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Original article The incidence of exercise-associated hyponatraemia in the London Courtney Kipps,1 Sanjay Sharma,2 Dan Tunstall Pedoe3

1London Marathon and ABSTRACT to 24 h after prolonged physical activity.4 The Specialty Trainee in Sport and Background Exercise-associated hyponatraemia disorder is broadly classifi ed into symptomatic Exercise Medicine,Charing Cross Hospital and Queen (EAH) is a potentially fatal cause of collapse in or asymptomatic hyponatraemia by the presence Mary, University of London, endurance exercise. It is understood to be a dilutional or absence of signs or symptoms rather than by London, UK hyponatraemia caused by an increase of total body the absolute value of [Na+] as this is not a reli- 2London Marathon water relative to the amount of exchangeable sodium able predictor of clinical severity.4 Early signs and Consultant Cardiologist, stores. Fourteen runners presented to one London and symptoms of hyponatraemia are non-specifi c Kings College Hospital, London, UK hospital with symptomatic EAH several hours after such as bloating, nausea, vomiting and headache. 3London Marathon fi nishing the 2003 , and more recently, The more severe manifestations of hyponatra- and Retired Consultant a young male runner died from the complications of emia, hyponatraemic encephalopathy caused by Cardiologist, Homerton severe EAH after crossing the fi nish line of the London cerebral oedema, can lead to confusion, seizures, Hospital, London, UK Marathon. coma and death.4 Correspondence to Objectives To determine the incidence of EAH in EAH is widely understood to be a dilutional Dr Courtney Kipps, runners in the London Marathon. hyponatraemia caused by an increase of total 20 Elsenham Street, Methods Volunteers were recruited at race registration body water relative to the amount of exchange- London, UK; where they were weighed, had blood tests and able sodium stores.4 Aetiological factors include [email protected] completed a demographic and experience questionnaire. excessive fl uid consumption in excess of total Weights, blood tests and a fl uid intake questionnaire body fl uid losses,4 6 altered renal function,3 7 Accepted 01 June 2009 8 9 Published Online First were repeated after the fi nish. Blood was analysed longer race duration, female gender and smaller 11 June 2010 on-site using hand-held i-STAT blood analysers. size.6 Excessive sodium loss may also have an Results Of the 88 volunteers, 11 (12.5%) impact on the development of EAH, although it developed asymptomatic hyponatraemia (serum has not been shown to be a primary causative sodium 128–134 mmol/l). They consumed more fl uid factor.4 (p<0.001) and gained more weight (p<0.001) than In an attempt to reduce the morbidity and mor- did those without hyponatraemia. tality associated with EAH, the International Conclusions A signifi cant proportion (12.5%) of healthy EAH Consensus Development Conference has volunteers developed asymptomatic hyponatraemia met twice in recent years, publishing Consensus running a marathon in cool conditions. On average, Statements with recommendations for fl uid these runners consumed more fl uid and gained more replacement during endurance exercise.4 10 weight than did non-hyponatraemic runners, although Guidance has also been produced by the American fl uid intake was not related to weight gain in this study. College of Sports Medicine11 and the International Four of the 11 hyponatraemic runners lost weight over Marathon Medical Directors Association.12 Yet the course of the marathon, strengthening the case for in studies on volunteers running in an additional factor, such as inappropriate antidiuretic Europe and the USA, the incidence of hyponatra- hormone release during exercise, in the development emia is between 3% and 22%.13 14 After running of EAH. the London Marathon in 2003, 14 runners pre- sented to one London hospital with symptomatic EAH.15 More recently, a young male runner died of pulmonary and cerebral oedema consequent to INTRODUCTION EAH after crossing the fi nish line of the London 5 Over 710 000 runners have successfully completed Marathon. This study aimed to examine the inci- the London Marathon in its 28-year history. While dence of hyponatraemia in fi nishers in the London it is generally considered to be a safe event, medi- Marathon. cal staff at the marathon assess and treat up to 2% of runners annually for problems ranging from METHOD muscle cramps and exercise- associated collapse Study setting to hyperthermia and cardiac arrest. Marathon The London Marathon is a full 42.2 km mara- runners are at risk of collapse from causes related thon held over a fl at city course in the spring. to exercise1 not commonly seen in the general Bottles of water (330 ml) are available from population. A life-threatening cause of collapse water stations situated every mile (1.6 km) during endurance exercise is exercise-associated from the third mile onwards. Additionally, hyponatraemia (EAH), which has been respon- 330 ml sachets of a sports drink containing sible for the deaths of at least fi ve runners in the 22 mmol/l [Na+]16 are available at 4.6, 8.8, 15.3 USA and UK in the last few years.2–5 and 23.7 miles. Runners are advised in the pre- EAH is defi ned as serum sodium concentra- race literature not to drink at every station and tion ([Na+]) less than 135 mmol/l during or up not to drink excessively.

