Hydration Issues in the Athlete and Exercise Associated Hyponatremia

Disease/Disorder

Definition

Hydration issues in the athlete occur when there is an imbalance of the body’s two extracellular fluid compartments: total body sodium and total body water (TBW).

Abnormal hydration can result in a variety of changes which can affect performance or cause symptomatic disease. The most common disorders include dehydration, hypernatremia, Exercise-associated hyponatremia (EAH), as well as hypomagnesemia.

Dehydration is defined as loss of approximately 5% TBW. For practical purposes, change in body weight is used as a practical surrogate with dehydration defined as a body weight loss of >3%.^1,2

Exercise-associated hyponatremia (EAH) occurs during or within the first 24 hours after physical activity when the serum sodium ([Na⁺]) concentration drops <135 millimoles per liter (mmol/L)¹ Hyponatremia is clinically divided into two categories, asymptomatic and symptomatic. As sodium drops <128 mmol/L, or with rates of sodium losses of 7-10%, there is an increased risk of developing symptomatic hyponatremia, with more severe hyponatremia typically occurring as levels fall  <125 mmol/L.^1,3

Etiology

Dehydration in the athlete develops as a result of imbalance between the intake and absorption of free water before and during exercise, and fluid losses during exercise as a consequence of perspiration, respiration, as well as urinary and bowel sources and in some cases due to vomiting.

Two mechanisms are implicated in the etiology of hyponatremia: dilutional and depletional.^1,3 The dilutional model proposes that sustained overconsumption of hypotonic fluids in the setting of impaired water clearance mediated by arginine vasopressin (AVP) secretion results in euvolemic or hypervolemic hyponatremia and is associated with weight gain. The depletional model proposes that dehydration from excessive loss of under-replaced solute (sodium and potassium) in sweat, without adequate rehydration, can lead to hyponatremia. It is widely accepted that EAH is multifactorial but is predominately caused by the proposed dilutional mechanism through excessive fluid intake and impaired urinary water excretion.³

Epidemiology including risk factors and primary prevention

The overall incidence and prevalence of dehydration in athletes depends on duration and intensity of the sport, as well as nutritional and ambient factors. Dehydration affects performance through a variety of physiological and perceptual factors (including reduced cardiac output due to reduced plasma volume, increased perceived exertion, and increased body temperature due to decreased ability to thermoregulate). Besides the deleterious effects on performance, dehydration increases risk of heat-related illness. It is estimated that for every 1% of body weight lost due to dehydration, core body temperature can rise by an additional 0.15-0.2 degrees C.

Adequate hydration prior to athletic activity and drinking to thirst during activity is recommended to prevent dehydration.

In the past, guidelines and public education messaging regarding hydration strategies during athletic activities to prevent dehydration were focused on encouraging drinking fluids on a schedule, and beyond normal thirst signals, but more recently these have been controversial due to their contribution to incidence of EAH.

It is now known that the most important risk factor for EAH is sustained, excessive intake of hypotonic fluid greater than the fluid lost through sweat, respiratory, and renal excretion, leading to a positive fluid balance.¹

Risk factors for EAH include weight gain during exercise signaling fluid retention, exercise duration >4 hours, event inexperience, inadequate training, high or low body mass index (BMI), and potentially, high ambient temperature.^1,3 The use of non-steroidal anti-inflammatory drugs (NSAIDs) has also been proposed as a risk factor, presumably due to the potentiation of renal water retention.¹

The incidence of EAH is difficult to determine as most asymptomatic individuals are unlikely to obtain sodium laboratory workup, and many symptomatic individuals may be treated or recover without access to laboratory testing in the field.

