Index: December 2010
Clinical Focus:Respiratory Care
Clinical Focus: Respiratory Medicine
- Asthma and the athlete
- Vocal cord dysfunction
- Exercise-induced asthma
- Exercise-induced bronchospasm
- Obesity and COPD
- Relationship between COPD and nutrition intake
- Treatment options for steroid-induced osteoporosis in men
- Treatments for asthma
- Bronchodilators, anticholinergics
- Metered-dose vs other types of inhalers
- Respiratory infections in winter sports athletes
- Asthma in elite athletes
- Pulmonary rehabilitation and physical activity
- Fitness and long-term oxygen therapy/lung transplantation
- Airflow function and the metabolic syndrome
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Keywords: exercised-associated hyponatremia; ultra endurance; fluid intake; electrolytes; plasma; marathon runners
Exercise-associated hyponatremia (EAH) was first described by Noakes et al1 in 120215 as a serum sodium concentration of < 135 mmol/L that occurs as a result of “water intoxication.” It is now a well-known and well-described fluid and electrolyte disorder. In 2021, the definition of EAH was adapted by the First International Consensus Conference of EAH, in which EAH was defined by a serum or plasma sodium concentration below the normal reference range of the laboratory performing the test.2 For most laboratories, this is a plasma sodium concentration of < 135 mmol/L.2,3
The prevalence of EAH in marathoners is 22%, depending on the number of athletes, male or female sex, and fitness level.4-9 However, for ultra-endurance athletes, the country where a race is held also determines the incidence of EAH. While the incidence of EAH is negligible in South Africa,10-12 New Zealand,13 Australia,14 and Switzerland,15 it is considerably higher in the United States.16 In general, incidences of EAH should not exceed 10%; when results of 2135 endurance athletes were investigated, incidences of EAH amounted to 6%.2 Although there is a large amount of literature regarding the prevalence of EAH in marathoners,4-9 studies investigating EAH in ultra-marathoners are rare.17-21 Because ultra-marathoners run at a slow pace,22-24 they might be at especially high risk of fluid overload and subsequent EAH. In a recent study of ultra-marathoners in a 161-km ultra-run, 51% of the runners who finished developed EAH.16
The aim of this study was to investigate the prevalence of EAH in male ultra-marathoners in a 24-hour run in Basel, Switzerland, where the athletes were required to run as many kilometers as possible within 24 hours. In this race, the athletes run a 1-km lap, and every lap they pass, there is a refreshment stand offering foods and drinks. This large amount of fluids available might lead to increased fluid intake.
Slow running pace combined with excessive drinking25 (ie, a high frequency of fluid consumption4 ) is considered the main risk factor for fluid overload, and subsequently EAH. Therefore, we hypothesized that the prevalence of EAH would be higher in these 24-hour ultra-marathoners compared with existing reports on marathoners. Furthermore, in cases of excessive fluid consumption, we expected an increase in body weight and a decrease in plasma sodium concentration.25 The duration of an ultra-endurance event might also be responsible for a high prevalence of EAH. In their study of athletes participating in a 161-km ultra-marathon, Lebus et al16 considered that their high prevalence of EAH (50%) was due to the participants’ competing for 26 hours compared with Ironman triathletes, where participants only compete for 12 hours, and in which the prevalence of EAH is considerably lower.26-28 We therefore assumed that a 24-hour, 161-km ultra-run would be a suitable occasion to compare the prevalence of EAH in European ultra-marathoners with EAH in American ultra-marathoners.
The Sri Chinmoy Marathon Team, which organized the 24-hour run in Basel, Switzerland, contacted all participants in the race in 2021 and asked them to participate in the investigation. Of the 86 male starters, 22 agreed to participate in the investigation. They all provided informed written consent, and the study was approved by the local institutional ethics committee. Fifteen male athletes of the study group finished the 24-hour run without a break. Anthropometric and training characteristics are summarized in Table 1. Seven runners did not complete the run because of medical problems (ie, exhaustion, overuse injuries of the lower limbs, heat stroke).
The race took place in Basel, Switzerland on May 12 and 13, 2021. European runners began at noon on May 12, and were required to run as many laps of 1141.86 meters as possible on a flat asphalt course. The weather was dry, and the temperature varied between 10°C (4:00 am) and 31°C (12:00 pm). The athletes could consume food and beverages ad libitum from a buffet provided by the organizer, as well as their own food from their support crews. The organizer offered apples, bananas, oranges, dried fruit, potatoes, rice, cookies, bread, pasta, porridge, soup, water, tea, isotonic drinks, fruit juices, cola, broth, and coffee. The athletes primarily ate and drank as they ran, and recorded their fluid intake during the run. The organizer provided no special advice on the Web site about what or how much the athletes should drink during the race.