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Study population linear regression. Data are presented as “mean (SD)” unless Healthy volunteers were recruited at race registration otherwise stated. Signifi cance was defi ned as p<0.05. from runners participating in the 2006 London Marathon. Written consent was obtained from each volunteer. Each RESULTS was weighed in light clothing and completed a question- The event was held in wet, rainy conditions with air tem- naire detailing demographics and marathon experience. A perature 9–12°C, humidity 73% and wind speed 3–9 km/h. 2 ml sample of venous blood was drawn from the antecubital Wet bulb globe temperature (WBGT) was 9°C at the start. fossa and analysed immediately for sodium on self-calibrat- The race started with 33 578 runners; 33 222 fi nished. At the ing, handheld i-STAT blood analysers (Abbott Point of Care, fi nish, 603 runners were seen in the medical tents. No cases of East Windsor, New Jersey, USA). (The i-STAT analyser has symptomatic EAH were found among these runners. been shown to have excellent reliability for measuring [Na+] when compared to simultaneous laboratory analyser mea- Volunteers surements.17 18 It has been used with success in the marathon Demographics setting14 19 and has been in use in the medical tents of the One hundred and sixteen volunteers were recruited. Prerace London Marathon since 2005.) As soon as possible after data sets on fi ve runners were incomplete, and they were fi nishing the marathon, volunteers were asked to report to not included in further analysis. The remaining 111 com- the medical tent on-site where they were weighed on the prised 42 female and 69 male runners with an average age same scales, had a postrace blood test analysed in the same of 38.8 years. Eighty-eight of these 111 (79.3%) returned for fashion as before and completed a fl uid intake question- postrace tests after the marathon. The returning runners naire. Estimated fl uid intake was calculated by multiplying had a lower baseline [Na+] (138 (3) mmol/l, p=0.044) and ran the number of drinks consumed by 330 ml (the volume of a the marathon 33 min faster (p=0.005) than did those who water bottle or sports drink sachet.) did not return for blood tests (baseline [Na+] 140 (2) mmol/l) (fi gure 1). Otherwise, the two groups were not signifi cantly different in terms of age, sex, body mass index (BMI) or pre- Statistical analysis vious experience. Statistics were calculated using GraphPad Prism (GraphPad All except two non-returners fi nished the marathon. One Software, San Diego, California, USA). Descriptive statistics did not start the race, and another withdrew after tripping and were used to illustrate demographics and to estimate the inci- injuring her leg. A third runner collapsed after fi nishing and dence of hyponatraemia. Differences between groups were was reviewed by the medical team. His [Na+] was found to be analysed with independent t tests for continuous variables, 138 mmol/l, excluding the diagnosis of EAH. χ2 for categorical variables and Mann–Whitney U tests for non-parametric data. Where appropriate, skewed data were Postrace results transformed to a logarithmic scale to follow a normal dis- Asymptomatic hyponatraemia was identifi ed in 11 (12.5%) of tribution. Relationships between continuous variables were the 88 volunteers. Their [Na+] ranged from 128 to 134 mmol/l. analysed using Pearson’s Product Moment correlation and This group was not signifi cantly different from the volunteers

Figure 1 Finishing times of all study volunteers.