Symptomatic EAH is less common than asymptomatic EA. Severe EAH is rare, with at least 14 reported deaths since 1981.^1,5 The incidence of EAH is greater in females compared to males, when adjusting for BMI and racing time, the apparent difference is not statistically significant.¹

Prevention is primarily aimed at organized educational programs advising athletes to drink to thirst, monitor their body weight, and be cognizant of symptoms of EAH. Pre-event sodium supplementation has proven to have little to no role in prevention.³

Despite the recent increased awareness regarding the potential consequences of excessive fluid intake, various sports have seen cases of EAH. Through routine screenings for research, cases of asymptomatic EAH have been diagnosed and documented in rugby players, elite junior rowers, Ironman triathletes, endurance cyclists, half-marathon, marathon, and ultramarathon runners, with variable rates dependent on sporting activity.^3,5

When organizing or supervising an event, careful consideration should be given both to the placement of hydration stations to reduce excessive fluid intake, and the types of fluids available, subsequently minimizing the incidence of volume, electrolyte, and fluid disturbances.^1,4

Patho-anatomy/physiology

As previously mentioned, EAH results from dilutional hyponatremia, the expansion of TBW relative to total body exchangeable solutes (sodium and potassium). The subsequent osmotic gradients result in water shifting into the intracellular compartment, leading to cellular edema. Symptoms result from pathologic central nervous system (CNS) tissue expansion and can become life-threatening with the elevation of intracranial pressures.¹

The excretory rate of the kidneys is between 800-1000 milliliters/hour (mL/h) in the normal resting adult, Depending on exercise intensity and ambient conditions, the athlete loses about 500 ml/h during exercise. Thus, fluid consumption at or below a rate of 1.5 liters/hour (L/h) theoretically should prevent overhydration.³ However, most of this data was generalized from male athletes in a limited range of conditions.

Osmoreceptors, which lack a blood-brain barrier and are in communication with the brain parenchyma, blood, and cerebrospinal fluid, and baroreceptors found in the carotid sinus, aortic arch, and great veins, act as physiological sensors to regulate plasma osmolality and volume by coordinating thirst and AVP secretion.¹

AVP is synthesized in the hypothalamus, stored in the posterior pituitary gland, and acts at the V2 receptor in the collecting ducts of the kidney to open aquaporin channels causing water resorption. Under normal circumstances, AVP is suppressed in the presence of hypoosmolality. In some athletes, AVP is not appropriately suppressed (as typified by the finding of inappropriately elevated urine osmolality). This release of AVP leads to water retention in the distal tubule of the kidney and impaired water excretion, and when coupled with excessive water intake, leads to hyponatremia.⁵

Non-osmotic AVP secretion or Syndrome of Inappropriate Antidiuretic Hormone (SIADH) may occur during exercise due to stimulation from elevated body temperature, volume contraction, hypoglycemia, interleukin-6 (IL-6) release, vomiting, and medication use (such as NSAIDs and selective serotonin reuptake inhibitors (SSRIs)).^1,3,5

Osmotic inactivation and/or impaired mobilization of osmotically inactive sodium stores has also been theorized to play a role in the development of hyponatremia during endurance events.² It has been hypothesized that athletes who develop EAH either cannot activate the exchangeable pool of sodium in response to sodium losses or alternatively, sodium may move into non-osmotically active forms. The mechanisms that control the exchange of sodium between these compartments remain unknown.^2,5

In addition, glycogen metabolism may be an important contributor to hyponatremia that occurs in the absence of weight gain. One kilogram of glycogen can contain upwards of 3 kg of associated water andas glycogen is metabolized, water is released. This contribution to TBW is relatively small, but could lead to depression of the serum sodium.⁶

Moreover, there is suggestion that drops in serum sodium could be attributed to the absorption of water retained in the gastrointestinal system at the end of a race or exercise, into circulation. This may explain a “transient lucid period” followed by an acute presentation of Exercise associated hyponatremic encephalopathy (EAHE) about 30 minutes after stopping physical activity.⁷

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Serum [Na⁺] is not always a good predictor of symptoms, as asymptomatic EAH is a biochemical finding. Athletes may only experience mild, transient complaints that are common with physical exertion. Mild symptomatic EAH may present with non-specific signs and symptoms such as light headedness, headaches, dizziness, nausea, bloating, puffiness, and/or increase in body weight, and athletes may maintain normal vital signs.^1,3,6 These athletes usually do not improve in the Trendelenburg position, and they do not have signs of encephalopathy.

