runner?

Hyponatraemia means the concentration of sodium in the blood has fallen below its normal range. Sodium is the main dissolved particle in the fluid outside the body's cells, so its concentration largely decides where water goes. When blood sodium falls, water shifts into cells. Brain cells sit inside a rigid skull and have little room to swell. That is the mechanism behind the dangerous form.

When the problem develops during or shortly after prolonged exercise, it is called exercise-associated hyponatraemia, usually shortened to EAH. American sources spell it hyponatremia. It should not be confused with dehydration, which is a loss of body water. It should also not be confused with heat illness, which is a failure to shed heat. All three can look similar at a finish line, and they can occur together. That overlap is why the distinction matters.

EAH is not confined to unusual athletes. A systematic review of ultra-trail racing starts from the observation that these races can cause both EAH and acute kidney injury (a sudden drop in kidney function) in healthy runners with no previous kidney disease. The review then examined how often each occurs in relation to race length and elevation: across the 28 studies it pooled, 9.11% of the runners analysed for it were diagnosed with EAH (195 of 2065) and 42.04% with acute kidney injury (468 of 1113). That evidence comes from ultra-trail events, not road marathons, so it shows the condition is possible in healthy runners rather than how common it is at your distance.

Is it mild, serious, or only a theoretical risk?

It helps to separate four categories, because each has a different evidential status and a different consequence.

Mild dilution

A slightly low sodium level can produce no symptoms at all, or vague ones such as bloating, nausea or swollen fingers. These symptoms are not specific. They fit fatigue, heat and dehydration just as well. Mild dilution may resolve as the kidneys excrete the excess water, but nobody can confirm that it is mild without a measurement.

Serious hyponatraemia

One case report describes a 57-year-old man who developed acute hyponatraemia during a 100-mile ultramarathon. His initial presentation was rapid neurological deterioration and transient cardiovascular instability. The report discusses treatment with hypertonic saline, a concentrated salt solution given under hospital monitoring. It describes a single patient, so it shows how severe EAH can become, not how often that happens.

Warning signs that need prompt medical review

These signs need medical review, particularly in a runner who has been drinking heavily:

confusion, disorientation or behaviour out of character;
a severe or worsening headache;
repeated vomiting;
unusual drowsiness or difficulty staying awake;
new breathlessness;
a seizure or collapse.

Risk added by medication

Anti-inflammatory painkillers (NSAIDs, such as ibuprofen) belong here. A Swiss review notes that endurance athletes, especially amateurs without medical supervision, take NSAIDs during training and races to treat or pre-empt pain. Many are unaware of the side effects. The review states that in combination with other risk factors such as overhydration, NSAIDs increase the risk of exercise-associated hyponatraemia, and that they raise the risk of acute kidney injury as well.

The mechanism offered is that NSAIDs reduce the kidney's ability to excrete excess water, which favours dilution. Two limits belong with that statement: it comes from a narrative review by nephrologists rather than from a trial, and the review itself says the frequency of exercise-associated hyponatraemia remains unknown. The direction is stated by the source; the size of the risk is not.

Why can drinking too much water lower blood sodium?

The intuitive explanation is that runners sweat out their salt. That is mostly wrong. Sweat contains sodium, but it is less concentrated than blood. Sweating on its own therefore tends to concentrate the blood rather than dilute it. Dilution needs water in excess of losses.

Healthy kidneys normally dispose of surplus water quickly. During prolonged exercise, however, antidiuretic hormone (also called vasopressin, the signal that tells the kidneys to retain water) can stay elevated. Triggers such as nausea, pain and sustained exertion can keep it high even when the blood is already dilute. This is a mechanism: it explains why a runner who keeps drinking may not pass the excess, not how often it happens.

The same chemistry applies to sports drinks. They contain sodium, but far less than blood does. In large enough volumes they still dilute. A sports drink lowers the rate of dilution compared with plain water. It does not cancel a large fluid surplus.

