The popularity of triathlons — races in which competitors run, bike and swim — has exploded over the past 15 years. According to USA Triathlon, the leading group that organizes races, the number of people with one-day memberships (indicating race participation) stood at more than 447,000 in 2014, compared with about 128,000 in 1999. 
 
 But a small yet persistent number of tragedies have marred the triathlon boom. Triathletes have a death rate of approximately 1.5 people per 100,000 participants, according to a 2010 article in the journal JAMA. That's not many, but it is two to three times higher than the rate seen in marathons. 
 
 Most of the deaths occur during the swim portion of the races, when participants are crowded together in the water. And when someone dies during a swim, it's tough to determine the cause. [The Odds of Dying: A Look At Your Chances of Death from Causes Both Common and Unusual] 
 
 Now, new research hints that a rush of fluid into the lungs may sometimes play a role. 
 
 In the new research, scientists looked at a condition called immersion pulmonary edema (IPO). When someone jumps into water — especially cold water — the body rapidly shunts blood away from the extremities and moves it toward the core. Sometimes, this can lead to a change in internal pressure that forces fluids from the blood into the lungs, leading to shortness of breath and blood-tinged mucus. If a swimmer can't get out of the water quickly, the fluid buildup (the edema) in their lungs may incapacitate them. 
 
 The researchers at Duke University Medical Center and the University of Iowa tracked triathlon deaths in the United States and Canada from October 2008 to November 2015. They found that 58 people died while training or during competitions, including 42 who died during the swim portion. Then, the researchers requested autopsy records from those swimming deaths. (They didn't compare the swimming deaths to the biking and running deaths because there were very few fatalities from those other portions of the race, and many of the deaths that did occur were the result of car collisions.) 
 
 Of the 23 records the researchers were able to secure, 19 belonged to men and four belonged to women. In some cases, there were obvious cardiac problems that could have contributed to the person's death. Four men had significant coronary artery disease, defined as blood vessels that were narrowed by more than 70 percent. Another man experienced a tear in his renal artery, causing him to hemorrhage; another died when his aortic artery tore open. A third man had heart stents, indicating existing cardiovascular disease. The researchers removed this group from their analysis, leaving 16 people without any obvious reason to have died in the water. 
 
 Of this remaining group, six people had excessively large hearts, the researchers found. In particular, the athletes showed evidence of left ventricular hypertrophy, meaning that the chamber of the heart that pumps blood to the body is larger than usual. 
 
 Elite athletes often have larger hearts than their sedentary counterparts because they work the muscle harder, but this so-called "athlete's heart" is usually not as pronounced as what was seen in the triathletes who died, the researchers reported Aug. 29 in the journal BMJ Open Sport & Exercise Medicine. 
 
 The researchers also compared the results of the autopsies to a cohort of 225 healthy triathletes and found vast differences in the proportion of people with thickening of their heart walls. The septum, or middle wall, of the ventricles was thickened in 1 percent of the healthy athletes, compared with 67 percent of the deceased athletes. Likewise, the posterior wall of the ventricles was overly thick in 0.5 percent of the healthy triathletes, compared with 50 percent of the deceased triathletes. [10 Amazing Facts About Your Heart] 
 
 Previous studies had found left ventricular hypertrophy to be a risk factor for immersion pulmonary edema. The new findings don't prove that the triathletes died of IPO, the researchers warned, but they do suggest a possible explanation for some deaths. 
 
 "The message is that if people have untreated hypertension or they're known to have ventricular hypertrophy, they need to get evaluated and treated before they embark on this sport," study researcher Dr. Richard Moon, a professor of anesthesiology and medicine at the Duke University School of Medicine, said in a statement. 
 
 Other explanations for triathlete deaths have been suggested as well. A 2015 commentary in the journal Current Sports Medicine Reports pointed to some possible explanations, such as panic attacks caused by crowded race conditions and cold-water races when athletes are used to training in warm pools. Some triathlon organizations are working to make changes to events that may decrease the risk. Ironman, for example, altered its swims in 2013 so that participants start in a staggered fashion rather than entering the water all at once. 
 