Tools exist for rapid sideline serum [Na⁺] testing, and they can and should be utilized in symptomatic athletes. Despite the lack of initially concerning symptoms, even mildly symptomatic athletes can progress rapidly to severe EAH with neurologic symptoms, and life-threatening EAHE.  EAHE is characterized by a change in mental status and can be accompanied by headache, vomiting, altered sensorium, seizures, dyspnea or frothy sputum (non-cardiogenic pulmonary edema), decorticate posturing or mydriasis (signs of brainstem herniation), and/or coma as sequelae of cerebral edema and brainstem herniation.^1,7

Specific secondary or associated conditions and complications

Athletes with asymptomatic EAH are at risk for developing symptomatic EAH up to 24 hours after a strenuous event.¹ A secondary potential complication of symptomatic EAH and subsequent EAHE, is central nervous system triggered non-cardiogenic pulmonary edema. This may present as dyspnea or frothy sputum and could require supplemental oxygen or intubation if adequate oxygen saturation is not maintained.

Essentials of Assessment

History

Signs and symptoms can overlap between EAH, dehydration, heat illness, and acute altitude illnesses. Correct diagnosis of EAH versus dehydration guides appropriate management and ensuing athlete outcome, therefore EAH should be considered in the differential diagnosis of an individual that has been, or is currently, participating in strenuous activity or prolonged exercise.⁷

Evaluation should include history of present illness, past medical history (with attention to hypertension, diabetes, hyperlipidemia, heart failure, chronic liver or kidney disease, and/or neurologic insults), family history, supplements and medications (with attention to diuretics, antihistamines, anti-hypertensives, lithium, SSRIs and NSAIDs), pre- and post-race weight, amount and type of fluid and food ingested during exercise, urine production (clear or dark and amount), vomiting or diarrhea, shortness of breath, history of problems in past races, and amount of training prior to current event.

Physical examination

Physical exam should focus on the central nervous system, pulmonary system, and cardiovascular system. Assessment of vital signs is essential. Tachycardia and hypotension are associated with dehydration, whereas vital signs (including body temperature) are usually not grossly abnormal in hyponatremia. A rectal temperature most accurately measures core body temperature in cases of suspected concomitant exertional heat-related illness.⁸ In the conscious athlete, a brief mental status exam can be performed if there is question for altered sensorium. Unconscious patients should be assessed for abnormal posturing and pupillary responses. An evaluation for peripheral and pulmonary edema should be performed. Weight gain or loss can be used to assess water balance and may provide indication of serum [Na⁺]. Physical signs of dehydration include dry mucous membranes, poor skin turgor, sunken eyes, and a delayed capillary refill.

Increased vulnerability to orthostatism is a common phenomenon after an endurance event that does not necessarily correlate with dehydration status, although the mechanism is not completely understood.⁹

Functional assessment

Presentation of EAH is variable and can range from being asymptomatic, to seizures, coma, and even death. Dehydration also has a wide range of presentations including mental status and behavioral changes, such as increased aggression.¹⁰

It is still controversial whether dehydration causes impairment in executive function and “mental readiness.” Differences have been noted in endurance versus track-and-field events with no consistently reported changes in endurance athletes when reporting perceived tiredness, alertness, confusion, fatigue, anger, or depression.^9,11

Laboratory studies

The International Exercise Associated Hyponatremia Consensus Development Conference has previously concluded that there should be availability of on-site serum [Na⁺] analysis.¹ On-site serum [Na⁺] can be rapidly obtained within minutes using the i-STAT^® handheld blood analysis system. Medical teams at most endurance events are equipped with i-STAT^® analyzers and accompanying testing cartridges. Depending on which cartridges are available, renal function labs may also be readily obtained which can provide information on hydration status. However, there are circumstances where such testing is not readily available or useful.⁷

