Exercise-Associated Hyponatraemia

Sodium largely determines the concentration of the blood and how water moves between the body's compartments. During prolonged exercise, blood sodium falls when fluid intake, particularly of water or low-sodium drinks, exceeds the body's ability to excrete the excess, diluting the blood. This is compounded by the release of the hormone that controls water retention, arginine vasopressin (AVP, also known as antidiuretic hormone), which is often inappropriately raised during endurance exercise and reduces the kidney's ability to clear the extra water. Overdrinking is the main mechanism, but not universal: a less common form arises when substantial losses of both water and sodium go under-replaced, leaving a low sodium in a depleted athlete.

As blood sodium falls, water moves into the cells, and the most dangerous consequence is swelling of the brain, which produces the neurological features and can be fatal; fluid can also accumulate in the lungs. The main risk factors cluster around drinking too much: excessive fluid intake during events, which is the key modifiable factor, longer and slower finishing times that allow more drinking, lower body weight, events where frequent drinking is encouraged, and relying on water or dilute drinks. Non-steroidal anti-inflammatory drugs (NSAIDs) are a possible though not firmly established contributor.

Mild exercise-associated hyponatraemia may cause no symptoms, or only vague ones such as nausea, headache, dizziness, bloating or puffiness, and is often found only when sodium is measured. As sodium falls further, features of brain swelling appear: a worsening headache, vomiting, confusion, agitation, unsteadiness, seizures and reduced consciousness, and severe cases can progress to coma and death. A counterintuitive point is that the athlete may look overhydrated, or have gained weight during the event, rather than showing the dehydration clinicians often expect. Weight gain or overhydration supports the diagnosis, but their absence does not exclude it.

The critical differential is exertional heat stroke, which also causes central nervous system dysfunction. As a rule it runs a high core temperature while exercise-associated hyponatraemia does not, but this is not a strict binary, since the two can overlap or coexist. Assessment therefore combines rectal temperature, point-of-care sodium, blood glucose, the history and the clinical picture rather than temperature alone, with low glucose and cardiac causes also considered.

The diagnostic test is the blood sodium concentration, ideally measured at the point of care at large events, since the result guides immediate management and the condition cannot be confirmed from history alone. A low sodium confirms the diagnosis, though clinical urgency is set primarily by the neurological and respiratory symptoms rather than the sodium value alone. Core temperature, measured rectally, helps separate this from exertional heat stroke, and blood glucose should be checked. In hospital, further tests assess sodium, kidney function and the concentration of the blood and urine. Where body weight before and after an event is known, weight gain supports a picture of fluid overload.

The guiding principle is broadly the opposite of that for dehydration. When exercise-associated hyponatraemia is suspected, the instinct to give dilute fluid must be resisted, since adding water lowers the sodium further and worsens the brain swelling. Mild cases, with no or minor symptoms, are managed by restricting fluid and observing, allowing the body to excrete the excess and correct the sodium. Restriction is not universal, however: where careful assessment confirms genuine hypovolaemic shock or significant muscle breakdown (rhabdomyolysis), isotonic fluid may be needed, so the clinical picture guides the decision.

Severe cases, with confusion, seizures, vomiting or reduced consciousness, indicate brain swelling (encephalopathy) and are a medical emergency. The definitive treatment is a small, controlled bolus of concentrated (hypertonic) saline, typically 3 percent, given under an appropriate protocol and repeated according to the symptoms and the sodium response, alongside calling emergency services and supporting airway, breathing and circulation. At events with the right protocols and trained staff this may be given on site, since rapid treatment is life-saving. What not to do matters as much: do not give large volumes of ordinary dilute fluid, and do not assume dehydration. If the diagnosis is uncertain and sodium cannot be measured, it is safer to withhold dilute fluid until the sodium is known.

Prevention rests on sensible fluid intake, and the clearest message is to avoid overdrinking. Drinking to thirst, rather than to a fixed schedule or as much as possible, is the practical guide, and athletes should be warned against the belief that more fluid is always better. Organisers can help by spacing and moderating fluid stations and educating participants, while being alert to those at higher risk, such as slower finishers. Extra salt alone does not reliably prevent the condition, so the focus stays on not overdrinking.

Return to sport follows resolution of symptoms and a normal blood sodium, with a review of fluid behaviour and any contributing factors so future events are safer. After a mild episode this is usually straightforward. After a severe or recurrent episode, return is individualised and includes specialist clearance before going back to endurance activity.

• •International consensus guidance on exercise-associated hyponatraemia sets out the definition, the central role of overdrinking, the avoidance of dilute fluid, and hypertonic saline for severe cases.
• •Wilderness and endurance medicine guidance addresses on-site management, including hypertonic saline protocols and when isotonic fluid is appropriate.
• •Guidance on the collapsed endurance athlete stresses measuring both sodium and core temperature, since heat stroke and hyponatraemia can overlap.
• •United Kingdom sports and endurance event medical resources support planning and safe fluid advice.

• •Exercise-associated hyponatraemia is a blood sodium below 135 millimoles per litre during or within about 24 hours of prolonged exercise, usually from overdrinking.
• •Management is broadly the opposite of dehydration: restrict dilute fluid rather than giving large volumes, guided by assessment.
• •Severe cases with brain swelling need concentrated (hypertonic) saline, typically 3 percent, not water.
• •Measure point-of-care sodium urgently in a collapsed endurance athlete, but never delay airway, breathing, circulation or cooling for suspected heat illness.
• •Heat stroke generally runs a high core temperature and hyponatraemia does not, though they can coexist, so check temperature, sodium and glucose.
• •Prevent it by avoiding overdrinking and drinking to thirst rather than to a schedule.