What is the mechanism by which endurance runners develop hyponatremia (low sodium levels in the blood) after extended runs?

Mechanism of Exercise-Associated Hyponatremia in Endurance Runners

Exercise-associated hyponatremia (EAH) is primarily caused by a dilutional mechanism where there is an increase in total body water relative to the amount of exchangeable sodium stores, rather than excessive sodium loss. 1

Primary Pathophysiological Mechanism

The development of hyponatremia in endurance runners occurs through the following process:

1. Dilutional Hyponatremia:

   • The fundamental mechanism is dilutional, where total body water increases disproportionately to sodium content 1
   • This occurs when fluid intake exceeds the body's capacity for fluid excretion during prolonged exercise 2

2. Role of Antidiuretic Hormone (ADH/Vasopressin):

   • Inappropriate secretion of arginine vasopressin (AVP) plays a critical role 2
   • During prolonged endurance running, AVP is stimulated by non-osmotic factors such as:
     • Exercise-induced plasma volume decreases
     • Physical stress of prolonged exertion
   • This leads to water retention despite low plasma sodium levels 2

3. Fluid Retention Mechanism:

   • With AVP inappropriately elevated, the kidneys continue to retain water
   • Excess fluid intake is not excreted properly
   • Sodium may continue to be excreted despite developing hyponatremia 2

Risk Factors Contributing to the Mechanism

Several factors increase the risk of this pathophysiological process:

• Excessive fluid consumption beyond total body fluid losses 1, 3
• Altered renal function during prolonged exercise 1
• Longer race times (typically greater than 4 hours) 1
• Female sex 1
• Low body mass index 1
• Slower competitors who spend more time on the course 4
• Non-acclimatized individuals 4

Secondary Contributing Factors

While dilution is the primary mechanism, other factors may contribute:

• Sodium losses through sweating may have an additional effect, though not identified as the primary factor 1, 5
• Inadequate sodium intake during prolonged events can exacerbate the condition 5
• Non-osmotic stimuli for AVP release during exercise 2

Clinical Progression

The mechanism leads to a progressive clinical picture:

1. Initial subtle symptoms (bloating, nausea, vomiting, headache) 1
2. Worsening to hyponatremic encephalopathy with altered mental status 1
3. Potential progression to seizures, coma, and death due to cerebral edema 1

Incidence and Occurrence

The incidence of EAH varies widely:

• 3-22% in marathon runners in Europe and USA 1
• Can occur in both warm and cold environments, with one study showing 44% incidence in a cold weather ultraendurance race 5

Prevention Considerations

Understanding this mechanism helps inform prevention strategies:

• Avoiding excessive fluid intake beyond thirst 1
• Monitoring body weight to avoid weight gain during events 1
• Appropriate sodium intake during prolonged events 5

This dilutional mechanism, driven primarily by inappropriate AVP secretion and excessive fluid intake relative to losses, explains why hyponatremia can develop in endurance runners even before they begin post-race fluid replenishment.