The hyponatremia of exercise may exist in symptomatic and asymptomatic forms. Symptomatic hyponatremia is usually characterized by severe alterations in cerebral function including coma and grand ma1 seizures; it develops especially in less competitive athletes who have maintained high rates of fluid intake during endurance events lasting at least 5 hours. The hyponatremia becomes symptomatic when the volume of excess fluid retained exceeds 2 to 3 liters. The etiology of the condition is unknown. Possibly as many as three or more pathologies (abnormal fluid retention possibly due to inappropriate ADH secretion, abnormal regulation of the extracellular fluid volume, translocation of sodium into a "third space") must be present for symptomatic hyponatremia to develop. The avoidance of overhydration would appear to be the only certain way that susceptible individuals can prevent symptomatic hyponatremia. Sodium chloride containing solutions ingested in physiologically significant concentrations would likely prevent a possible "third space" effect.
Timothy D. Noakes
Martin D. Hoffman, Kristin J. Stuempfle, Ian R. Rogers, Louise B. Weschler, and Tamara Hew-Butler
To determine the incidence of exercise-associated hyponatremia (EAH), the associated biochemical measurements and risk factors for EAH, and whether there is an association between postrace blood sodium concentration ([Na+]) and changes in body mass among participants in the 2009 Western States Endurance Run, a 161-km mountain trail run.
Change in body mass, postrace [Na+], and blood creatine phosphokinase (CPK) concentration, and selected runner characteristics were evaluated among consenting competitors.
Of the 47 study participants, 14 (30%) had EAH as defined by a postrace [Na+] <135 mmol/L. Postrace [Na+] and percent change in body mass were directly related (r = .30, P = .044), and 50% of those with EAH had body mass losses of 3–6%. EAH was unrelated to age, sex, finish time, or use of nonsteroidal anti-inflammatory drugs during the run, but those with EAH had completed a smaller (P = .03) number of 161-km ultramarathons. The relationship of CPK levels to postrace [Na+] did not reach statistical significance (r = –.25, P = .097).
EAH was common (30%) among finishers of this 161-km ultramarathon and it was not unusual for those with EAH to be dehydrated. As such, changes in body mass should not be relied upon in the assessment for EAH during 161-km ultramarathons.
Lawrence E. Armstrong, Elaine C. Lee, Douglas J. Casa, Evan C. Johnson, Matthew S. Ganio, Brendon P. McDermott, Jakob L. Vingren, Hyun M. Oh, and Keith H. Williamson
Exertional hyponatremia (EH) during prolonged exercise involves all avenues of fluid-electrolyte gain and loss. Although previous research implicates retention of excess fluid, EH may involve either loss, gain, or no change of body mass. Thus, the etiology, predisposing factors, and recommendations for prevention are vague—except for advice to avoid excessive drinking.
This retrospective field study presents case reports of two unacquainted recreational cyclists (LC, 31y and AM, 39 years) who began exercise with normal serum electrolytes but finished a summer 164-km ride (ambient, 34±5°C) with a serum [Na+] of 130 mmol/L.
To clarify the etiology of EH, their pre- and post-exercise measurements were compared to a control group (CON) of 31 normonatremic cyclists (mean ± SD; 37±6 years; 141±3 mmol Na+/L).
Anthropomorphic characteristics, exercise time, and post-exercise ratings of thermal sensation, perceived exertion and muscle cramp were similar for LC, AM and CON. These two hyponatremic cyclists consumed a large and similar volume of fluid (191 and 189 ml/kg), experienced an 11 mmol/L decrease of serum [Na+], reported low thirst sensations; however, LC gained 3.1 kg (+4.3% of body mass) during 8.9 hr of exercise and AM maintained body mass (+0.1kg, +0.1%, 10.6h). In the entire cohort (n = 33), post-event serum [Na+] was strongly correlated with total fluid intake (R2 = 0.45, p < .0001), and correlated moderately with dietary sodium intake (R2=0.28, p = .004) and body mass change (R2 = 0.22, p = .02). Linear regression analyses predicted the threshold of EH onset (<135 mmol Na+/L) as 168 ml fluid/kg.