Table 1 Demographics of returning volunteers* Volunteers (n=88) Hyponatraemic (n=11) Non-hyponatraemic (n=77) p Value† 95% CI χ2 Age (years) 37.1 (8.8) 39.7 (9.7) 0.412 –8.7, 3.6 – Sex (% male) 36.4 63.6 0.084 – 2.989 Weight (prerace, kg) 71.0 (12.6) 74.3 (12.9) 0.429 –11.5, 4.9 – Body mass index 25.6 (4.9) 24.4 (2.8) 0.231 –0.8, 3.2 – Previous marathons (median number) 1 (0–4) 1 (0–40) 0.542 – – *Data are presented as mean (SD) unless stated otherwise. †Continuous variables were analysed with independent t tests and categorical variables were analysed with the χ2 test..

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that did not develop hyponatraemia in terms of age (p=0.412), Among all volunteers, postmarathon [Na+] had a strong linear sex (p=0.084, χ2=2.989), prerace weight (p=0.429), BMI (p=0.231) relationship with change in [Na+] (r2=0.772, p<0.001) (fi gure 2). or previous marathon experience (median number of previous Postrace [Na+] was inversely related to fl uid intake (r2=0.160, marathons: p=0.545; proportion with experience: p=0.865, p<0.001) (fi gure 3) as well as to absolute weight change χ2=0.029) (table 1). There was no signifi cant difference in fi n- (r2=0.133, p<0.001) and relative weight change (r2=0.140, ishing times between hyponatraemic and non- hyponatraemic p<0.001) (fi gure 4). These relationships were similar when the runners (table 2). There were no cases of symptomatic change in [Na+] was modelled against fl uid intake (r2=0.169, hyponatraemia. p<0.001) and absolute (r2=0.096, p=0.003) and relative weight change (r2=0.097, p=0.003). Although there was a positive Fluid intake trend between fl uid intake and weight change, this relation- Average fl uid intake over the course of the marathon was ship was not signifi cant (p=0.217). 2144 ml; however, runners who developed hyponatraemia reported a signifi cantly larger fl uid intake (3683 ml vs 1924 ml, DISCUSSION p=0.001) and consumed fl uid at a higher rate than those with- Principal fi ndings out hyponatraemia (843 ml/h vs 451 ml/h, p=0.002) (table 2). There was no difference in frequency of drinking (p=0.138) Eleven of a control group of 88 healthy volunteers (12.5%) run- or frequency of urination (p=0.099) during the race. Runners ning the London Marathon had asymptomatic hyponatraemia who developed hyponatraemia reported drinking more fl uid in the time between fi nishing and their postrace review than did those who did not develop hyponatraemia, but this differ- ence was not statistically signifi cant (271 vs 186 ml, p=0.200). 150

Upper limit of Weight change 145 normal range ] (mmol/litre)

Runners with hyponatraemia completed the marathon 0.46 + (1.65) kg heavier than their baseline weight, while those with- 140

out hyponatraemia lost 1.46 (1.70) kg (p<0.001) over the same Lower limit of period. Relative weight change was also signifi cantly different 135 normal range 2 between the two groups (0.76 (2.8)% vs −1.9 (−2.2)%, p<0.001) 130 r = 0.772 (table 2). Sodium changes 125 Runners who developed hyponatraemia had a lower baseline Postmarathon [Na + [Na ] (albeit within the normal reference range) than those −10.0 −7.5 −5.0 −2.5 0.0 2.5 5.0 who did not develop hyponatraemia. They also exhibited Change in [Na+] (mmol/litre) a greater fall in [Na+] than those without hyponatraemia (table 3). Figure 2 Postmarathon [Na+] plotted against change in [Na+].

