Exercise-Associated Hyponatremia in Marathon Runners (original) (raw)
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The importance of exercise associated hyponatremia EAH in sports (Initial Version)
The importance of exercise-associated hyponatremia (EAH) in sports Exercise-associated hyponatremia (EAH) is not uncommon on different endurance sports. In Hong Kong, one confirmed case of EAH had been reported. A 35-year-old male runner was diagnosed as being EAH in the 2008 Standard Chartered Hong Kong International Marathon 1. In this essay, we review an up-to-date document 'Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California 2015' and summarize the importance of exercise-associated hyponatremia (EAH) in sports from this document together with the other related articles.
Medicina
Exercise-associated hyponatremia (EAH) is defined as a plasma sodium concentration of <135 mmol/L during or after endurance and ultra-endurance performance and was first described by Timothy Noakes when observed in ultra-marathoners competing in the Comrades Marathon in South Africa in the mid-1980s. It is well-established that a decrease in plasma sodium concentration <135 mmol/L occurs with excessive fluid intake. Clinically, a mild hyponatremia will lead to no or very unspecific symptoms. A pronounced hyponatremia (<120 mmol/L) will lead to central nervous symptoms due to cerebral edema, and respiratory failure can lead to death when plasma sodium concentration reaches values of <110–115 mmol/L. The objective of this narrative review is to present new findings about the aspects of sex, race location, sports discipline, and length of performance. The prevalence of EAH depends on the duration of an endurance performance (i.e., low in marathon running, high to very high ...
Exercise-Associated Hyponatremia: 2017 Update
Frontiers in Medicine
Exercise-associated hyponatremia (EAH) was initially described in the 1980s in endurance athletes, and work done since then has conclusively identified that overdrinking beyond thirst and non-osmotic arginine vasopressin release are the most common etiologic factors. In recent years, EAH has been described in a broader variety of athletic events and also has been linked to the development of rhabdomyolysis. The potential role of volume and sodium depletion in a subset of athletes has also been described. This review focuses on the most recent literature in the field of EAH and summarizes key new findings in the epidemiology, pathophysiology, treatment, and prevention of this condition.
The Physician and Sportsmedicine, 2010
Aims: In a recent study of male ultra-marathoners who participated in a 161-km ultra-run, the prevalence of exercise-associated hyponatremia (EAH) was reported to be 50%, which is a considerably higher percentage than that seen in marathoners. We investigated the prevalence of EAH in male ultra-marathoners competing in a 24-hour run held in Basel, Switzerland. Body weight, hematocrit levels, plasma volume, plasma sodium concentration, urine specific gravity, and fluid intake were recorded in 15 male ultra-marathoners (mean age ± standard deviation [SD], 46.7 [5.8] years; plasma sodium, 71.1 [6.8] kg; height, 1.76 [0.07] m; body weight, 23.1 [1.84] kg/m 2 ). Plasma sodium was measured at 135.3 (2.8) mmol/L before the race and remained unchanged at 135.4 (3.6) mmol/L after the race. The competitors consumed a total of 15.1 (5.1) L during the race, equal to 0.62 (0.21) L/hour. Fluid intake correlated to the mean running speed (r = -0.87; P = 0.0001). Body weight decreased significantly (P = 0.0009) by 2.2 kg. Hematocrit remained unchanged, and urine specific gravity increased significantly (P = 0.0005). Plasma volume increased by 4. . Changes in body weight showed no association with post-race plasma sodium. The normal resting value should be 140 mmol/L so that a decrease of 5 mmol/L is described as EAH. Because the starting plasma sodium in this study was 135 mmol/L, it is not possible to define EAH as a value that is < 135 mmol/L. Instead, the correct definition should be a plasma sodium concentration of 130 mmol/L (ie, 5mmol/L below the normal resting value). Following this definition, it was determined that no athlete developed EAH in this 24-hour run.