 Original article on Live Science. ||||| Conclusions LVH—a marker of SIPO susceptibility—was present in a greater than the expected proportion of triathletes who died during the swim portion. We propose that IPO may be a significant aetiology of death during the swimming phase in triathletes. The importance of testing for LVH in triathletes as a predictor of adverse outcomes should be explored further. 
 
 Results We identified 58 deaths during the time period of the review, 42 (72.4%) of which occurred during a swim. Of these, 23 postmortem reports were obtained. Five individuals had significant (≥70%) coronary artery narrowing; one each had coronary stents; retroperitoneal haemorrhage; or aortic dissection. 9 of 20 (45%) with reported heart mass exceeded 95th centile values. LV free wall and septal thickness were reported in 14 and 9 cases, respectively; of these, 6 (42.9%) and 4 (44.4%) cases exceeded normal values. 6 of 15 individuals (40%) without an obvious cause of death had excessive heart mass. The proportion of individuals with LVH exceeded the prevalence in the general triathlete population. 
 
 Methods Deaths while training for or during triathlon events in the USA and Canada from October 2008 to November 2015 were identified, and postmortem reports requested. We assessed obvious causes of death; the prevalence of left ventricular hypertrophy (LVH); comparison with healthy triathletes. 
 
 In a series of deaths occurring during the swim portion of triathlon events, a high proportion of autopsies demonstrated cardiac anomalies, in particular left ventricular hypertrophy (LVH). LVH is a marker of immersion pulmonary oedema (IPO) susceptibility, and the authors propose that many of these deaths were due to swimming-induced pulmonary oedema (SIPO). 
 
 The results suggest that screening examinations for triathletes should search for conditions that predispose to SIPO, such as hypertension, LVH and obstructive sleep apnoea. A risk reduction strategy that may prevent some of these deaths should include optimisation of blood pressure and body weight, and treatment of sleep apnoea. 
 
 The current investigation was performed to test the hypothesis that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training have a higher prevalence of cardiac anomalies that could predispose to IPO. 
 
 Immersion pulmonary oedema (IPO, also known as swimming-induced pulmonary oedema, SIPO) is one such potential cause. IPO presents as rapid onset of dyspnoea, wheezing, hypoxaemia and expectoration of blood-tinged sputum, which can incapacitate a swimmer. A recent comprehensive review of swimming-related death identified IPO as a possible cause. 11 Although IPO usually occurs in healthy individuals without an obvious predisposing factor, many victims have left ventricular hypertrophy (LVH), hypertension and other cardiovascular comorbidities—potential markers of susceptibility. 12–15 
 
 Drowning, the process of experiencing respiratory impairment from submersion/immersion in liquid, 4 is often the official reported cause of swimming death; 1 however, drowning seems unlikely in experienced swimmers. Predictors of cardiac death—the overwhelming primary cause of sudden death in most other sports 2 , 5–8 —remain elusive in triathletes. Arrhythmic causes, including prolonged QTc and autonomic conflict (simultaneous activation of sympathetic and parasympathetic), 4 , 9 have been proposed in triathlete cardiac death. Other suggested causes include exertional heat stroke, myocardial infarction, head trauma, panic attack and arrhythmia. 10 Cause of death uncommonly can be attributed to an anatomic cardiac anomaly; 1 thus, in most cases, physiological causes must be sought. 
 
 The triathlon is a sequence of consecutive races consisting of a sequence of swim (750–3800 m), bicycle (13–112 km) and foot (5–42 km) races. As in all competitive sports, there is a modest sudden death rate, which has been estimated at 1.5 per 100 000 participants, 1 in sanctioned triathlon events, two to three times greater than the marathon rate. 2 , 3 As most deaths occur during the swim when the victim's plight is not readily distinguishable among the large number of swimmers, the proximate cause of sudden death in the swim portion of the triathlon remains elusive. 
 
