Introduction

Ironman triathlons were first undertaken in Hawaii 36 years ago, and consist of a continuous 2.4 mile swim, 112 mile cycle and a marathon-length run. These three events all occur in one day, therefore making it one of the most difficult sporting events in the world1. As a result of training for and partaking in aerobic endurance events, such as marathons, cross-country skiing, triathlons and ironman triathlons, the heart can undergo changes which enable it to elevate cardiac output for prolonged periods of time. These changes include both structural remodelling of the chambers and production of cardiac biomarkers2.

Recently, there has been increased interest in these kinds of extreme competitions due to so-called ‘super fit’ athletes dying prematurely, for example the ‘ultrarunner’ Micah True, who died aged 58 whilst on a long-distance run in a forest in New Mexico3. Cardiologist Dr James O'Keefe's TEDx talk and review article4, 5 discuss this issue, suggesting athletes should cut back on the amount of intense endurance events they partake in. He contends there is a maximum amount of exercise that is beneficial, after which it has a detrimental long term effect on the body.

This WordPress will look into these claims, discovering how many athletes are actually dying as a result of the sporting practices and patterns, and whether it is justified to recommend a maximum exercise dosage.

Aims and Objectives

1. The main aim of our project was to find evidence which discusses whether long term participation in extreme, endurance sports (like iron-man triathlons) is overall beneficial or detrimental to the cardiovascular system.

2. To find out if there is sufficient evidence that supports an optimal exercise threshold

3. To develop our understandings of the benefits of exercise and the risk factors  that could lead to long-term cardiovascular health problems.

4. To learn to critically appraise articles and decide what information is useful and can be applied to our research

5. To critically appraise a paper as a group

This site was made by a group (Author's Contributions page) of University of Edinburgh medical students who studied this subject over 10 weeks as part of the SSC (SSC web pages).

This website has not been peer reviewed.

We certify that this website is our own work and that we have authorisation to use all the content (e.g. figures / images) used in this website

We would like to thank Dr Rob Sutherland for his help and guidance with this project.

Total Website Word Count (including all appendices):

Word Count (minus contribution page, references page, Critical Appraisal Appendix, Information Search Report and other sections clearly marked as Appendices):

The benefits of Exercise

The claim that regular physical activity improves health and disease is well supported [6,7,8]. Through the use of many study and review articles we have gathered enough evidence to establish a strong link between exercise and improved mental and physical health. Stroke and coronary heart disease (CHD) are two notable diseases in which a change in lifestyle can have a huge impact. Moreover there is evidence to show that exercise can reduce mortality and morbidity among all ages, as well as body weight.

Prevention of heart problems

Exercise plays an important role in the prevention of CHD and stroke as it helps to combat raised blood cholesterol and high arterial blood pressure. The American College of Medicine has supported the theory that even brisk walking everyday will have a positive effect on the cardiovascular system.

[6] This particular study has also highlighted the improvements exercise has on hypertension. It found that adults with mild, moderate or labile systemic arterial hypertension who undertook regular physical activity had decreased systolic and diastolic blood pressure. However a larger sample size would be required to fully support these findings.[6]

One final thing this study recognised was that exercise will increase a patients general capacity for physical work as it reduces the work therefore the stress load on the heart. This means a reduction in blood pressure and reduces the likelihood of myocardial infarction. On top of this the maximum myocardial performance will further increase thus allowing you to do more exercise and maintain a training regime.[6] Further, vigorous exercise can leads to physical changes of the heart, grouped under the term “athletes heart. ” Another study looks at the effects of exercise on cardiovascular disease. In this study were 936 woman undergoing coronary angiography for suspected myocardial ischemia. The results from the study show that higher physical fitness scores were significantly associated with fewer coronary artery disease risk factors, less angiographic coronary artery disease, as well as heavily reduced risk for any other adverse cardiovascular event.[6] The results from this study have been supported by many other large scale studies that provide support for the notion that exercise has a significant effect on mortality and myocardial ischemia incidence.