The wide range of serum [Na+] changes (+6 to -11 mmol/L) led us to recommend an individualized rehydration plan to athletes because the interactions of factors were complex and idiosyncratic.
James M. Winger, Martin D. Hoffman, Tamara D. Hew-Butler, Kristin J. Stuempfle, Jonathan P. Dugas, Kevin Fogard, and Lara R. Dugas
To determine if beliefs about physiology and rehydration affect ultramarathon runners’ hydration behaviors or if these beliefs increase the risk for exercise-associated hyponatremia (EAH).
Participants of the 2011 161-km Western States Endurance Run completed a prerace questionnaire, prerace and postrace body-mass measurements, and postrace assessment of serum sodium ([Na+]).
Of 310 finishers, 309 (99.7%) completed the prerace questionnaire and 207 (67%) underwent postrace blood studies. Twelve (5.8%) finishers had asymptomatic EAH ([Na+] range 131–134 mmol/L). The most common hydration plan (43.1%) was drinking according to schedule, and these runners did so to replace fluid lost when sweating (100%) and to avoid dehydration (81.2%). Prerace drinking plan was not associated with postrace [Na+] or the development of postrace hyponatremia. There also were no group differences between those with and those without EAH for any other variables including planned energy intake or knowledge of fluid balance. Runners not planning to drink to thirst trended toward more influence from advertisements (P = .056) and were significantly more influenced by scientific organizations (P = .043) than runners with other drinking plans. Finally, runners who believe that EAH is caused by excessive drinking adopted a lower-volume drinking plan (P = .005), while runners who believe that EAH is caused by sodium loss via sweating reported more common use of sodium supplementation during the race (P = .017).
Beliefs regarding the causes of EAH alter race behaviors including drinking plan and sodium supplementation but do not appear to affect the likelihood of developing EAH during a 161-km ultramarathon.
Beat Knechtle, Patrizia Knechtle, and Thomas Rosemann
Fluid overload is considered a main risk factor for exercise-associated hyponatremia (EAH). The aim of this study was to investigate the incidence of EAH in ultra-runners at the 100 km ultra-run in Biel, Switzerland.
Pre- and postrace, body mass, urinary specific gravity, hemoglobin, hematocrit, plasma [Na+], and plasma volume were determined.
Of the 145 finishers, seven runners (4.8%) developed asymptomatic EAH. While running, the athletes consumed a total of (median and interquartile ranges) 6.9 (5.1-8.8) L over the 100 km distance, equal to 0.58 (0.41-0.79) L/h. Fluid intake correlated negatively and significantly with race time (r = -.50, P < .0001). Body mass decreased, plasma [Na+] remained unchanged, hematocrit and hemoglobin decreased, and urinary specific gravity increased. Plasma volume increased by 4.6 (-2.3 to 12.8) %. Change in body mass correlated with both postrace plasma [Na+] and Δ plasma [Na+]. Postrace plasma [Na+] correlated to Δ plasma [Na+]. Fluid intake was associated neither with postrace plasma [Na+] nor with Δ plasma [Na+]. Fluid intake was related to Δ body mass (r = .21, P = .012), but not to postrace body mass. Fluid intake showed no correlation to Δ plasma volume. Change in plasma volume was associated with postrace [Na+].
Incidences of EAH in 100 km ultra-marathoners were lower compared with reports on marathoners. Body mass decreased, plasma volume increased, and plasma [Na+] was maintained. Since fluid intake was related neither to Δ plasma volume nor to Δ plasma [Na+], we assume that factors other than fluid intake maintained body fluid homeostasis.