 Each medical examiner report was examined to determine whether there were any abnormalities of coronary arteries, cardiac muscle or valves, or obvious cause of death other than coronary disease. Heart mass and myocardial thickness were recorded. Heart mass was classified relative to normal reference ranges: for men 233–383 g; 16 for women 148–296 g. 17 Heart mass and ventricular wall thickness were also compared with the 95th centile values of normal heart mass scaled to height and sex. 18 Values also were compared with echocardiographic data obtained from a population of triathletes. 19 Also recorded were age, sex, height, body mass, body mass index, event date, death date, autopsy results and any other available pertinent information. Significant coronary artery disease (CAD) was enumerated as ≥70%; ≥50% coronary narrowing was also recorded. 20 LV mass was conservatively estimated as 75% of total heart weight. 21 
 
 The study was approved by the Duke Medicine Institutional Review Board. Using the search phrase ‘triathlon death’, deaths during triathlon events or while in training for triathlons in the USA and Canada from October 2008 to November 2015 were identified using manual internet searches and Google Alerts. The phase of the event when death occurred was obtained from news sources such as newspaper articles or internet postings. Medical examiner reports for those participants who died during a swim were requested, and the phase of the race in which each acute event occurred was confirmed from the report. 
 
 Excluding those with an obvious possible cause of death (coronary disease ≥70% narrowing (n=4), presumed coronary disease due to history of stent placement (n=1), retroperitoneal haemorrhage (n=1), aortic dissection (n=1)), 16 individuals remained. Of these, 6 (37.5%) had excessive heart mass, one of whom also had acute myocarditis. In this group, there was a higher proportion of individuals with thickened LV compared with the general triathlete population (p<0.001, table 6 ). 
 
 Four individuals had significant (≥70%) CAD. A man aged 58 years died of a massive retroperitoneal haemorrhage due to renal artery dissection. Death was attributed to acute dissection of the descending aorta in a man aged 66 years. A man aged 46 years had a history of atrial fibrillation, and flecainide was detected in his urine. A man aged 68 years was known to have coronary stents; his death was presumed to have been due to coronary disease and a full autopsy was not performed. Post-resuscitation ECG revealed prolonged QTc interval in a man aged 44 years whose initial cardiac rhythm was ventricular fibrillation. A woman aged 38 years had acute myocarditis. All individuals had pulmonary oedema. 
 
 We identified 58 deaths during the time period of the review, of which 42 (72.4%) occurred during the swim ( tables 1 and 2 ). A total of 23 medical examiner reports were obtained and reviewed. There were 19 men and 4 women ( table 3 ). The age distribution of the population of individuals for whom medical examiner report was available did not differ from the total population of swimming deaths ( table 4 , χ 2 =1.274, p=0.74). Further details are provided in table 5 and the online supplementary file . 
 
 Discussion 
 
 Albeit the probability of death during a triathlon is low, when occurring in a highly publicised event it inevitably raises a great deal of public concern about the sport's safety. This impelled the largest North American triathlon organisation to initiate an inquiry into triathlon deaths.22 ,23 Unfortunately, good data are difficult to obtain and hence specific screening or aftercare recommendations could not be made. The current investigation was performed to test the hypothesis that, when compared with triathletes and the general population, individuals who died swimming during a triathlon or in training have a higher prevalence of cardiac anomalies that predispose to IPO. 
 