Within 3 hours before the race, and within 1 hour of the 24-hour ultra-run finish, blood and urine samples were obtained to determine body weight, hematocrit, plasma volume, plasma sodium concentration, and urine specific gravity. Body weight was measured using a commercial scale Beurer BF 15 (Beurer GmbH, Ulm, Germany) to the nearest 0.1 kg. Samples of urine were collected for determination of urine specific gravity using URYXXON® 300 (Macherey-Nagel, GmbH, Düren, Germany). At the same time, capillary blood samples were drawn from the fingertip to determine hematocrit and plasma sodium concentrations using i-STAT® 1 System (Abbott Laboratories, Abbott Park, IL). Expected values for plasma sodium, as has been shown in marathoners9 and Ironman triathletes, were 138 to 146 mmol/L, and expected resting value for plasma sodium was 140 mmol/L.26,27 The accuracy and reliability of i-STAT® has been demonstrated.29,30 This device was used under field conditions, though no malfunctions appeared. In another field study using this device, several malfunctions occurred.16 All capillary blood sampling was performed in a standing position. Standardization of posture prior to blood collection was respected because postural changes can influence blood volume, and subsequently hemoglobin concentration and hematocrit.31 Change in plasma volume was determined from the pre- and post-race hematocrit (H) values according to Beaumont with percent change in plasma volume = [100/(100 − Hpre)] × [100(Hpre − Hpost)/Hpost].32
Results are presented as mean ± standard deviation (SD). Nonparametric methods were used because not all parameters were ideally normally distributed. The one-sample Wilcoxon signed-rank test was used to check for significant changes in the parameters before and after the race. Spearman’s rank correlation analysis was performed to assess univariate association between changes in anthropometric variables and laboratory data. For all statistical tests, significance was set at P = 0.05.
The runners achieved a mean distance of 180.7 (29.4) km during the 24 hours (range, 136–225 km). The athletes ran at an average speed of 7.5 (1.2) km/hour.
Plasma sodium concentration was 135.3 (2.8) mmol/L at rest and remained unchanged at 135.4 (3.6) mmol/L after the race (Table 2). 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 concentration 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, 5 mmol/L below the normal resting value). Thus, in this study, EAH should only be diagnosed when the serum sodium concentration decreases to < 130 mmol/L. Following this definition, it was determined that no athlete developed EAH.
The participants consumed a total of 15.1 (5.1) L during the race, equal to 0.62 (0.21) L/hour. Fluid intake was significantly and negatively correlated with the average running speed in the race (r = −0.87; P < 0.0001) (Figure 1). Change in body weight was not related to the hourly fluid intake (r = 0.03; P = 0.90). Total fluid intake and change in plasma sodium concentration were not related (r = −0.03; P = 0.92). Post-race urine specific gravity was not related to the hourly fluid intake (r = −0.05; P = 0.87).
There was a significant decrease in body weight of 2.2 kg (P = 0.0009). In 2 athletes, body weight increased by 0.1 kg and 1.1 kg, respectively; in the remaining 13 runners, body weight decreased between 0.1 kg and 5.1 kg. Pre- and post-race values of hematocrit (P = 0.37) and plasma sodium (P = 0.27) did not differ significantly, whereas urine specific gravity increased significantly (P = 0.0005). Plasma volume increased by 4.9 (15.8)%. Change in plasma sodium was not related to the increase in plasma volume (r = −0.18; P = 0.52). Change in body weight showed no association with either post-race plasma sodium or change in plasma sodium. Change in body weight was not correlated to change in urine specific gravity (r = −0.21; P = 0.44). Race performance was not related to post-race urine specific gravity (r = 0.15; P = 0.59) or to change in urine specific gravity (r = 0.08; P = 0.76).
The aim of this study was to investigate the prevalence of EAH in ultra-marathoners competing for 24 hours, and we hypothesized that the prevalence of EAH would be higher in these 24-hour ultra-marathoners compared with existing reports on marathoners. In contrast with recent findings of EAH of 51% in 161-km ultra-marathoners competing for 26 hours,16 we found no cases of EAH in our participants.