Glucometers can rapidly determine blood glucose levels, providing important information considering serum [Na+] is artificially lowered (i.e., pseudohyponatremia) by hyperglycemic states and must be corrected using correction factors.¹² Other causes of pseudohyponatremia include hyperlipidemia and hyperproteinemia, both of which need to be verified with laboratory blood panels.¹²

In the hospital setting, serum and urine osmolality should also be obtained. Additional studies can include other serum electrolytes such as calcium, potassium and magnesium, hormones such as Copeptin, AVP, and aldosterone, and urinalysis to evaluate for urine lactate levels, urine protein, and urine myoglobinuria for rhabdomyolysis. These laboratory tests require more studies and clinical correlation to determine their diagnostic and treatment value.

Imaging

Neuroimaging such as computerized tomography (CT) of the brain may be obtained once an athlete with EAHE is at an advanced medical care facility, however this must not delay acute stabilization.¹

Supplemental assessment tools

Body weight scales prior and during events for monitoring body weight should be considered when organizing an athletic event, especially for long-duration events or events at risk due to environmental factors. Athletes should obtain their baseline event-day weight as it acts as a surrogate measurement of TBW. If pre-race weight is not obtained, the history of the athlete’s normal weight is an appropriate substitute. Lack of weight loss or weight gain during an endurance event is a positive indicator of fluid overload and possible hyponatremia, and fluid intake should be reduced.¹ Some weight loss (1.5-2.5 kilograms) is expected during an endurance race, but athletes who exceed 2% loss of body weight should be assessed for dehydration.¹² Interestingly, some athletes have better results despite more than 2% body weight loss in endurance races.^9,13,14,15 Recent studies suggest tailoring recommendations to individual performance, but more studies need to be done for better understanding of safety and performance guidelines. Event climate including weather, altitude, humidity, temperature, and subsequent athlete clothing are also potential factors that should not be neglected.

Early predictions of outcomes

Severity of initial presenting symptoms, not absolute serum [Na⁺], better predict outcome and should guide treatment.¹ Any athlete suspected of having EAH should have rapid determination of serum [Na⁺]. With appropriate recognition and management, the vast majority of asymptomatic or mildly symptomatic EAH and dehydration cases resolve without long-term sequelae. For both EAH and dehydration, loss of consciousness or disorientation suggests more severe abnormalities and should be acted upon emergently.

Social role and social support system

Athletes with asymptomatic EAH or those treated for mild symptomatic EAH should be discharged from the event’s medical assessment area with a companion to monitor for the development of neurological symptoms that would prompt immediate medical attention.¹Anyone with suspected functional neurological deficits and delayed reaction times should be encouraged to avoid high risk activities such as riding a bicycle, swimming, or driving.

Environmental

Extreme environmental temperatures can affect the likelihood of developing either dehydration or EAH. Cold may elevate the osmotic set-point for secretion of AVP, especially when age >65 years.¹⁶ Non-acclimatized athletes may require hydration beyond thirst drive in temperatures >38ºC (100.4ºF) to improve performance and prevent dehydration.¹⁶ Prolonged exercise (generally longer than 90 minutes of activity) in warmer climates has been suggested as causing excessive sodium losses driving the primary mechanism for EAH, however evidence to date is limited.^2,17

When organizing or supervising a sporting event, it is important to consider that fluid requirements ae individualistic and can vary widely among athletes. Sweat rate, exercise mode, activity intensity, environmental conditions, and the participant’s incoming hydration and nutrition status as well as body composition, can all play a role.⁴

Professional issues

Medical personnel at the sports events should be aware of proper treatment of EAH and differential diagnoses, as incorrect treatment can further compromise serum [Na⁺] and further deteriorate the athlete’s condition. Medical directors should consider education via pre-race briefings/webinars and by providing suggested reading material and/or educational videos and podcasts.⁷