Table 2 Hyponatraemic and non-hyponatraemic volunteers’ fi nishing times, weight change and fl uid intake* Volunteers (n=88) Hyponatraemic (n=11) Non-hyponatraemic (n=77) p Value† 95% CI χ2 Finishing times (min) 266 (48) 252 (43) 0.303 −13.6, 43.0 – Weight change Absolute (kg) 0.46 (1.65) −1.46 (1.70) <0.001 0.8, 3.0 – Relative (%) 0.76 (2.8) −1.90 (2.2) <0.001 1.2, 4.1 –

Log10 (fl uid intake (ml))‡ 3.49 (0.27) 3.20 (0.28) 0.001 1.32, 2.98§ –

Log10 (fl uid rate (ml/h))‡ 2.86 (0.267) 2.58 (0.26) 0.002 1.28, 2.75§ Frequency of fl uid consumption – – 0.138 – 3.960 Every mile Number 5 14 – – – % 45.5 18.2 – – – Every other mile Number 4 36 – – – % 36.4 46.6 – – – Every third mile or less often Number 2 24 – – – % 18.2 31.2 – – – Frequency of urination during race Median 1 1 0.099 – – Range 0–6 0–6 – – – *Data are presented as mean (SD) unless stated otherwise. †Continuous variables were analysed with independent t tests, and categorical variables were analysed with the χ2 test. Non-parametric data were analysed with the Mann–Whitney U test. ‡Data transformed to follow normal distribution. §95% CI of the geometric means.

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Table 3 Volunteers’ pre- and postmarathon [Na+] and change in [Na+] Volunteers (n=88) Hyponatraemic (n=11) Non-hyponatraemic (n=77) [Na+] (mmol/l) Mean (SD) Range Mean (SD) Range p-Value* 95% CI Premarathon 138 (1.8) 135–140 140 (1.4) 136–143 0.010 −2.1, −0.3 Postmarathon 132 (2) 128–134 139 (2) 135–143 <0.001 −8.2, −5.5 Change −6 (1.4) −8 to −4 −1 (2) −5 to 4 <0.001 −6.9, −4.4 *Continuous variables were analysed with independent t tests.

150

Upper limit of 145 normal range

] (mmol/litre) 140 + Lower limit of 135 normal range

130

2 125 r = 0.164

120 Postmarathon [Na 0 1000 2000 3000 4000 5000 6000 7000 8000 9000 Fluid intake (ml)

Figure 3 Postmarathon [Na+] against fl uid intake.

at the fi nish. On average, these runners consumed more fl uid and gained more weight than did non-hyponatraemic runners, although fl uid intake was not related to weight gain in this 150 study, and four of the 11 hyponatraemic runners lost weight over the course of the marathon. Female gender and slow race Upper limit of

] (mmol/litre) 145 normal range

pace were not associated with the development of EAH in this + study. Five of the 11 runners who developed hyponatraemia 140 fi nished the race within 4 h. Lower limit of 135 normal range Discussion 130 The primary aetiological factor in the development of EAH 4 6 8 2 is fl uid consumption in excess of total body fl uid losses. 125 r = 0.1395