 

Adapted from P H Fentem . Benefits of Exercise in Health and Disease . ABC of Sports Medicine 1994; 308(): 1291-1295 [6]

BMI exercise and physical functioning

A large scale study in America investigated the relationship between overall health and exercise regime. 7867 peoples aged from 51 to 61 between the years of 1992 and 1996 were investigated in a longitudinal study. Adjusted relative risk for health decline and new physical activities were determined with logistic regression. All levels of no job related physical activity were associated with a lower risk of decline in overall health compared to the control group who did very little exercise.[7] The speed at which the subject's overall health declined decreased from 20.8%[7]  among those who never did light exercise to 8.4% in those who did a little exercise. Decline in overall health was 30% lower for individuals who performed light exercise, however the benefits were similar no matter it was carried out. The rates of developing new physical difficulties decreased from 28.2% to 16.9% [7] for those who did a little physical exercise at least 3 times a week.  [7] In terms of vigorous exercise which was categorised as running, cycling or swimming [7] , the results were much more prominent. Individuals who participated in vigorous exercise at least 3 times a week experienced a drop in decline from 22.2% to 12% [7] . Comparative risks for developing a new mobility issue were 0.45 for obese individuals who performed vigorous exercise 1 or 2 times a week compared to 0.46 for those who did it 3 times or more per week. The results highlights that exercise of any form had a positive effect on overall health and physical functioning. A parallel cross sectional study reported that the likelihood of developing a physical difficulty could be reduced by half by a physically active occupation. [7]

Exercise helps reduce diabetes

Along with obesity physical activity of any form has been shown to reduce risks associated with type 2 diabetes and several studies have identified ethnic minorities at elevated risk. Findings suggest that engaging in some physical exercise such as leisure activities may have some benefits, however exercising at a higher intensity improves physical functioning and reduce blood glucose therefore reducing the risk of Non-insulin dependant diabetes

mellitis. Lab studies have shown that exercise can increase insulin sensitivity and improves glucose tolerance which supports the findings in the study. [7]

Cancer

Several studies have evaluated the association amoung lifestyle factors such as physical activity and health related quality of life in cancer survivors. In a study of breast, colorectal and prostate cancer survivors, participants who engage in 30 minutes of moderately intense exercise at least 5 times a week reported significantly health related quality of life. These benefits were so significant that they surpassed the benefits or any modifications in your diet. [8]

Osteoporosis

Weight bearing exercise prevents osteoporosis so regular physical exercises is one of the best ways to prevent fractures as it increases the mineral content of bones thus making them stronger.

Mental health

There have been many studies carried out to show that physical activity helps to improve mood, depression and general mental wellbeing. One particular study looked at the effects of resistant training over a 24 week period in health older adults. Following the programme it was concluded that exercise caused a reduction in confusion, anger and tension, as well as improving general mood, with the adults having higher mood scores. [9] Furthermore it was discovered that even unusual methods of exercise such as African dancing can enhance mood and even self esteem in people. [8]

Sudden Death and Causation

Incidence of sudden death in endurance events such as marathons, half-marathons and triathlons has been extensively recorded  10-17. The occurrence of such deaths merits discussion over the safety of these events and whether the immediate risk to the individual could outweigh the aforementioned benefits of endurance training and exercise.

Marathons

A study of approximately four million marathon runners in the US found the risk of cardiac arrest to be 1.01 per 100,000 participants.17 With regard to actual sudden death, one large American study stated the risk per 100,000 participants to be around 0.75,18 with another at approximately 0.8.19 The size and concurrence of multiple studies18,19 improves the reliability of their results. Though there are studies which indicate a higher risk of sudden death,20 Redelmeier and Greenwald19 suggest this may be an overestimation due to their relatively small sample size.

Triathlons

A study by K.M.Harris et al., which investigated death in triathlons of varying lengths, found the risk of death to be 1.5 per 100,000 participants.11 Of a total 14 deaths across all triathlons, 13 occurred in the swimming segment.11 Many reasons are suggested to explain why almost all deaths in these triathlons occur during the swim. Clearly, there are unique practical issues here which hinder the identification of troubled swimmers and performance of CPR. It is suggested that some triathletes are not as suited to the swimming part; being both unpracticed at swimming in the presence of waves or crowds.1,11 Aside from the logistical, there are also underlying physiological mechanisms which can contribute to swimming deaths.1, 21-25  From literature on swimming deaths21,22,23there appear to be two opposing autonomic responses at play. Shattock and Tipton clarify these responses as the sympathetic ‘cold shock response’ and the parasympathetic ‘diving response.23 Such antagonism of these systems is postulated to account for the potentially fatal arrhythmias which can arise on swimming in cold water.23