 IPO and its causes Water immersion causes blood redistribution from the periphery to the heart and pulmonary vessels, causing an increase in central blood volume and pulmonary vascular pressures.24 This can be extreme and precipitate pulmonary oedema in IPO-susceptible individuals, even in those without any obvious comorbidities.25 The effect is augmented—especially during exercise—in cold versus warm water.26 Those triathletes susceptible to IPO are therefore believed to have abnormal myocardial diastolic compliance (lusitropy)—or stiff hearts. Abnormal LV diastolic compliance is partly responsible for elevated LV end-diastolic pressure during exercise in patients suffering from heart failure with preserved ejection fraction (HFpEF).27 IPO seems to be a form of HFpEF precipitated by increased preload due to immersion with heavy exertion. In the initial publication of IPO, a number of individuals exhibited a hypertensive response to cold exposure; thus, it is plausible that they had LVH.12 In a recent review of published cases, nearly 50% of published civilian IPO cases had identifiable predisposing factors, and most were cardiac.15 The association of IPO susceptibility with LVH and risk factors for LVH12–15 strongly implicates abnormal LV diastolic compliance. Since most sudden deaths occur during the swim portion of the triathlon, it is certainly plausible that IPO is a cause. IPO tends to occur in susceptible individuals most frequently in cold water, and often during heavy exertion.12 ,28–30 Typical IPO symptoms—cough productive of pink frothy or blood-tinged secretions occurring during a swim—have been reported by 1.4% of triathletes,31 and in 1.8–60% during 2.4–3.6 km open sea swimming trials in young, fit naval recruits.29 ,32 The prevalence of LVH in the general population is estimated to be 12–21%.33 ,34 In well-trained triathletes, LV dimensions are usually within the normal range for the general population.19 ,35 ,36 In a group of 235 triathletes (168 men, 67 women) participating in the Hawaii Ironman Triathlon from 1985 to 1995, the overall prevalence of LVH by echocardiography was 24% (LV mass >294 g in men, >198 g in women).19 Chronic, high-intensity exercise can also lead to LVH (athlete's heart); this was the most likely cause of the enlarged LV in most cases in the quoted series. Diastolic filling properties in athlete's heart under dry, resting conditions are normal;37 ,38 thus, it is unlikely that athlete's heart is a precipitating cause of IPO. LV thickness in athlete's heart very rarely exceeds 13 mm.39 ,40 In contrast, in the current series, a pathological cause of enlarged hearts was more prevalent, including extreme values of septal thickness and estimated LV mass (figure 1), significantly beyond the range expected from hypertrophy due to athlete's heart.36 ,39 ,41 Thus, diastolic filling properties were more likely to be abnormal. All autopsied cases in this series had pulmonary oedema, which is usually the end result from any attempt at cardiopulmonary resuscitation and water aspiration during terminal event. Thus, the existence of pulmonary oedema at autopsy provides little insight. 
 
 Possible causes of death in triathlons In some cases, cardiac anatomy at autopsy after a triathlon may occasionally provide clues to the cause of death.1 Of nine athletes autopsied after a triathlon-related death, only two had cardiac anomalies that could be construed as being a primary cause of death: one with Wolff-Parkinson-White syndrome, the other with a congenital coronary artery anomaly. On the other hand, six had LVH.1 IPO is a plausible cause of triathlon death, particularly since it has been suggested as one possible mechanism in the pathophysiology of drowning.4 In contrast, due to the rarity of IPO-related deaths and lack of known history of IPO in any triathlon death, some have concluded that it is an unlikely cause of death in triathletes.10 ,22 ,23 Nevertheless, several IPO-related deaths have been reported in other settings.42–47 Fatal cases of IPO may be rare but probably under-recognised; unless an episode is witnessed and survival is sufficiently long enough to obtain adequate clinical information to make the diagnosis, attribution of an in-water death to IPO is exceedingly difficult.48 It is impossible to exclude primary arrhythmia as the cause of death in these individuals. Indeed, it has been proposed that cardiomegaly is an independent risk factor for cardiac arrhythmia.35 ,49–51 However, in a series of cardiac arrests during long-distance runs (where diagnostic facilities are more likely to be available and thus early detection of an arrhythmia more likely), primary arrhythmia was the purported cause in only a minority of instances. Non-ischaemic ventricular tachycardia was observed in only 7%, with ‘presumed arrhythmia’ the attributed cause in an additional 7%.3 One individual in our series had a history of atrial fibrillation and was taking an antiarrhythmic. It is not possible to know whether his propensity towards atrial arrhythmias contributed to his death; however, any rhythm other than sinus rhythm is likely to cause a rise in pulmonary artery and capillary pressures in the face of increased preload as occurs during immersion. In fact, atrial fibrillation has been proposed as a predisposing condition for IPO.52 In another case in the present series, prolonged QTc was noted after resuscitation. Swimming can be a trigger for arrhythmias in long QTc syndrome;53 however, prolonged QTc could also be secondary to antiarrhythmic drug administration after cardiopulmonary resuscitation or the cardiac injury itself. Information about genetic predisposition was unavailable. On the other hand, additional information from bystanders and others suggests that at least some of the deaths in the current series were not sudden and had features consistent with IPO (eg, cases 2, 10, 23 in the online supplementary material). It might also be argued that demand ischaemia might be more likely during swimming, even in those with minimal coronary narrowing, because of the central redistribution of blood and higher LV volume. For a given level of exercise, this might lead to greater myocardial wall tension and myocardial oxygen consumption compared to dry land. However, in patients with known CAD, a study of swimming in cold water versus cycling demonstrated that ST segment depression occurred at similar levels of exercise during both activities.54 The distribution of cardiac pathologies in this series is in marked contrast with other similar studies: in younger cohorts of sudden death cases, myocarditis, hypertrophic cardiomyopathy (HCM) and coronary artery abnormalities are more common.55 In case series with age distribution similar to the current series, atherosclerotic disease predominates.56 ,57 Of those in our cohort in whom coronary arteries were mentioned in the medical examiner's report, only four individuals had ≥70% coronary narrowing; six individuals had ≥50% narrowing. One additional person who did not have an autopsy but had coronary artery stents was presumed to have ≥50% narrowing. Whereas HCM is a common cause of sudden cardiac death in most series of land-based athletic events, no mention of it was made in any of the medical examiner reports in this series. While it can be difficult to distinguish HCM from undifferentiated LVH at autopsy,58 the apparent lack of HCM in this series is consistent with the physiology of swimming: blood redistribution during immersion dilates the LV and thus reduces the likelihood of LV outflow obstruction even when present. 
 
