Exercise-Associated Hyponatremia: Role of Cytokines
Section snippets
Pathogenesis of exercise-associated hyponatremia
Representing diametrically opposite disorders of body fluid homeostasis, dehydration due to sodium depletion and abnormal fluid retention leading to water intoxication have been proposed as primary causes of EAH in triathletes after iron-distance races.7, 8 A depletional mechanism, which might arise from sodium loss during sweating combined with free water intake, would infer preventive and therapeutic roles for electrolyte supplements, including sports drinks, in accordance with the position
Relative risk and prevention of exercise-associated hyponatremia
A recent study of the Boston Marathon indicated higher risk for EAH in slower recreational marathon runners at extremes of body mass index who gained weight during the race.2 Although sex was not an independent risk factor, women may be at increased relative risk owing to a tendency to drink more fluids than men in proportion to their body weight.18 In addition to zealous drinking, slow pace, and less racing experience, use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been associated
Diagnosis and treatment
Although they are opposite disorders of body fluid balance, EAH and dehydration may present with similar nonspecific symptoms including fatigue, headache, nausea, and vomiting. Associated mental status changes, such as confusion and disorientation, should heighten clinical suspicion for EAH, which was observed in 17 runners after the 2004 London Marathon.23 Cognitive deficits may be accompanied by delirium with psychomotor disturbances as neuropsychiatric manifestations of hypotonic
Muscle-derived interleukin-6 in the nonosmotic stimulation of arginine vasopressin
Given that SIADH is the dominant clinical paradigm for EAH, the mechanism for nonosmotic stimulation of AVP remains unknown. Pain, nausea, and vomiting are acute physiologic stimuli for AVP secretion that frequently occur in collapsed marathon runners, and enhanced release of muscle-derived IL-6 during glycogen depletion may induce nonosmotic stimulation of AVP secretion, which has been shown to occur with recombinant IL-6 administered to human research subjects.33 Correlation of plasma IL-6
Summary
EAH is a dilutional hyponatremia occurring during prolonged exercise in athletes, associated with positive fluid balance mediated in part by the secretion of AVP. Understanding SIADH as the clinical paradigm for EAH suggests well-described and validated strategies for prevention and treatment. Monitoring weight changes during races, especially among slower runners, may be used for early detection of fluid retention before the onset of mental status changes. Diagnosis of EAH optimally by
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Cited by (64)
Exercise-associated electrolyte disorders
2019, Current Opinion in Endocrine and Metabolic ResearchMolecular Biology and Gene Regulation
2017, Textbook of Nephro-EndocrinologyFatal water intoxication and cardiac arrest in runners during marathons: Prevention and treatment based on validated clinical paradigms
2015, American Journal of MedicineHigh incidence of hyponatremia in rowers during a four-week training camp
2015, American Journal of MedicineWilderness medical society practice guidelines for treatment of exercise-associated hyponatremia: 2014 update
2014, Wilderness and Environmental MedicineCitation Excerpt :Although the incidence of women experiencing symptomatic hyponatremia appears to be greater than that of men in some environments,22,24,26,51 when adjusted for BMI and racing time, the apparent sex difference has not been shown to be statistically significant.51 Along with other nonosmotic stimuli to AVP secretion,40,52–57 nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated as a risk factor in the development of EAH22,25,58 by potentiating the water retention effects of AVP at the kidney.59,60 However, data are still conflicting,24,49 and further investigation is necessary to determine whether NSAID usage—with respect to both classification and dosages—is a clear risk factor for the development of EAH.
Efficacy of oral versus intravenous hypertonic saline in runners with hyponatremia
2014, Journal of Science and Medicine in SportCitation Excerpt :The mean non-suppressed AVP concentrations of ∼1.4 pg/mL associated with the mean low sodium values (∼130 mmol/L) at race finish would also suggest that sustained hypovolemia may have been a physiologically appropriate non-osmotic stimulus to AVP secretion, similar to cases of thiazide-induced hyponatremia.24 Thus, a unifying pathogenic hypothesis for hypo-, eu- and hyper-volemic classifications of EAH would be persistent secretion of AVP following intake of hypotonic fluids which exceeds the renal capacity for free water excretion.25 With further regard to volemic status, the main physiological difference between the routes of HTS administration was significant (p < 0.05) plasma volume expansion with the IV (9%) but not the oral (1%) administration of HTS.