Causation

Fatal health complications are very rare in recreational exercise.25 In young people (aged under 30), sudden deaths during recreational exercise are commonly due to congenital heart diseases. On the other hand, deaths in the over-thirties occur as a result of arterial hypertension, CHD and sequelae of cardio-metabolic syndrome.25 These patterns held true for participants of competitive endurance exercise.17 Deaths among older participants of US marathons / half-marathons were found more likely to be due to ischaemic heart disease whereas deaths among younger people were more likely to be due to hypertrophic cardiomyopathy.17 This finding also agrees with another

study which recorded that MI and atherosclerotic heart disease accounted for 93% of deaths in marathon participants over 45.18

Seen in figure No.1 are the causes of cardiac arrest for both survivors and non-survivors as adapted from Kim et al’s study.17

  

figure No.1 as adapted fromKim et al’s study.17

Spread of deaths:

Several studies have elucidated differences in spread of deaths along a marathons distance.17,19 As can be seen in figure No.2, deaths are more heavily distributed in the latter half of the race. With almost 50% of deaths occurring in the last mile of the race despite only representing less than 4% of the total distance.19 Other studies have reported similar findings such as Kim et al.’s study which found 78.6% of deaths occurred in the last quartile (20-26.2miles).17 This may be due to the increased physiological stress of longer races resulting, resulting increased chance of such cardiac event precipitating.17

figure No.2 as adapted from Redelmeier and Greenwald's study.19

CPR:

As indicated by studies on the London marathon and US marathons,  14,17 the performance of CPR and early defibrillation has a large impact on the survival of a cardiac arrest. In Kim et al.’s study, of those who survived a cardiac arrest, all received bystander-administered CPR.17 The initiation time of CPR greatly affected the outcome for the runner with average time of survivors being 1.5 minutes compared to 5.2 minutes in non-survivors.17  In contrast to survivors, only 43% of non-survivors received any bystander-administered CPR.17

Making defibrillators available is also an important aim for race organisers. Studies of the London Marathon found survival rates to be directly related to the speed of defibrillation from ventricular fibrillation, the most common heart arrhythmia in cardiac arrest.14 In comparison to others, The London Marathon appears to have a relatively high resuscitation rate of 50%.13 To meet the optimum chance for defibrillation of 2 minutes or less, defibrillators would be required every 300m, though the study stresses that the duty of care of organisers does not necessitate deployment of resources disproportionate to risk.14

Screening and Prevention:

As a first-line preventative measure it is prudent to first ensure participants are capable of participating in such demanding events. A swimming proficiency test has been suggested to combat some triathletes’ inexperience in cold, crowded open water.11 In more accessible events, there may be a role for physicians to exclude high risk runners – such as those with coronary artery disease16 – though this claim has insufficient evidence to merit limiting public participation at this stage.15

Second, numerous studies have questioned the efficacy of screening in excluding susceptible individuals.14+19 Low specificity generates false positives, perhaps causing these individuals to unnecessarily refrain from exercise or endure undue anxiety.14 Low sensitivity, on the other hand, may result in potentially life-threatening conditions slipping through the net.14+16 Therefore we believe screening is not yet a sufficiently effective preventative measure to be implemented universally.

Risk in context:

A US retrospective analysis study claims that the relative risk of death of marathon runners is smaller than risk of motor fatality occurring, for the same roads and similar time intervals.19 Such estimates places the risk within the realms of everyday activities as also indicated by a UK study.13 Risk of deaths are low even compared to other athletic populations such as in collegiate athletics or jogging.17  A UK study argues that even in light of events of sudden death, unseen from the public eye are potentially “thousands of runners who are postponing or preventing their heart disease” through their training for such an event.13

The benefits of exercise are well promoted, however an untrue lay understanding, popularised by running gurus such as James Fixx and Dr Tom Bassler, is that marathon runners are immune to coronary heart disease, an idea which has been largely discredited.15 Deaths in athletes clearly do occur, such as that of Phiddipidees26 and of Micah True.3 Such beliefs, are postulated to potentially lead to a dangerous denial in symptoms,15 and athletes “should not ignore untoward symptoms.”16

Conclusion:

Although the concept of risk can be difficult to present as a public health message, there is a very low risk of sudden death associated with extreme endurance exercise.10-17 Given the huge 30% reduction of risk of all causes of death as a result of regular exercise for any age or gender,27 it would appear that living a sedentary lifestyle is far more dangerous in the long run than participating in even extreme endurance events.