Good Samaritan laws vary among states, however, generally only cover doctors who are also bystander fans. Physicians might be participating and can help in the event of an emergency on the course if Good Samaritan laws are in place. If a doctor is an official race event volunteer, then additional malpractice insurance should be obtained. Recently insurance policies have been developed specifically for volunteer medical teams.¹⁸

Rehabilitation Management and Treatments

Available or current treatment guidelines at different disease stages

Treatment should be driven by the degree of neurological impairment, not just serum [Na+] because both the magnitude and rate of development of hyponatremia influence brain edema.¹ On-site treatment guidelines for hyponatremia are now organized by whether serum [Na⁺] has or has not been confirmed by measurement and whether the athlete is asymptomatic, symptomatic, or in severe EAHE.^1,3

If EAH is confirmed by [Na⁺] measurement, and there are no neurological symptoms beyond headache, limiting further fluid intake until onset of urination is typically sufficient for treatment. A salty snack or an oral hypertonic fluid (i.e., a salty soup or bouillon) especially in those with [Na⁺] <130 mmol/L, may also be used in the resolution of hyponatremia. It is essential to monitor  the athlete for at least 60 minutes or until symptoms resolve and educate the athlete and the athlete’s team (coaches, trainers, family, etc.) on the neurologic signs and symptoms of EAH.^1,5  It is appropriate to discharge athletes from the medical area with a companion and advise them to seek immediate medical attention should new or worsening neurologic symptoms develop. In the case of severe EAH or EAHE, emergent treatment with IV hypertonic saline (100 mL 3% bolus) to decrease intracranial pressure is warranted. Up to three 100mL boluses of 3% hypertonic saline at 10-minute intervals may be given.

On site treatment of suspected EAH, but not confirmed by serum [Na⁺] measurement, is challenging as symptoms are similar to that of volume depletion and heat illness. Healthcare providers should consider a broad differential and weigh the risks and benefits of fluid restriction on a case by case basis. Hypotonic fluids should be restricted in suspected EAH with consideration of the potential harm that could result from fluid restriction if the diagnosis is incorrect. If there are symptoms of severe EAH or EAHE, and the clinical suspicion is high, empiric treatment with rapid infusion of IV hypertonic saline should be initiated emergently to prevent further neurological deterioration. As EAH is an acute process, there is no risk of osmotic demyelination. If EAHE is wrongly assumed, a bolus of hypertonic saline has minimal negative consequences, even in the case of hypovolemia or hypernatremia, and may provide beneficial volume expansion.¹ When serum [Na⁺] cannot be determined and field treatment has not been successful, emergency transport to a definitive care facility should be expedited. If possible, information about the patient’s neurological and cardiopulmonary history; i.e. if they have a history of seizures, arrhythmias, anemia, clots, strokes, or syncope should be obtained.

Coordination of care

It is critical that medical personnel in emergency transport services are aware of the athlete’s suspected (or confirmed) diagnosis, and treatment. The importance of avoiding isotonic or hypotonic fluid resuscitation is critical as this would worsen hyponatremia.

Measurement of treatment outcomes

There are no current guidelines necessitating ongoing serum [Na⁺] measurement during management for EAH. Treatment is dictated primarily by symptoms however, this may be practiced in asymptomatic or mild symptomatic EAH athletes before discharge to ensure that the serum [Na⁺] is at least >130 mmol/L.

Patient & family education

Prevention through education is the main goal and requires broad programs targeted to athletes, coaches, trainers, and parents emphasizing the importance of appropriate hydration practices of drinking to thirst, recognition of EAH signs and symptoms, and urgency of intervention.^1,16 They must understand that excessive fluid intake will not prevent muscle cramps and exertional heat stroke. This education, along with management protocols, must also reach onsite, emergency, and hospital medical personnel.