 Limitations There are several limitations to our study showing that markers of IPO susceptibility are common among victims of sudden death during triathlons. It cannot be definitively concluded that the cause of death in individuals with LVH was IPO. IPO has been considered by some to be an unlikely cause of triathlon death due to lack of prior history among victims. However, instances of IPO are most likely under-reported. Most triathletes train for the swim portion in pools, which are generally warmer than open bodies of water where events are held, and during a pool swim mild IPO symptoms can be relieved at an early stage by exiting the water. Primary arrhythmias cannot be excluded; indeed, it has been suggested that arrhythmias are more common among individuals with LVH.34 Among those classified as having no obvious cause of death, one (woman aged 38 years, see online supplementary case 3) had histologic evidence for acute myocarditis. Two others (man aged 57 years, see online supplementary case 6 and man aged 48 years, see online supplementary case 18) had 50–60% coronary stenosis. Although this degree of stenosis is not conventionally considered to be critical, the true degree of narrowing could have been underestimated at autopsy. Another (man aged 46 years, see online supplementary case 10) had no CAD but did have areas of myocardial fibrosis and chronic inflammation suggesting remote infarction. Finally, one case (man aged 43 years, see online supplementary case 12) had scattered intramural adipose and focal loose interstitial fibrous tissue. Although not identified as such by the examining pathologist, this could be consistent with arrhythmogenic right ventricular dysplasia. We cannot exclude the possibility that these individuals might have died of an arrhythmia. While there could be inconsistencies in attempting to compare LVH using echocardiography with heart mass determined at autopsy (table 6), we feel that gross errors are unlikely as echo has been validated against postmortem measurements.59 Among 775 sports-related sudden death cases during moderate-to-vigorous exertion among men and women, fewer deaths occur during swimming than cycling or jogging.60 This could be a consequence, in individuals at risk for athletic sudden death, of fewer person-hours spent swimming. However, in triathlons, a specific swimming-related mechanism for death would be expected to predominate where swimming is the first of three events. Nevertheless, observations demonstrating that IPO is relatively common in competitive swimming such as military training and triathlons—and has been the cause of deaths42–47—implicate this condition as a likely cause of at least some deaths in triathlons. It would have been ideal to compare autopsies of triathletes dying during the bicycle or run portions; however, this was not possible due to fewer of those deaths, with a significant proportion due to motor vehicle trauma. Interestingly, scuba diving is another precipitating activity for IPO; indeed, LVH has been observed in a high percentage of scuba diving deaths.61 ||||| Heart abnormalities linked to immersion pulmonary edema were present in a greater-than-expected proportion of triathletes who died during the competition's swim portion, according to a study led by researchers at Duke Health. 
 
