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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 longdistance 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
2.
3.
4.
5.
long term participation in extreme, endurance sports (like iron-man
triathlons) is overall beneficial or detrimental to the cardiovascular system.
To find out if there is sufficient evidence that supports an optimal exercise
threshold
To develop our understandings of the benefits of exercise and the risk
factors that could lead to long-term cardiovascular health problems.
To learn to critically appraise articles and decide what information is useful
and can be applied to our research
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This website has not been peer reviewed.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, halfmarathons 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 (2026.2miles).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 ultraendurance 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 ultraendurance 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 longterm, 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 longterm 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 diseasespecific 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 allcause 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 mediumvigorous, and 8.5 for high-vigorous exercise. The study adjusted for 13 prespecified 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]
Limitations
One 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 highintensity endurance events. We contend our conclusions are valid insofar as
the current research permits.
Further Research
Future 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 Recommendations
We 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 Health
Media 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 exercise 10, 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 gains 19.
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
Aim
To investigate life expectancy and mortality among former elite athletes and
controls.
Study Design
It 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 Population
Male former athletes who had represented Finland between 1920 and 1965 at
least once in international competitions (n=2675). The athletes were subdivided 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 Population
Controls 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.
Results
117 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).
Bias
Cause-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.
Comments
This 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.
Conclusion
This 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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