Cardiac Damage and Remodelling

In their attempts to establish the long term effects of endurance exercise, many studies investigated biochemical markers of cardiac damage. Though many markers were recorded and analysed, authors were particularly interested in Cardiac Troponin T (CT-T). CT-T is a chemical which leaks out of cardiac myocytes when they are damaged, for example in ischaemic necrosis28. In a myocardial infarction, CT-T levels are found to rise up to twelve hours after and then drop anywhere from five to fourteen days after the actual infarction incident29,30.

In James O’Keefe’s review5, he cites the temporarily raised CT-T in half of marathon runners during and after the event as evidence that continued ultra-endurance exercise causes myocardial cell damage “at the sites of myocyte slippage of one cell along another due to loss of integrity of desmosomal connection”.

Many primary studies give similar results and conclusions to O’Keefe with regard to CT-T. One paper published in the British Journal of Sports Medicine in 2006 found small significant changes in CT-T levels in participants of the 2001 Australian Ironman triathlon. In a clinical context such CT-T changes may represent ischaemic heart damage, however their significance in these athletes  is unclear.31

Interestingly, the study details the “biphasic pattern” of CT-T release – the first peak caused by cytoplasmic CT-T released when the myocyte cell membrane is destabilised (reversible), and the second due to disintegration of the entire structure’s contractile ability (irreversible). Further research to establish the contribution of each phase to overall CT-T release is vital to understand the

link between CT-T and permanent cardiac damage, and the extent to which the changes that occur are pathological.

Though most papers showed significant changes in CT-T, various conclusions were drawn from the results. A paper published in the Journal of the American college of Cardiology (JACC) challenged the view that the release of CT-T is a certain indicator of cardiac necrosis32. Instead, they propose that CT-T changes represent reversible cardiomyocyte membrane damage that is part of the remodelling process that an athletic heart undergoes. It states a need for distinguishing between the aforementioned clinical presentation of raised CT-T (an MI) and this athletic appearance. Once more, establishing the mechanism and timing of CT-T release is essential to accurately assessing the validity of this paper’s conclusion.

One study, by G. Whyte et al., notably found insignificant CT-T alterations in their participants, opining that the changes did not resemble those seen after a myocardial infarction.32 The paper also studied the structure of the heart and investigated whether there were any changes in several different dimensional measures of the chambers of the heart, including IVSd (intraventricular septal width during diastole), LVIDd (left ventricular internal dimension during diastole) and LVPWd (Left ventricular posterior wall during diastole). The study found no significant dimensional changes, suggesting that even if ultra-endurance exercise causes changes at the cellular level of the heart, it has no effect on its ventricular structure.

Although Whyte’s32 study suggests there are no changes to LV size, most studies seem to suggest that there are in fact alterations to left atrial (LA) diameter, and this may cause the long term cardiovascular problems33,34. This is due to the structural adaptations that occur to the heart as a result of long-term, aerobic exercise. Left atrial enlargement allows an increased cardiac output for longer periods of time to meet the demands of high dynamic sports such as long distance running and cycling35. The effects of these modifications are shown on an ECG. Sinus bradycardia appears, as well as increased QRS voltage, to give a slower yet more forceful contraction35.

 

Despite these alterations having a positive effect on the athlete’s ability to carry out intense aerobic exercise, there is potential for them to have a long-term negative effect on the heart - namely causing lone atrial fibrillation (LAF)33,34,35,36. Many studies agree that there is a correlation between LA enlargement and increased risk of developing LAF. Although there was no control group for comparison in Grimsmo’s 28-30 year follow-up study into cross-country skiers34, the skiers presenting with LAF had a larger LA diameter than those who did not have the condition, with a positive correlation between increasing LA diameter and LAF of 0.41. These results are in agreement with Molina’s 200836 follow- up study, which looks at the incidence of LAF in a group of marathon runners compared to a sedentary control group.  It split the marathon group up into those with and without LAF, allowing comparison between the two. Although there were only 9 participants with LAF compared to 174 without, there was a statistically significant association between increased LA inferosuperior diameter and higher risk of incident LAF. This is a result of long-term pressure and volume overload in the atrium causing it to stretch, leading to myocyte hypertrophy. This process is thought to trigger the development of LAF in certain individuals37.