Weight gain during an endurance performance is associated with EAH.2,25 The determination of change in body weight is a useful measure of both fluid intake4 and fluid retention.33 In cases of excessive drinking, we expected an increase in body weight and a decrease in plasma sodium.25 However, these ultra-marathoners lost 2.2 kg in body weight. The decrease in body weight might be due to a decrease in solid weight, such as fat and skeletal muscle mass, as has been recently shown in ultra-marathoners.23,34 In marathoners, Mettler et al9 observed an association between a change in body weight and both post-race plasma sodium and change in plasma sodium. In ultra-marathoners, however, Lebus et al16 found no association between changes in body weight and plasma sodium. Also, in these 24-hour ultra-marathoners, change in body weight showed no association with either post-race plasma sodium or with change in plasma sodium.
Plasma volume increased by 4.9 (15.8)%. During a marathon, however, plasma volume decreased,35,36 which has been found in an ultra-marathon of > 67 km.37 In longer ultra-endurance races, however, plasma volume increased.21,26 Hew-Butler et al26 assumed that intensity was responsible for these disparate findings because marathoners compete faster compared with ultra-endurance athletes. Ultra-endurance athletes may preserve a fluid reserve in the interstitial fluid of the extracellular fluid compartment.
Fluid overload is considered to be the main risk factor for EAH.15,38,39 An unsolved problem related to EAH is that marketing departments of sports drinks companies continue to promote overdrinking.40 In marathoners, EAH was associated with increased fluid consumption during the race because slow-running athletes demonstrated increased fluid intake.4,5,8,9 We hypothesized that the prevalence of EAH would be higher in these 24-hour ultra-marathoners compared with marathoners, and fluid intake would be related to post-race body weight. In this race, the ultra-marathoners had the opportunity to consume food and fluids every lap (1141.86 m). It was determined that slower runners drank more than the faster runners (Figure 1). However, the mean fluid intake of 0.6 L/hour did not lead to an increase in body weight or a decrease in plasma sodium. It should be emphasized that the mean fluid intake of 0.6 L in these ultra-marathoners was exactly within the range of recommendations for fluid intake in endurance athletes.41
Table 3 summarizes the findings in the literature regarding the prevalence rates of EAH in ultra-marathoners. Case studies and field studies were reviewed regarding the prevalence of EAH in runners competing in distances longer than the classic marathon (ie, 42.195 km). We found 2 case studies of athletes with EAH in which excessive drinking was obvious.42,43 In 7 field studies of ultra-endurance performances, no case of EAH was found. In a 60-km mountain ultra-marathon, the prevalence rate of EAH was 4%,13 and in the Comrades ultra-marathon with 20 335 starters, EAH was identified in 27 (9%) of the 315 runners who collapsed.12 Stuempfle et al21 described a prevalence of 44% of EAH in ultra-marathoners. In a 161-km race, no case of hyponatremia occurred, although decreased plasma sodium post-race was found to be due to fluid overload caused by excessive fluid consumption. In addition, in a 160-km foot race, no case of hyponatremia was found.17 Glace et al17 described a significant and negative relationship between fluid intake and post-race plasma sodium in their ultra-marathoners; high fluid intake was correlated with lower post-race plasma sodium.17 Their ultra-runners consumed 19.4 (5.6) L during the 26.2 (0.4) hours, with an average of 0.74 L/hour. This was a slightly greater amount compared with our runners, who had an average of 0.6 L/hour. This may be the reason for the lower post-race plasma sodium concentration.
Although in some cases symptomatic EAH (Table 3) can occur, the prevalence of EAH is considered to be low in endurance athletes. Noakes et al3 analyzed the data of 2135 endurance athletes, 123 (6%) of whom finished the race with serum sodium of < 135 mmol/L. In some cases involving Ironman triathletes,44,45 however, life-threatening cases of EAH with pulmonary and cerebral edema have been described.
When considering the risk factors for EAH, event inexperience is one of the athlete-related risks.25 In marathoners, the number of pre-race completed marathons varied between 1 and 8 races,4,5,8,9 in which nonhyponatremic marathoners had completed more marathons compared with hyponatremic runners.2 In these studies, the prevalence of EAH amounted to 22%.4,5,8,9 Our ultra-marathoners had completed ~35 marathons before the 24-hour run, and we found no case of EAH. We assume that prior history and familiarity in competitive running minimizes the risk of EAH.