EAH can also develop in a controlled setting. One case report describes a 21-year-old male volunteer who unexpectedly developed symptomatic hyponatraemia during a research study of prolonged exercise in the heat. The measurements are specific: he drank 10.3 litres over seven hours and retained 2.77 of them, his sodium losses in sweat and urine stayed at or below those of the nine unaffected volunteers, and his plasma sodium fell below 130 mEq/l after four hours of mild, intermittent exercise in the heat. An unusually large release of vasopressin coincided with his urine output falling to zero. It shows that supervision and youth are not protection in themselves. As a single case, it cannot tell you who else is at risk.

Is a risk factor the same as a cause?

No. This is where most online advice on running hydration goes wrong. Case reports describe what happened to one person. They cannot identify risk factors. Factors commonly listed for EAH, such as a long time on course, are best read as mechanistically plausible. More hours on course means more opportunity for intake to outrun losses.

A factor found alongside cases in a finish-line sample is a cross-sectional association. Measurements of this kind are taken at the same time as the problem appears. Only data collected before the race can show that a factor predicts EAH. When you see a confident list of causes, check whether it was built on that kind of data.

Which prevention measures are actually supported?

Ranked by the strength of what supports them, not by how often they are marketed:

Not drinking beyond what you lose. Mechanistically plausible, resting on well-established physiology, and consistent with the case literature. This addresses the cause rather than a side issue.
Drinking in response to thirst rather than to a fixed schedule. Mechanistically plausible and widely used in general practice. It is a convention with a sound physiological rationale, and none of the studies cited here tested it against a fixed schedule as an intervention.
Avoiding NSAIDs around long races. The cited review states that NSAIDs increase the risk of both acute kidney injury and exercise-associated hyponatraemia, with overhydration among the combining factors. It is a narrative review, not a trial, so take the direction as stated and the size as unquantified.
Weight change across long training runs as a personal check. A practical proxy, not a diagnosis. Finishing heavier than you started means intake exceeded losses. It does not measure sodium.
Salt tablets or high-sodium drinks as a licence to drink freely. Not supported by any source cited here, and the chemistry argues against it: their sodium concentration is far below that of blood, so they cannot offset a large water surplus.
Fixed rules such as drinking at every aid station. No study cited here tests them, and a fixed volume takes no account of what you are actually losing. They are coaching conventions.

The variables that change your exposure are race duration, heat, and how much you drink relative to what you sweat. A drinking plan that works for a short race in cool conditions does not automatically transfer to a long race in heat, or to a slower pace that adds hours on course.

When is it a medical question, and how does a runner return after an episode?

The trigger is any warning sign listed above, especially confusion, vomiting or worsening headache in someone who has drunk a lot. At a race, that is a reason to go to the medical tent rather than the drinks table. Away from a race, it is a matter for emergency services. Telling EAH apart from dehydration needs a blood sodium test, and treatment decisions such as hypertonic saline belong to clinicians.

Return after a confirmed episode is decided by criteria, not by a calendar. The criteria are:

symptoms fully resolved;
sodium documented as back in range;
the cause understood, whether drinking volume, medication or both;
a revised drinking approach tried on long training runs before any race.

The stopping condition is a return of bloating, hand swelling, headache or weight gain during long runs. Any of these means stepping back and reviewing the plan with a clinician rather than pushing on.

Verdict

If your goal is to avoid EAH, the measure with the clearest rationale is not drinking more than you lose. Salt products do not replace that: no source cited here supports them as prevention, and their sodium is too dilute to offset a fluid surplus. If you take NSAIDs during long efforts, the review cited here states that both the kidney risk and the hyponatraemia risk go up, without quantifying either. If you have had a confirmed episode, your return is a clinical decision built on criteria.

When you see the next hydration claim, ask one question: does it address the balance between fluid in and fluid out, or does it sell a product around it?

Feeling worse after drinking a lot is the one moment in a race when more water is the wrong answer.

This article is general information, not a diagnosis. Suspected hyponatraemia needs assessment by a clinician.