Although these structural changes are fairly common in athletes who have participated in long term aerobic exercise, not everyone develops LAF. In Wilhelm’s study on cardiac remodelling in non-elite marathon runners33 57% of those who had participated in 1-5 marathons in their lifetime had enlarged LA, which increased to 74% in those who had run in over 6 marathons. These percentages were based on defined ranges for LA enlargement - when LA volume index >29ml/m2. Yet only 2% and 5% of the group who had competed in 1-5 marathons and 6 marathons respectively had actually developed LAF based on their history. This is in agreement with other studies; structural changes are common in all athletes, but only a small proportion of these go on to develop LAF36.

Long term Outcomes

Exercise is said to have positive effects on health and is thought to lower a variety of risk factors. There is debate as to whether these benefits remain with long-term vigorous exercise. Does exercise translate to an overall mortality reduction, or do morbidities arise?

Increased Life Expectancy

Kettunen et al found that elite athletes achieved 5-6 years additional life expectancy over the control group(38). The case population consisted of male Finnish athletes who had competed at international level between 1920 and 1965 (n=2675), with an average follow-up of 50 years. They were categorized into endurance, team and power sport athletes to allow for more event specific analysis. The control group consisted of Finnish men who were declared healthy (military class A1) at age 20 (n= 1712). This excluded possible control subjects with early onset chronic conditions who might confound the results. The compulsory nature of this military health assessment also helped to minimize any selection bias. Moreover, controls were matched for socioeconomic status and birth cohort with the athlete population. The matching of controls for some team and power sport athletes was incomplete in the original study(39), and therefore results regarding endurance athletes will be of most interest to us. Median life expectancy was calculated by the Kaplan-Meier method, and Cox proportional hazard model analysis used for hazard ratios (HR). HR, adjusted for socioeconomic status and birth cohort, were significantly lower in endurance athletes (HR=0.70 (0.61 to 0.79) 95% confidence limits, p<0.05). This trend held true for disease-specific mortality, as endurance athletes were better off for ischemic heart disease (HR=0.68), cancer (HR=0.62) and stroke (HR=0.52).

Of particular interest to our review was the finding that the same proportion of endurance athletes as controls died from IHD (20.4% to 19.3%), but that the mean survival age for athletes was 72.4 years compared to 67.4 years. Therefore, this study suggests that elite athletes die from the same causes as the healthy general population, and in the same proportions; they simply live an additional 5-6 years on average. This finding was consistent with a large case-control study conducted by Marijon et al, in which 41% lower mortality was observed in French Tour de France participants(40).

The major limiting factor in both papers was the possible selection bias in studying healthy elite athletes, and the presence of unadjusted for confounding factors. Lower smoking rates, a heavily selected for genetic profile and the maintenance of an active lifestyle make it impossible to isolate the effect of long-term vigorous exercise alone.

Risk of Atrial Fibrillation

Research(41) suggests that long-term vigorous exercise is linked to the development of atrial fibrillation. This is of particular significance due to the absence of other cardiovascular risk factors in the former elite athletes under investigation. Baldesberger et al conducted a 30 – 50 year case-control study of 62 male former Tour de Suisse cyclists and 62 male leisure-time golfers. At the end of the follow-up, they found that atrial fibrillation was more prevalent among the former athletes than the controls. 6 of the 62 male former athletes developed atrial fibrillation, compared with 0 of the 62 controls (P = 0.028). The study group was matched for age, BMI, hypertension and current hours of physical training, but the researchers failed to match the study group for levels of smoking. Controls smoked significantly more than the former athletes. Therefore, smoking was a confounding factor that could be investigated to assess whether or not it provided a protective effect against atrial fibrillation. Also, a high percentage (77%) of the former athletes admitted to the use of performance enhancing agents, which could be a contributing factor to the development of atrial fibrillation.

The proposal that the incidence of atrial fibrillation increases with age is supported by data found in the study by Grimmso et al following cross-country skiers over 28 – 30 years(42).