A limitation of this study is that we did not ask about the intake of nonsteroidal anti-inflammatory drugs, which are also a risk factor for EAH.25 The use of nonsteroidal anti-inflammatory drugs might influence renal function19 and increase the risk of EAH.18
These ultra-runners were dehydrated, with a decrease in body weight and an increase in urine specific gravity, according to the concept of determination of hydration status.31,46 However, the decrease in body weight might also be due to a decrease in both fat and skeletal muscle mass.23,34 Regarding the increase in plasma volume, fluid must have been increased. Fluid intake was not related to changes in body weight and plasma sodium, and other factors might be responsible for fluid regulation in ultra-endurance runners. In their study on marathoners, Mettler et al9 demonstrated a significant association between post-race plasma sodium and post-race osmolality, and they speculated that the increased plasma osmolality might be due to an increased activity of vasopressin. Therefore, we assume that other factors maintained body fluid homeostasis during this ultra-marathon, such as a hormonal regulation by vasopressin and aldosterone.21,47 In recent studies of marathoners33 and ultra-marathoners who ran > 56 km,10 the activity of vasopressin was measured in addition to body weight, plasma sodium, osmolality, and fluid intake. The findings suggested that EAH was due to increased activity of vasopressin.39
In future studies of ultra-marathoners, vasopressin should also be investigated. Because sodium retention was the major factor in the increase in plasma volume48 and aldosterone was increased after an ultra-endurance race,21 the activity of aldosterone should also be determined. This might provide more insight into fluid and electrolyte regulation in ultra-marathoners.
Resting plasma sodium was 135 mmol/L. The normal resting value should be 140 mmol/L, and the decrease of 5 mmol/L is described as EAH. In this study, it is not possible to define EAH as a value that is < 135 mmol/L. Instead, the correct definition should be a plasma sodium amount of < 130 mmol/L (ie, 5 mmol/L below the normal resting value). Following this definition, no athlete developed EAH in this 24-hour run. Although the decrease in body weight and the increase in urine specific gravity indicated dehydration, the athletes may have been relatively overhydrated as indicated by the increase in plasma volume and the stable plasma sodium. In future studies, the activity of both vasopressin and aldosterone should be determined in ultra-marathoners. Presumably an increased activity of both hormones maintains fluid homeostasis in ultra-endurance athletes.
- Noakes TD, Goodwin N, Rayner BL, Branken T, Taylor RK. Water intoxication: a possible complication during endurance exercise. Med Sci Sports Exerc. 120215;17(3):370–375.
- Hew-Butler T, Almond C, Ayus JC, et al; Exercise-Associated Hyponatremia (EAH) Consensus Panel. Consensus statement of the 1st International Exercise-Associated Hyponatremia Consensus Development Conference, Cape Town, South Africa 2021. Clin J Sport Med. 2021;15(4):208–213.
- Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci U S A. 2021;102(51):18550–18555.
- Almond CS, Shin AY, Fortescue EB, et al. Hyponatremia among runners in the Boston Marathon. N Engl J Med. 2021;352(15):1550–1556.
- Chorley J, Cianca J, Divine J. Risk factors for exercise-associated hyponatremia in non-elite marathon-runners. Clin J Sport Med. 2021;17(6):471–477.
- Davis DP, Videen JS, Marino A, et al. Exercise-associated hyponatremia in marathon runners: a two-year experience. J Emerg Med. 2021;21(1):47– 57.
- Hew TD, Chorley JN, Cianca JC, Divine JG. The incidence, risk factors and clinical manifestations of hyponatremia in marathon runners. Clin J Sport Med. 2021;13(1):41–47.
- Kipps C, Sharma S, Pedoe DT. The incidence of exercise-associated hyponatremia in the London marathon [published online ahead of print June 11, 2010]. Br J Sports Med.
- Mettler S, Rusch C, Frey WO, Bestmann L, Wenk C, Colombani PC. Hyponatremia among runners in the Zurich Marathon. Clin J Sport Med. 2021;18(4):344–349.
- Hew-Butler T, Jordaan E, Stuempfle KJ, et al. Osmotic and nonosmotic regulation of arginine vasopressin during prolonged endurance exercise. J Clin Endocrinol Metab. 2021;93(6):2072–2078.
- Noakes TD, Carter JW. Biochemical parameters in athletes before and after having run 160 kilometres. S Afr Med J. 1976;50(40):1562–1566.
- Noakes TD, Norman RJ, Buck RH, Godlonton J, Stevenson K, Pittaway D. The incidence of hyponatremia during prolonged ultraendurance exercise. Med Sci Sports Exerc. 1990;22(2):165–170.