Some practical recommendations from the International Marathon Director’s Association include¹⁶

• Drink to thirst. Obey the body’s natural physiological cues.
• Water, sodium, and glucose should be available at fluid replacement stations spaced 1.6 km (minimum) to 5 km (maximum) apart.
• Calibrated scales along a marathon course should be at the discretion of the medical team and weight loss of >4% or any weight gain constitutes justification for medical consultation.
• Many sports drinks contain a lower concentration of sodium than body fluids and consumption can worsen EAH.¹⁹

However, there are circumstances where drinking to thirst may not be recommended. This strategy may be inappropriate in shorter durations of exercise (<1 h to 90 min); exercise in cooler conditions, and lower-intensity exercise. It remains consistent that athletes should never drink to the point of weight gain.²⁰

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

It is important to be aware of factors that contribute to excessive hydration, as the most common cause of EAH is sustained hypotonic fluid intake greater than fluid volume lost. These risk factors include exercise duration >4 hours (i.e., slow pace), event inexperience or inadequate training, and encouragement to overconsume readily available fluids.¹ Athletes should be educated to “drink to thirst” in order to avoid overhydration. Finely tuned osmoreceptors and baroreceptors regulate both plasma osmolality and circulating volume through thirst and AVP secretion. Hence using thirst as guide is the best strategy to avoid overhydration. During exercise, the recommendation is to drink no more than 500-1200 mL/h, depending on body size, training level and environmental factors.¹⁶ Nonetheless, thirst is the best gauge for hydration status. Sports drinks should not be used to maintain serum [Na⁺], and can worsen EAH,¹⁹ as most sports drinks are hypotonic to plasma.¹

Cutting Edge/Emerging and Unique Concepts and Practice

The increasing usage of i-STAT^® handheld blood analysis systems has advanced on-site care of EAH by improving early recognition. Evidence suggests that some athletes mobilize sodium stores more than others, yet this is not well understood and further research may investigate related genetic markers.² A small prospective observational study by Whatmough et al.demonstrated that marathon runners who used an NSAID before or during a marathon had a decrease in serum [Na⁺] compared to a control that did not use NSAIDs. Mechanistically, this is consistent with the ramifications of renal artery vasoconstriction attributed to prostaglandin inhibition, resulting in water retension.¹⁷

Gaps in the Evidence-Based Knowledge

Current controversy exists over the hypovolemic variant of EAH, particularly the contribution of sodium loss through hypotonic sweat and role of brain natriuretic peptide in urinary sodium losses. Current guidelines are to treat these individuals with IV hypertonic saline bolus followed by IV normal saline to replete volume.¹ Other areas of future investigation include the role of diet and sodium supplementation, success of the “drink to thirst” strategy, recurrence rates of EAH, long-term health implications, possible genetic markers, the role of NSAIDs, investigating alternative treatments for mild EAH, and the variability in serum [Na⁺] and body weight in the days leading up to an event and at event start.¹