Athletes drink more during exercise in hot conditions than in Postmarathon [Na cool conditions,20 and unusually hot environmental conditions are a recognised risk factor for EAH.4 A cluster of 14 cases of −7.5 −5.0 −2.5 0.0 2.5 5.0 7.5 10.0 EAH after a previous London Marathon was partly attributed Relative weight change (%) to the hot conditions on the day (WBGT 15.2°C, 0.43 cases of symptomatic EAH per 1000 fi nishers); cooler conditions on Figure 4 Postmarathon [Na+] versus relative weight change. each of the following 2 years were associated with only single cases (2004: WBGT 10.8°C, 0.03/1000; 2005: WBGT 12°C, However, in this study, estimated fl uid intake was not related 0.03/1000).15 In the cool, wet conditions encountered during to weight gain. Several reasons may account for this. First, fl uid this current event, none of the collapsed runners seen by medi- intake was self-reported and subject to recall bias. Second, cal staff in the medical tents had hyponatraemia (unpublished runners should expect to lose some weight over the course of data). However, despite these conditions, 12.5% of a group of a marathon due to substrate oxidation;21 neutral weight bal- healthy volunteers running the London Marathon drank suf- ance therefore suggests over-hydration. A recent study calcu- fi cient quantities of fl uid to lower their [Na+] by an average of lated that weight loss of 0.75 kg was the minimum necessary 6 mmol/l, thereby developing hyponatraemia. over the course of a marathon to reduce the risk of developing Weight change is a useful objective measure of fl uid hyponatraemia.14 Finally, weight gain and subsequent EAH intake6 and retention.3 Consistent with data from the Boston may be related to factors other than fl uid intake. The volumes Marathon,6 hyponatraemic runners in this study reported a consumed by participants in this study were on the whole not signifi cantly larger fl uid intake and exhibited considerable exceptional quantities, although the differences between the weight gain compared with non-hyponatraemic runners. two groups are signifi cant. The larger group of 77 unaffected Signifi cant inverse relationships between [Na+] and weight runners drank less than 2 litres each over the course of the change and [Na+] and fl uid intake in this study lend support race, while runners who developed hyponatraemia drank an to the fi ndings of Almond et al,6 providing further evidence average of over 3.5 litres per person. Unaffected runners drank for the role of excessive fl uid intake in the aetiology of EAH. at an average rate of 450 ml/h; hyponatraemic runners drank