Maximum Dose

Public health agencies and researchers have sought to better understand the relationship between exercise and the health benefits it provides. This has led to the hypothesis of an exercise threshold, based upon activity duration, frequency and intensity, and the pursuit of a dose-response curve.

The Copenhagen City Heart Study(43) comprised 17,589 participants in a prospective study to investigate the association between jogging and all-cause mortality in men and women. HR for increasing duration of exercise were adjusted for confounding factors and plotted to produce a U-shaped curve for mortality risk. The data suggests that 1 – 2.4 hours of slow or average paced jogging per week is associated with the lowest mortality. Crucially, joggers had a lower mortality than non-joggers, irrespective of duration and intensity.

Wen et al(44) produced a large-scale prospective cohort study to investigate the minimum amount of physical activity that would provide health benefits. 416175 men and women in Taiwan reported their weekly-exercise volume in a self-administered questionnaire, and were allocated into 5 categories based on exercise volume. Metabolic equivalent values were used to quantify exercise volume, where 1MET = 1 kcal per hour per kg of bodyweight. The categories were assigned an MET of 2.5 for light, 4.5 moderate, 6.5 medium-vigorous, and 8.5 for high-vigorous exercise. The study adjusted for 13 pre-specified confounding factors and tested the reliability of the data by comparing it to the Spearman’s correlation tested in the same period. They found that all-cause hazard ratios had a negative correlation with increasing activity level, refuting the validity of a U-shaped curve. Moreover, a threshold, rather than a U-shaped curve, appears at around 50 minutes of vigorous exercise a day. This suggests a substantially higher amount of vigorous exercise is beneficial than the modest 1-2.4 hours of jogging recommended by the Copenhagen City Heart Study.

These papers come to contrasting conclusions, making it difficult to prescribe an optimum exercise dose. On the one hand, the Copenhagen study suggests an optimum range, whereas the Taiwan study suggests a threshold at which benefits of increasing exercise plateau, and after which further effects are unknown. Unfortunately, there was no standard measurement for exercise

volume, strongly limiting the validity of any comparison. Further research using an agreed definition of exercise intensity is required in order to establish the optimum range of exercise from a public health perspective.

Conclusion

We set ourselves the task of determining whether by participating in extreme endurance exercise, such as ironman triathlons, one is running away from or towards ‘the grim reaper’. To explore this, we answered the following questions:

Is the work of the heart during extreme endurance exercise beneficial or detrimental?There can be no doubt that exercise is generally beneficial to health6, 7, 8. The risk of stroke, cancer, coronary heart disease and many other diseases is significantly reduced by exercise and also has a positive effect on mental health8,9.

On the other hand, intense endurance exercise causes release of cardiac troponin T, suggesting myocardial damage was suffered5. However, in the case of exercise, it is inconclusive whether CT-T is a marker of pathology, or simply the physiological remodelling of an athlete’s heart31.

A significant correlation does exist between long-term vigorous exercise and the structural enlargement of the left atrium33,34. There is sufficient evidence that this predisposes susceptible individuals to develop lone atrial fibrillation33,34,36. However, the absolute risk of developing atrial fibrillation remains low33,36.

Is long-term vigorous exercise the key to a longer life, or an early grave?There is no doubt that deaths can occur as a result of participating in endurance events. Nevertheless, the fact remains that less than 1 in 100,000 runners die while participating in a marathon19.

Moreover, elite athletes boast increased life expectancy and significantly reduced mortality from heart disease, stroke and cancer, suggesting their exercise history is protective [38] Indeed, the only clear evidence we found that long-term vigorous exercise is disadvantageous was the increased incidence of atrial fibrillation [40]

LimitationsOne obstacle was the absence of a universal definition of what constituted long-term vigorous exercise, making comparisons across our wide range of research difficult.

The study populations investigated were disproportionately male, limiting the applicability of our conclusions for the female population.

Athletes demonstrated healthier lifestyles overall – their rates of smoking were lower, they maintained an active lifestyle, and they were likely to have a favourable genetic profile8. These confounding factors limit our ability to isolate the contribution of intense exercise to the greater life expectancy observed.

There is huge potential for investigation into the genetic profiles of elite athletes, so as to elucidate the factors behind both their exceptional fitness and any susceptibility to health conditions.