 The findings, published Aug. 29 in the journal BMJ Open Sport & Exercise Medicine, are based on an analysis of autopsy reports of people who died in the United States and Canada between 2008 and 2015 while participating in triathlons. Triathlon competitions involve consecutive races of swimming, bicycling and running. 
 
 Study investigators identified 58 deaths during the time period, with 42 of those occurring during the swim. Researchers examined autopsy reports on 23 of the 42 deaths. 
 
 Richard Moon, M.D., the study's first author and a professor of anesthesiology and medicine at the Duke University School of Medicine, said he and co-investigators reviewed the autopsy reports to identify whether conditions were present that may have made the athletes susceptible to immersion pulmonary edema (IPE, in the study abbreviated as IPO based on the Greek spelling of oedema). 
 
 IPE, also known as swimming-induced pulmonary edema, occurs when the lungs suddenly fill with body fluids during activities in cold water, such as swimming and diving. IPE can lead to difficulty breathing, wheezing and confusion, which can be serious and even fatal. 
 
 While IPE can occur in healthy individuals, Moon said its onset is often seen in those with left ventricular hypertrophy (LVH), a condition where the heart muscle becomes thickened or heart mass increases. LVH typically occurs in people with high blood pressure and is a marker for susceptibility to IPE. A mildly enlarged heart -- commonly referred to as athlete's heart -- can also develop among endurance athletes, although athlete's heart is not believed to predispose to swimming-induced pulmonary edema. 
 
 Moon and co-researchers compared figures from the autopsy reports in the current study to data from previous studies, including one published in 1997 led by Pamela Douglas, M.D., professor of medicine at Duke. Douglas' investigation looked at the prevalence of LVH in 225 athletes who completed a triathlon in Hawaii from 1985-95. 
 
 "Among the autopsy reports of the deceased triathletes, we found a much higher prevalence of LVH than the healthy athletes in Dr. Douglas' study," Moon said. "The degree of enlargement was also much greater in the triathletes who died." 
 
 Specifically, the 16 triathletes who died from unclear causes had higher measures of heart wall thickness. The autopsy reports showed abnormal cardiac septal thickness in 67 percent of the deceased athletes and abnormal posterior wall thickness in 50 percent. In the Douglas study, it was one percent and one-half percent, respectively. 
 
 While it cannot be definitively concluded that IPE was the cause of the triathlete deaths during swimming, Moon said the autopsy reports demonstrate a plausible link. He recommended that potential triathletes and their health-care providers be aware of the known connection between LVH and the potential risk of immersion pulmonary edema. 
 
 "The message is that if people have untreated hypertension or they're known to have ventricular hypertrophy, they need to get evaluated and treated before they embark on this sport," Moon said. 
 
 ### 
 
 In addition to Moon, study authors include Stefanie D. Martina and Drs. Dionne F. Peacher and William E. Kraus of Duke. 
 
 The study was funded by the U.S. Naval Sea Systems Command (N0463A-07-C-0002 and N61331-03-C-0015). The authors report no disclosures.
– Researchers believe they may know why so many people die during triathlons compared to other races, such as marathons. Approximately 1.5 people die out of every 100,000 who participate in a triathlon—which includes running, biking, and swimming portions, LiveScience reports. That's two to three times the death rate for marathon participants. According to a study published Monday in BMJ Open Sport & Exercise Medicine, more than 72% of triathlon deaths looked at by researchers happened in the water during the swimming portion of the race. And researchers believe the culprit is something called immersion pulmonary edema, or IPE. IPE occurs when a person quickly gets into water, especially cold water. That causes the body to take blood from the arms, legs, and other extremities and move it toward the core. This changes the body's internal pressure and may force fluids from the blood into the lungs. This can cause people to experience confusion and difficulty breathing, sometimes to the point of death, according to a press release. A number of triathletes who died for no discernible reason had significantly enlarged hearts, even to a greater degree than other athletes. Researchers say this condition—left ventricular hypertrophy—is a risk factor for IPE. Researchers conclude future triathletes should be checked for the condition before participating in or training for a race. (A boy with cerebral palsy inspires in triathlon finish.)