British Journal of Sports Medicine, 2006
Background: The development of symptomatic hyponatraemia consequent on participation in marathon and ultraendurance races has led to questions about its aetiology and prevention. Objectives: To evaluate: (a) the assertion that sweat sodium losses cannot contribute to the development of hyponatraemia during endurance exercise; (b) the adequacy of fluid replacement recommendations issued by the International Marathon Medical Directors Association (IMMDA) for races of 42 km or longer; (c) the effectiveness of commercial sports drinks, compared with water, for attenuating plasma sodium reductions. Methods: A mathematical model was used to predict the effects of different drinking behaviours on hydration status and plasma sodium concentration when body mass, body composition, running speed, weather conditions, and sweat sodium concentration were systematically varied. Results: Fluid intake at rates that exceed sweating rate is predicted to be the primary cause of hyponatraemia. However, the model predicts that runners secreting relatively salty sweat can finish ultraendurance exercise both dehydrated and hyponatraemic. Electrolyte-containing beverages are predicted to delay the development of hyponatraemia. The predictions suggest that the IMMDA fluid intake recommendations adequately sustain hydration over the 42 km distance if qualifiers-for example, running pace, body size-are followed. Conclusions: Actions to prevent hyponatraemia should focus on minimising overdrinking relative to sweating rate and attenuating salt depletion in those who excrete salty sweat. This simulation demonstrates the complexity of defining fluid and electrolyte consumption rates during athletic competition. S ymptomatic hyponatraemia associated with athletic competition was first described in 1985, 1 and more than 100 cases have been documented. 2-4 Although most cases develop during participation in endurance events lasting eight hours or more, this syndrome also develops in slower runners participating in marathon (42 km) races. Most cases are associated with excessive fluid intake and weight gain. 2 5 However, there is evidence that some athletes finish ultraendurance competition with plasma sodium concentrations below 130 mEq/l and have body mass losses greater than or equal to the weight loss expected from cellular respiration and respiratory water loss. 6 7 The latter suggests that, in certain situations, hyponatraemia can occur without excessive fluid consumption. As sweat sodium concentrations can be high, 8 9 it has been proposed that excessive fluid consumption and sweat sodium losses can contribute to symptomatic hyponatraemia. 5 Noakes and colleagues have discounted the idea that sweat sodium losses contribute to the development of symptomatic hyponatraemia 10 11 and argue that all cases would be prevented if athletes refrained from drinking excessively large volumes during endurance events. 10 11 In response to the symptomatic hyponatraemia cases during marathon competitions, the International Marathon Medical Directors Association (IMMDA) of the Association of International Marathons published a position stand recommending that marathon runners drink ad libitum 400-800 ml/h, with the higher rates for the faster, heavier runners competing in warm environmental conditions and the lower rates for the slower runners/walkers completing marathon races in cooler environmental conditions. 12 IMMDA has not made any recommendations about sodium intake. The adequacy of the IMMDA recommendation for preventing excessive dehydration or the development of symptomatic hyponatraemia has not been systematically evaluated. Excessive dehydration was not defined and probably refers more to minimising its contributions to heat exhaustion rather than to sustaining race pace. The IMMDA fluid consumption rates were stated as being ''applicable to other distance running races'', so perhaps including ultraendurance events, such as Ironman distance triathlons. The effect of using the IMMDA recommendation for races longer than a marathon has also not been systematically evaluated.
2021
Introduction: Hyponatremia often occurs during the practice of endurance sports. We evaluated the impact on hyponatremia of the hydration recommendations of the Third International Exercise-Associated Hyponatremia Consensus Development Conference 2015 (3IE-AHCD) during the 2017 Gran Trail de Peñalara marathon (GTP) and the Vitoria Gasteiz Ironman triathlon (VGI). Methods: Prospective study of GTP and VGI athletes participating in four information sessions in the months prior to the events, to explain that hydration should only be according to their level of thirst, per the recommendations of the 3IE-AHCD. Consenting event finishers were included in final analysis. Pre-and post-race anthropometric and biochemical parameters were compared. Results: Thirty-six GTP (33 male) and 94 VGI (88 male) finishers were evaluated. GTP race median fluid intake was 800 ml/h, with 900 ml/h in the VGI race. 83.3% GTPfin and 77.6% VGIfin remained eunatremic (blood sodium 135-145 mmol/L). Only 1/36 GTP and 1/94 VGI participant finished in hyponatremia, both with a sodium level of 134 mmol/L. Fourteen percent of GTP, and 21.2% of VGI participants finished in hypernatremia, with no increase in race completion times. No participating athlete required medical attention, except for musculoskeletal complaints. Pro-BNP and Copeptin levels rose significantly. Changes in copeptin levels did not correlate with changes in plasma osmolality, nor total body water content in impedance analysis. Conclusions: Recommending that athletes' fluid intake in endurance events be a function of their thirst almost entirely prevented development of hyponatremia, without induction of clinically significant hypernatremia, or a negative repercussion on race completion times.