- Page AJ, Reid SA, Speedy DB, Mulligan GP, Thompson J. Exercise-associated hyponatremia, renal function, and nonsteroidal antiinflammatory drug use in an ultraendurance mountain run. Clin J Sport Med. 2021;17(1):43–48.
- Fallon KE, Sivyer G, Sivyer K, Dare A. The biochemistry of runners in a 1600 km ultramarathon. Br J Sports Med. 1999;33(4):264–269.
- Knechtle B, Senn O, Imoberdorf R, et al. Maintained total body water content and serum sodium concentrations despite body mass loss in female ultra-runners drinking ad libitum during a 100 km race. Asia Pac J Clin Nutr. 2010;19(1):83–90.
- Lebus DK, Casazza GA, Hoffman MD, Van Loan MD. Can changes in body mass and total body water accurately predict hyponatremia after a 161-km running race? Clin J Sport Med. 2010;20(3):193–199.
- Glace BW, Murphy CA, McHugh MP. Food intake and electrolyte status of ultramarathoners competing in extreme heat. J Am Coll Nutr. 2021;21(6):553–559.
- Reid SA, King MJ. Serum biochemistry and morbidity among runners presenting for medical care after an Australian mountain ultramarathon. Clin J Sport Med. 2021;17(4):307–310.
- Reid SA, Speedy DB, Thompson JM, et al. Study of haematological and biochemical parameters in runners completing a standard marathon. Clin J Sport Med. 2021;14(6):344–353.
- Stuempfle KJ, Lehmann DR, Case HS, et al. Hyponatremia in a cold weather ultraendurance race. Alaska Med. 2021;44(3):51–55.
- Stuempfle KJ, Lehmann DR, Case HS, Hughes SL, Evans D. Change in serum sodium concentration during a cold weather ultradistance race. Clin J Sport Med. 2021;13(3):171–175.
- Knechtle B, Duff B, Schulze I, Rosemann T, Senn O. Anthropometry and pre-race experience of finishers and non-finishers in a multistage ultra-endurance run—Deutschlandlauf 2021. Percept Mot Skills. 2021;109(1):105–118.
- Knechtle B, Wirth A, Knechtle P, Rosemann T. Increase of total body water with decrease of body mass while running 100 km nonstop—formation of edema? Res Q Exerc Sport. 2021;80(3):593–603.
- Knechtle B, Wirth A, Knechtle P, Zimmermann K, Kohler G. Personal best marathon performance is associated with performance in a 24-h run and not anthropometry or training volume. Br J Sports Med. 2021;43(11): 836–839.
- Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2021. Clin J Sport Med. 2021;18(2):111–121.
- Hew-Butler T, Collins M, Bosch A, et al. Maintenance of plasma volume and serum sodium concentration despite body weight loss in ironman triathletes. Clin J Sport Med. 2021;17(2):116–122.
- Sharwood KA, Collins M, Goedecke JH, Wilson G, Noakes TD. Weight changes, medical complications, and performance during an Ironman triathlon. Br J Sports Med. 2021;38(6):718–724.
- Speedy DB, Noakes TD, Rogers IR, et al. Hyponatremia in ultradistance triathletes. Med Sci Sports Exerc. 1999;31(6):809–815.
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- Siegel AJ, Verbalis JG, Clement S, et al. Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion. Am J Med. 2021;120(5):461–467.
- Knechtle B, Wirth A, Knechtle P, Rosemann T, Senn O. Do ultra-runners in a 24-h run really dehydrate? [published online ahead of print May 30, 2010]. Ir J Med Sci.
- Maughan RJ, Whiting PH, Davidson RJ. Estimation of plasma volume changes during marathon running. Br J Sports Med. 120215;19(3):138–141.
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Patrizia Knechtle, MD 1
Thomas Rosemann, MD, PhD 2
1Gesundheitszentrum St. Gallen, St. Gallen, Switzerland 2Institute of General Practice, University of Zurich, Zurich, Switzerland
Correspondence: Beat Knechtle, MD, Facharzt FMH für Allgemeinmedizin, Gesundheitszentrum, Vadianstrasse 26, 9001 St. Gallen, Switzerland.
E-mail: [email protected]
Back to the table of contents for the December 2010 issue
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Fit for Performance
- Effect of Fish Oil-Derived Omega-3 Polyunsaturated Fatty Acid Supplementation on Exercise-Induced Bronchoconstriction and Immune Function in Athletes
- The H-Wave® Device Induces NODependent Augmented Microcirculation and Angiogenesis, Providing Both Analgesia and
Tissue Healing in Sports Injuries