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842 ml of fl uid/h on average, almost twice the rate. However, hyponatraemia becomes symptomatic is highly variable four of the hyponatraemic runners in this study consumed and therefore unpredictable. Following Almond et al, if this fl uid at rates (less than 450 ml/h) unlikely to cause fl uid over- incidence of EAH is representative of all fi nishers in the load purely by overwhelming the renal excretory capacity. London Marathon, 4152 runners are likely to have fi nished Additionally, four hyponatraemic runners actually lost weight with asymptomatic hyponatraemia, despite the cool wet over the course of the run (two of these four consumed fl uid weather conditions discouraging excessive drinking. This at less than 450 ml/h). Inappropriate antidiuretic hormone life-threatening condition, which recently claimed the life of (ADH) release during exercise causing altered renal function a healthy runner in the London Marathon,5 appears to remain and secondary fl uid retention is one such mechanism by which a real threat despite recent EAH Consensus Statements4 10 EAH can develop in the absence of excessive fl uid intake.3 4 and an Advisory Statement from the International Marathon 22 Inappropriate ADH release increases the risk of developing Medical Directors Association12 on safe drinking habits EAH even when relatively “normal” volumes of fl uid are con- during exercise. This signifi cant incidence of asymptomatic sumed.4 Non-osmotic stimulation of ADH causing EAH has hyponatraemia which developed in cool running conditions in been linked to the release of interleukin-6 in exertional rhab- a healthy running population should alert marathon medical domyolysis in marathon runners.3 23 Evidence of inappropri- staff and organisers to the potential for an increase in more ately concentrated urine would be a useful surrogate marker severe hyponatraemia in warmer weather conditions which of the syndrome of inappropriate secretion of antidiuretic hor- encourage excessive drinking. Runners should continue to be mone (SIADH) for future studies. educated about fl uid intake during exercise and the symptoms Recent experience from the London Marathon indicates of early hyponatraemia such as weight gain. that runners with hyponatraemia have tended to present to hospital several hours after fi nishing the event apparently Limitations well, suggesting that fl uid consumed after exercise may add Logistical considerations determined that prerace weight 3 8 19 24 to the risk of developing hyponatraemia. One theory and [Na+] were measured at registration rather than at the suggests that as blood fl ow returns to the gut with the ces- start; thus, we cannot ascertain the true prerace hydration sation of exercise and before the renal system has returned status of the volunteers immediately before the race. Fluid to normal, increased absorption of water from the gut con- intake in this study was self-reported. Runners often take tributes to fl uid overload and the subsequent risk of EAH. great care over their training and race schedules; however, Runners in this study who developed hyponatraemia tended fl uid intake was reported retrospectively and therefore must to drink more after the race than those who did not develop be treated as an estimate. Fortunately, weight change, a hyponatraemia, but this difference did not reach statistical more reliable and objective measure of fl uid balance,3 pro- signifi cance. Persistent SIADH may explain postrace onset duced similar results. of EAH as runners continue to consume fl uids under the Twenty-three volunteers (20.1%) did not return for a blood mistaken impression that delayed urination signifi es dehy- test after the marathon. There could be many reasons for 3 dration. For practical reasons, volunteers in this study were this, but we do know this group fi nished the marathon later asked to report for follow-up blood tests as soon as possible than those who did return. If prolonged duration of exer- after fi nishing the marathon. The incidence of hyponatra- cise is a recognised risk factor and had this group returned emia may well have been higher if blood samples had been for blood tests, might the incidence of EAH have been even taken later. Development of EAH in the hours after the mara- higher? thon is worthy of further investigation. EAH is more common after exercise of more than 4 h dura- CONCLUSION tion: slower runners have more opportunity to consume exces- A signifi cant proportion (12.5%) of healthy volunteers sive volumes of fl uid.6 8 9 25 In this study, however, fi ve of the developed asymptomatic hyponatraemia running a marathon 11 runners (45.5%) who developed hyponatraemia fi nished in cool conditions. On average, these runners consumed more the race within 4 h, and, contrary to other studies,8 the current fl uid and gained more weight than did non-hyponatraemic study did not fi nd a correlation between fi nishing times and runners, although fl uid intake was not related to weight gain [Na+]. Closer analysis reveals that three of these fi ve con- in this study, and four of the 11 hyponatraemic runners lost sumed at least 600 ml in the time between fi nishing and their weight over the course of the marathon. Female gender and review, thereby increasing their total fl uid intake by 25–30% slow race pace were not associated with the development after stopping exercise. These two observations enhance the of EAH in this study. Five of the 11 runners who developed case for the presence of an additional factor, such as altered hyponatraemia fi nished the race within 4 h. Three of these renal function persisting after the precipitating activity, in the fi ve consumed up to 30% of their total fl uid intake after they development of EAH. had fi nished the marathon. These observations enhance the A limitation noted by other studies was a lack of baseline or case for the presence of an additional factor in the develop- premarathon [Na+].6 Without a baseline, it could be argued that ment of EAH, such as inappropriate ADH release during development of hyponatraemia is related to low premarathon exercise causing altered renal function and which may persist [Na+]. Although those who developed hyponatraemia did start after cessation of the precipitating activity. with a lower premarathon [Na+], they were all within the normal range. Notably, however, these runners demonstrated Acknowledgements The authors would like to thank all the runners who kindly a signifi cantly greater fall in [Na+] than those who did not volunteered to help us in this study. Thanks must also go to Abbott Point of Care, develop hyponatraemia. who kindly supplied the i-STAT blood analysers and cartridges for this study and The incidence of asymptomatic hyponatraemia in this continue to support the London Marathon medical team. study group is consistent with the experience at the Boston Funding Abbott Point of Care supplied the i-STAT blood analysers and cartridges Marathon supporting the contention that EAH is under- for this study. recognised.6 The tipping point at which asymptomatic Competing interests None.

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The incidence of exercise-associated hyponatraemia in the London marathon

Courtney Kipps, Sanjay Sharma and Dan Tunstall Pedoe

Br J Sports Med 2011 45: 14-19 originally published online July 20, 2009 doi: 10.1136/bjsm.2009.059535

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