References

1. Hew-Butler T, Rosner MH, Fowkes-Godek S. Statement of the third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clin J Sport Med. 2015;25(4):303-320.
2. Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: Evidence from 2,135 weighed competitive athletic peformances. Proc Natl Acad Sci U S A. 2005;102:18550-18555.
3. Krabak BJ, Parker KM, DiGirolamo A. Exercise-associated collapse: is hyponatremia in our head? PM R. 2016;8:S61-S68.
4. Belval LN, Hosokawa Y, Casa DJ, et al. Practical Hydration Solutions for Sports. Nutrients. 2019;11(7):1550. Published 2019 Jul 9. doi:10.3390/nu11071550
5. Hew-Butler T, Loi V, Pani A, Rosner MH. Exercise-Associated Hyponatremia: 2017 Update. Front Med (Lausanne). 2017;4:21. Published 2017 Mar 3. doi:10.3389/fmed.2017.0002
6. Rosner MH, Kirven J. Exercise-associated hyponatremia. Clin J Am Soc Nephrol (2007) 2(1):151–61.10.2215/CJN.02730806 
7. Rosner MH. Exercise-Associated Hyponatremia. Trans Am Clin Climatol Assoc. 2019;130:76-87. PMID: 31516170; PMCID: PMC6735969.
8. O’Connor FG and Casa DJ. Exertional heat illness in adolescents and adults: Management and prevention. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on April 3^rd, 2024.)
9. Martínez-Navarro I, Chiva-Bartoll O, Hernando B, Collado E, Porcar V, Hernando C. Hydration Status, Executive Function, and Response to Orthostatism After a 118-km Mountain Race: Are They Interrelated? J Strength Cond Res. 2018 Feb;32(2):441-449. doi: 10.1519/JSC.0000000000001614. PMID: 27548786.
10. Speedy DB, Noakes TD, Rogers IR, et al. Hyponatremia in ultradistance triathletes. Med Sci Sports Exerc. 1999;31(6):809-815.
11. Casa DJ, Cheuvront SN, Galloway SD, Shirreffs SM. Fluid Needs for Training, Competition, and Recovery in Track-and-Field Athletes. Int J Sport Nutr Exerc Metab. 2019 Mar 1;29(2):175-180. doi: 10.1123/ijsnem.2018-0374. Epub 2019 Apr 4. PMID: 30943836
12. Sterns RH. Overview of the treatment of hyponatremia in adults. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on April 3^rd, 2024.)
13. Kenefick RW. Drinking Strategies: Planned Drinking Versus Drinking to Thirst. Sports Med. 2018;48(Suppl 1):31-37. doi:10.1007/s40279-017-0844-6
14. Krabak BJ, Waite B, Lipman G. Evaluation and treatment of injury and illness in the ultramarathon athlete. Phys Med Rehabil Clin N Am. 2014 Nov;25(4):845-63. doi: 10.1016/j.pmr.2014.06.006. Epub 2014 Jul 19. PMID: 25442162.
15. Grozenski A, Kiel J. Basic Nutrition for Sports Participation, Part 1: Diet Composition, Macronutrients, and Hydration. Curr Sports Med Rep. 2020 Oct;19(10):389-391. doi: 10.1249/JSR.0000000000000753. PMID: 33031200.
16. Hew-Butler T, Verbalis JG, Noakes TD. Updated fluid recommendation: position statement from the International Marathon Medical Directors Association (IMMDA). Clin J Sport Med. 2006;16(4):283-292.
17. Whatmough S, Mears S, Kipps C. Serum sodium changes in marathon participants who use NSAIDs. BMJ Open Sport Exerc Med. 2018 Dec 5;4(1):e000364. doi: 10.1136/bmjsem-2018-000364. PMID: 30588325; PMCID: PMC6280910.
18. West B, Varacallo M. Good Samaritan Laws. [Updated 2022 Sep 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542176/
19. Cohen D. The truth about sports drinks. BMJ. 2012;345:e4737.
20. Speedy DB, Rogers IR, Noakes TD, Thompson JM, Guirey J, Safih S, Boswell DR. Diagnosis and prevention of hyponatremia at an ultradistance triathlon. Clin J Sport Med. 2000 Jan;10(1):52-8. doi: 10.1097/00042752-200001000-00010. PMID: 10695851.

Original Version of the Topic

Robert Irwin, MD, Michelle D. Francavilla, MD. Hydration Issues in the Athlete and Exercise Associated Hyponatremia. 12/28/2012.

Previous Revision(s) of the Topic

Richard G. Chang, MD, Jameel J Khan, MD. Hydration Issues in the Athlete and Exercise Associated Hyponatremia. 8/25/2016.

Julio Vazquez-Galliano, MD, Daniela Mehech, MD, Cecilia Cordova Vallejos, MD, Jasal Patel, MD. Hydration Issues in the Athlete and Exercise Associated Hyponatremia. 4/29/2021

Author Disclosures

Ilona Schwarz, MD
Nothing to Disclose

Marcel Souffrant, MD
Nothing to Disclose

Ziva Petrin, MD
Nothing to Disclose