Martin D. Hoffman and Thomas M. Myers
Symptomatic exercise-associated hyponatremia (EAH) is known to be a potential complication from overhydration during exercise, but there remains a general belief that sodium supplementation will prevent EAH. We present a case in which a runner with a prior history of EAH consulted a sports nutritionist who advised him to consume considerable supplemental sodium, which did not prevent him from developing symptomatic EAH during a subsequent long run. Emergency medical services were requested for this runner shortly after he finished a 17-hr, 72-km run and hike in Grand Canyon National Park during which he reported having consumed 9.2–10.6 L of water and >6,500 mg of sodium. First responders determined his serum sodium concentration with point-of-care testing was 122 mEq/L. His hyponatremia was documented to have improved from field treatment with an oral hypertonic solution of 800 mg of sodium in 200 ml of water, and it improved further after significant aquaresis despite in-hospital treatment with isotonic fluids (lactated Ringer’s). He was discharged about 5 hr after admission in good condition. This case demonstrates that while oral sodium supplementation does not necessarily prevent symptomatic EAH associated with overhydration, early recognition and field management with oral hypertonic saline in combination with fluid restriction can be effective treatment for mild EAH. There continues to be a lack of universal understanding of the underlying pathophysiology and appropriate hospital management of EAH.
Michelle A. Cleary and Douglas J. Casa
Michelle A. Cleary and Douglas J. Casa
Beth Glace, Christine Murphy, and Malachy McHugh
The purpose of this study was to document eating strategies employed by runners during a 160-km race, and to identify eating patterns that predispose the runner to disturbed mental or gastrointestinal functioning. We monitored intake in 19 volunteers during the 12 hours pre-race. Intake was determined by interview with runners approximately every 12 km throughout the race. The mean finish time was 24.3 hours, with 4 runners not completing the race. Body mass decreased during the race, 75.9 ± 2.3 kg to 74.4 ± 2.2 kg (p < .001). Runners ingested 2643 kcals during the 12 hours prerace (68% carbohydrate) and 3.8 L of fluid. During the race 6047 kcal, 18 L of fluid, and 12 g of sodium were consumed. Gastrointestinal distress (GI) was experienced by half of the participants, but was unrelated to food or fluid intake. Upper GI symptoms were more prevalent than lower and occurred mainly after 88 km. Runners with GI distress tended to complete fewer training miles (p = .10) and to do shorter training runs (p = .08). Half of the volunteers reported mental status changes (MSC), such as confusion or dizziness. Runners with MSC had greater intake of total calories, carbohydrate, and fluid (p < .05) than runners without MSC. They also completed shorter training runs (p = .03). Caloric and moisture intake for all runners far exceeded intakes described previously. Although intake did not match energy expenditure, it may represent the upper limit for absorption during exercise, and very high food and/or fluid intake appears to lead to perturbed mental status.
Katherine Elizabeth Black, Jody Huxford, Tracy Perry, and Rachel Clare Brown
Blood sodium concentration of tetraplegics during exercise has not been investigated. This study aimed to measure blood sodium changes in relation to fluid intakes and thermal comfort in tetraplegics during wheelchair rugby training. Twelve international male wheelchair rugby players volunteered, and measures were taken during 2 training sessions. Body mass, blood sodium concentration, and subjective thermal comfort using a 10-point scale were recorded before and after both training sessions. Fluid intake and the distance covered were measured during both sessions. The mean (SD) percentage changes in body mass during the morning and afternoon training sessions were +0.4%1 (0.65%) and +0.69% (1.24%), respectively. There was a tendency for fluid intake rate to be correlated with the percentage change in blood sodium concentration (p = .072, r 2 = .642) during the morning training session; this correlation reached significance during the afternoon session (p = .004, r 2 = .717). Fluid intake was significantly correlated to change in thermal comfort in the morning session (p = .018, r 2 = .533), with this correlation showing a tendency in the afternoon session (p = .066, r 2 = .151). This is the first study to investigate blood sodium concentrations in a group of tetraplegics. Over the day, blood sodium concentrations significantly declined; 2 players recorded blood sodium concentrations of 135 mmol/L, and 5 recorded blood sodium concentrations of 136 mmol/L. Excessive fluid intake as a means of attenuating thermal discomfort seems to be the primary cause of low blood sodium concentrations in tetraplegic athletes. Findings from this study could aid in the design of fluid-intake strategies for tetraplegics.