Ironman triathletes were initially suggested as a study population to allow the focussed examination of extreme endurance exercise. However, given how recently ironman triathlons were established29, there is a lack of research available. Thus, we widened the scope of our study to include other high-intensity endurance events. We contend our conclusions are valid insofar as the current research permits.

Further ResearchFuture papers should focus on:

Understanding CT-T release at the cellular level in order to establish its contribution to cardiac damage in long-term exercise.

The influence of biological differences between men and women. Ironman triathlons, to understand the health implications of long-term

participation in one of the most demanding endurance events in the world. Comparing extreme endurance athletes to an additional study population

of moderate This would allow for investigation of whether the increases in life expectancy begin to plateau, and/or damage occurs, above an optimum exercise threshold.

Clinical RecommendationsWe support the following proposed measures be taken to reduce sudden deaths in extreme endurance events:

Implement a swimming proficiency test to combat some triathletes’ inexperience in cold, crowded open water11

Prioritise resuscitation over screening in resource allocation19

Develop more specific, cost-effective screening methods19

Increase clinical awareness of conditions associated with endurance exercise, such as hypertrophic cardiomyopathy17

Promote safety in the swimming section of triathlons by adding rest platforms.

Potentially exclude high risk runners, such as those with coronary artery disease15

Public HealthMedia furore surrounding deaths in marathons and other events in the public eye has continually prompted re-evaluation of the question “to what extent is exercise good for you?”

Ultimately, the benefits of exercise outweigh the risk6. We acknowledge that the chance of cardiac arrest is temporarily elevated during exercise10, and that, if you are susceptible, a lifetime of endurance exercise may lead to the development of AF34, 36. However, the alternative – leading a sedentary lifestyle – is a risk you cannot afford to take 27

Furthermore, the aforementioned risks are likely to be given disproportionate significance by the general public to justify reticence towards exercise.

Redelmeier encapsulates this problem perfectly when he writes that, in the public psyche, “Losses loom larger than the corresponding gains19.

Thus, we believe that while information must never be withheld, it is a responsible course of action to downplay the risks of extreme exercise in order to nurture a positive societal attitude towards habitual exercise.

Reconciling this with the priority of fostering a culture of trust between the public and the medical profession is the essence of good public health practice

Critical Appraisal

AimTo investigate life expectancy and mortality among former elite athletes and controls.

Study DesignIt is a case-control study with 50 years follow-up, based on the 1993 paper ‘Increased life expectancy of world class male athletes’ by Sarna S et al.

Study PopulationMale former athletes who had represented Finland between 1920 and 1965 at least once in international competitions (n=2675). The athletes were sub-divided into three categories based on the nature of their sport: endurance (long and middle distance running, cross-country skiing); team and power (including boxing and weightlifting).

Control PopulationControls consisted of Finnish men declared healthy at age 20 (Class A1) in a military health assessment. The controls were matched for the same age cohort and area of residence as the athletes (n=1712).

Statistical Tests

The Kaplan-Meier method was used to calculate median life expectancy and 95% confidence limits.

Hazard ratios (HR) were determined by Cox proportional hazard models. HR included were non-adjusted; adjusted for different sports and the control group, and those adjusted for birth cohort and/or socioeconomic status.

These corresponded to the appropriate outcome measures of median life expectancy and HR.

Results117 men were lost from the study due to uncertain birth or death data - final n=4019.

During the average 50 year follow-up, 67.1% of athletes and 70.5% of controls died.

Median life expectancy for endurance (79.1 years, 95% CI 76.6 to 80.6), team (78.8 years, 95% CI 78.1 to 79.8), and power (75.6 years, 95% CI 74.0 to 76.5) athletes were higher than controls (72.9 years, 95% CI 71.8 to 74.3).

All-cause mortality HR adjusted for socioeconomic status and birth cohort were 0.70 for endurance (p<0.05) and 0.80 for team sport athletes (p<0.05), compared to controls.

Endurance athletes had notably lower disease-specific mortality adjusted HR for ischaemic heart disease (0.68), cancer (0.62) and stroke (0.52), as did team sport athletes (0.73, 0.72, 0.59 respectively).