Exercise-Associated Hyponatremia during the Olympus Marathon Ultra-Endurance Trail Run
Nutrients
Research on hyponatremia during mountain marathons is scarce. The present study aimed to investigate the prevalence of exercise-associated hyponatremia during a 44-km trail running race that reached an altitude of 2780 m (Olympus Marathon). Sixty-two runners (five women) who completed the race participated in the study (age: 34.4 ± 8.6 years; height: 1.77 ± 0.06 m; and weight: 75.3 ± 10.0 kg). Anthropometric characteristics, blood, and urine samples were collected pre- and post-race. Food and fluid intake were recorded at each checkpoint. Due to race regulations, the runners could not carry any additional food and fluids besides the ones provided at specific checkpoints. Five runners (8%) exhibited asymptomatic hyponatremia (serum sodium <135 mmol∙L−1). Serum sodium in the hyponatremic runners decreased from 138.4 ± 0.9 (pre) to 131.4 ± 5.0 mmol∙L−1 (post), p < 0.05. Plasma osmolality increased only in the eunatremic runners (pre: 290 ± 3; post: 295 ± 6 mmol∙kg−1; p < 0.05)...
Hyponatremia among Runners in the Boston Marathon
New England Journal of Medicine, 2005
Hyponatremia has emerged as an important cause of race-related death and life-threatening illness among marathon runners. We studied a cohort of marathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors. methods Participants in the 2002 Boston Marathon were recruited one or two days before the race. Subjects completed a survey describing demographic information and training history. After the race, runners provided a blood sample and completed a questionnaire detailing their fluid consumption and urine output during the race. Prerace and postrace weights were recorded. Multivariate regression analyses were performed to identify risk factors associated with hyponatremia.
Proceedings of The National Academy of Sciences, 2005
To evaluate the role of fluid and Na ؉ balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na ؉ concentrations ([Na ؉ ]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na ؉ ]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na ؉ ] between 129 -135 mmol͞liter, and 11% a serum [Na ؉ ] of <129 mmol͞liter. Serum [Na ؉ ] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na ؉ ] in a subset of 18 subjects was predicted from the amount of Na ؉ that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na ؉ ] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na ؉ ], requiring the addition of significant amounts of Na ؉ (>500 mmol) into an expanded volume of total body water. This Na ؉ likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who (i) drink to excess during exercise, (ii) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and (iii) osmotically inactivate circulating Na ؉ or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985.
Incidence of Hyponatremia During a Continuous 246-km Ultramarathon Running Race
Frontiers in Nutrition
The purpose of this observational study was to examine the incidence of exercise-associated hyponatremia (EAH) in a 246-km continuous ultra-marathon. Methods: Over 2 years, 63 male finishers of the annual Spartathlon ultra-marathon foot race from Athens to Sparta, Greece were included in the data analysis. A blood sample was drawn from an antecubital vein the day before the race as well as within 15 min post-race and analyzed for sodium concentration. During the second year of data collection, blood was also drawn at the 93-km checkpoint (n = 29). Height and weight were measured pre and post-race. Results: Mean race time of all subjects was 33 ± 3 h with a range of 23.5 and 36.0 h. Of the 63 finishers recruited, nine began the race with values indicative of mild hyponatremia. Seven runners were classified as hyponatremic at the 93-km checkpoint, three of whom had sodium levels of severe hyponatremia. After the race, 41 total finishers (65%) developed either mild (n = 27, 43%) or severe hyponatremia (n = 14, 22%). Mean change in bodyweight percentage and serum sodium from pre-race to post-race was −3.6 ± 2.7% (−2.5 ± 1.9 kg) and −6.6 ± 5.6 mmol•L −1 , respectively. Pre-race serum sodium level was not a significant predictor of post-race serum sodium levels (β = 0.08, R 2 = 0.07, P = 0.698), however, there was a significant negative association between change in bodyweight percentage and post-race serum sodium concentration (β = −0.79, R 2 = 0.29, P = 0.011). Conclusion: The incidence of EAH of 52 and 65%, when excluding or including these individuals with pre-race hyponatremia, was the highest reported in current literature.