BiasCause-of-death data from national registries enabled differentiation between sport-specific and disease-specific mortalities, reducing selection bias. Moreover, few missing causes meant comprehensive data on participants was available . By selecting men who were declared healthy at age 20, those with early-onset chronic conditions were eliminated. This created a control group more favourable than the general population.

However, the study acknowledges some selection bias may exist, as elite athletes are likely to present as healthy given the competitive nature of sport. Their health and fitness will have been heavily selected for in the process of reaching top-level performance.

Confounding Factors 

The original study issued a questionnaire in 1985 to both populations, achieving response rates of over 80%. 60% of the former athletes who responded reported maintaining an active lifestyle in adulthood, compared to 17% of controls. Furthermore, 17% of cancer deaths among athletes were smoking related in comparison to 32.3% in controls. Neither active lifestyles nor smoking rates were adjusted for so they remain major confounding factors.

CommentsThis was a well-executed study that met its aims through appropriate study design, statistical analysis and outcome measurements. Their results are supported by the 2012 study ‘Mortality of French participants in the Tour de France (1947-2012)’, which observed greater life expectancy among athletes compared to controls randomly selected from the general population.

Their conclusion that “elite athletes have 5-6 years additional life expectancy compared to men who were healthy” appears justified. However, they acknowledge that conclusions specific to the effect of long-term vigorous exercise cannot be extrapolated from their results.

ConclusionThis study gives an excellent statistical analysis of increased life expectancy in world-class athletes, with a large sample size significantly decreasing the effects of chance on the results.

Information Search Report

Our first introduction to the topic was watching James O’Keefe’s TED talk ‘Run for your life! At a comfortable pace and not too far’, which discusses the structural and biological changes to the heart as a result of chronic competing in extreme endurance events, and reading his review article which accompanies the talk[4,5]. 

.From this we looked into some of the papers referenced in the talk and looked for other articles which discussed the adverse effects of excessive endurance exercise. We used websites such as ‘Medline’ and ‘SPORTDiscus with Full Text’ which were of particular use as multiple searches could be combined to find more specific articles that covered a number of topics. For example, when searching on Medline for articles about the occurrence of atrial fibrillation amongst people who have previously competed in intense aerobic exercise, the subject heading ‘atrial fibrillation’ is searched, with all subheading included. Then the term ‘endurance exercise’ is searched, which is covered under the subject heading ‘physical endurance’, including all subheadings. Then, on the search history, these two can be selected and combined with ‘AND’, to produce articles that cover both topics.

We then split into pairs, each finding articles that covered one particular aim. Initially, it was useful to find review articles, as they gave a good overview of the topic, before researching for more specific studies. One way of doing this was by looking at the studies that the review articles referenced, and then looking at articles which cited those studies, using the ‘cited by’ option below the articles on Google Scholar. Sometimes, we did not have permission to access certain articles, but by using the University computers, this problem was normally overcome using the findit@:Edinburgh software which gives students access to journals that are typically subscription only.

Contributions

Anita Balaji researched into and contributed to the writing of the beneficial effects of exercise section. She also wrote the aims and objectives, after discussing it with the group, and edited the critical appraisal into the final draft that features on the website. She also did the final editing of the site.

Peter Eves looked into the long term outcomes of intense endurance exercise, and co-wrote this section. He also completed the critical appraisal since it was based on a paper which he found in his research.

 

David Henshall researched into the short-term effects of partaking in endurance events and wrote part of this section and did additional reading into other people’s papers, analysing and reviewing them.

 

Alice Horne researched into the cardiac structural remodelling that occurs as a result of endurance exercise. She also completed the information search report and wrote the final draft of the introduction.

 

Callum Innes also researched into and wrote the section on the beneficial effects of exercise. He also edited the critical appraisal, compiled the final reference list as well as organising meetings. He also did the final editing of the site.

 

Jack Irvine researched and wrote the section on long-term outcomes, and took a lead role in collating all the references together from each individual’s section into a final reference list.

 

Fergus Jones researched into and wrote part of the short-term effects section alongside David and formatted the website.

 

Fady Samy researched into and wrote the section on the chemical changes that occur to the heart as a result of participation in extreme endurance events. He also took a lead role in the editing of the whole website.

 Everyone contributed to the writing of the conclusion, and the editing and proof reading of the whole website.

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