I just thought I would share this question we were asked recently:
“Do you have any data on the incidence of AFib in people who say competed in the Tour de France in past years to see how the risks in this population compare with the public as a whole.”
There is no doubt that I see a lot of people with atrial fibrillation (AFib, AF). Most of the people I see are cyclists. And that makes me think that there is something about cycling that leads to AF. But, it could be a sampling error – all the people who get AF from other sports might go and see someone else. It doesn’t feel like that though. As I supervise the nurse led AF clinic. There are plenty of people who run too in Somerset – I only see a few of those.
Tour De France cyclists are an unusual breed. They may well be genetically different to you and I. Or at least me. And remember, at least (hopefully) until recent times, these riders were (probably) systematically doped. There were probably teams in France doping kids from the age of 11 (according to some of my French contacts), and many domestiques had to take drugs or be dropped. It started with amphetamines in the 1900s.
There are descriptions of arrhythmias in former cyclists (e.g. Europace. 2015 Mar;17(3):387. doi: 10.1093/europace/euu399. Epub 2015 Feb 12.); A left atrial tachycardia is often the start of AF. But, there are no systematic studies that I am aware of. Overall, however, being a TdF cyclist seems beneficial to health however – they seem to live longer at least. See Eur Heart J. 2013 Oct;34(40):3145-50. doi: 10.1093/eurheartj/eht347. Epub 2013 Sep 3 and Int J Sports Med. 2011 Aug;32(8):644-7. doi: 10.1055/s-0031-1271711. Epub 2011 May 26.
That doesn’t mean it’s the cycling though. It could be the diet, the genes, or even the drugs. We perceive drugs as harmful, but that doesn’t mean they are. When the stigma dies down, we should probably try them in the elderly. It might improve the quality of their life – sarcopenia (a loss of muscle) and a loss of cardiovascular fitness really hits the elderly hard in a variety of ways.
I’m afraid that endurance exercise does appear to predispose to AF – at least in men. The paradox is that those who exercise appear to live longer, which can get lost in all the concerns.
So AF may need to be reconsidered as one of those things that happens – like tendonitis, stress fractures and muscle strains (although a bit more serious, in my view).
If I don’t get AF this year, I’ll be doing the Dublin Marathon again in October.
I think most of us reflect on what we have achieved in the past year. For me, it’s been a mixed year with regards to exercise. I did my first sprint and Olympic distance triathlons. I completed my first marathon for 16 years (I only ran one before) – in just under 4 hours.
But I didn’t get my sub 20 minute 5K time. Close at 20:38. And my cycling went to pieces with the focus on running.
Just recently I spent some time looking at my run data on Crickles. Taking a few of the runs I plotted out the relationship between heart rate, speed and gradient. It’s a bit messy (although I have some ideas to tidy that), but the curve/surface is quite interesting. I plotted the curves initially to help statistically create a normal range for my running conditions, with a longer term view to help track abnormal heart rates for a given situation.
I then limited the curve to gradients of +/- 2 degrees gradient initially. And I was struck by what it showed, but not entirely surprised.
As I start to run my heart rate speeds up. No great insights there. There is then a plateau until just over 11Km/h. That fits with what I experience. I know from my Garmin that up to 11-11.5Km/h I can sustain. It’s comfortable. My legs wear out first.
Go too much above that speed and everything becomes harder. That is my lactate threshold for running. That’s where the pain starts and I have to breathe harder to clear the carbon dioxide generated by lactic acid in the muscles from my system. They have to work anaerobically at these sorts of speeds.
The curve kicks up again just over 14Km/h. That’s the respiratory compensation point. Beyond that I can’t clear the lactic acid from my system by breathing and I am on borrowed time.
And that is why I can’t do a 5K in under 20 minutes yet. Sometimes you hit psychological blocks as a runner. I have watched my son streak away in the last few months having joined a running club. He was stuck, probably because of his brain, but his heart rate data suggested he could run much faster. And they unlocked that speed in him. But I am stuck by physiology at the moment.
So, I’ll be sprinting and running up hills in the new year. And working on some algorithms to track my progress. My Garmin says I can do sub 20. I know I can’t. Yet.
Have a great Xmas. And good luck for 2018.
Let us know your goals and what you want to see from the site.
I have updated this post now. Previously I just attached the word file – time constraints. But today I have some time, so here goes. As far as I can tell, this is the most complete analysis of the data that exists to date.
A search using the term “Marathon” and “Death” or “Mortality” on Pubmed yielded 167 references (most recently performed 20/10/17). The abstracts of these were reviewed. The reference lists of the final articles included in this paper were scanned for further relevant literature and review articles were obtained and read and their reference lists reviewed. On-line web searches and direct approaches to authors were made to provide additional data.
The End-Note library can be found here. It does not include the texts of some of the papers which were behind pay-walls.
A total of 8 papers were included in the final analysis. The papers can be divided into two categories. The first category comprises a series of papers which looked broadly at hundreds of marathons run across the USA over the past 40 years. The second category comprises a number of papers that have focused on two marathons in the USA – The Marine Corps Marathon and the Twin Cities Marathon – and also the London Marathon.
I have not included results relevant to half marathons or ultra-marathons or other events, such as triathlons, except where indicated in the text. Furthermore, I have not included mortality from marathons run as part of an event, such as a triathlon.
There have been a number of efforts to collect data from a larger number of marathons that have been staged across America. It is probable that the data from these papers overlaps. Furthermore, it is more likely that deaths will be missed compared with the studies which have focused on specific marathons, and therefore these papers have the potential to underestimate the true fatality rate.
Redelmeier et al. 20071
Redelmeier and Greenwald published an analysis of 26 marathons and their related deaths, staged in the USA, which they followed for up to 30 years. The principal focus of the paper was to compare the number of marathon deaths with the expected number of motor vehicle fatalities to determine whether running a marathon was safer than not running one.
The authors screened the 328 American marathons listed in Runner’s World on 01/01/2005. They excluded those with less than 20 years of data, fewer than 1000 participants annually, or those that were located primarily on off-road trails or that were part of triathlons or other combined endurance events. They selected 26 marathons randomly from the remainder. Note that the Marine Corps data is included in this analysis.
Data on “sudden cardiac deaths” was obtained from local newspapers on the days after each marathon. Race directors were contacted.
A total of 3,292,268 participants were included in the analysis. There were 26 “sudden cardiac deaths”. 15 marathons had no death, 6 had one death, and 5 had more than one (Boston, New York, Chicago, Honolulu and the Marine Corps Marathon). New York had 2 deaths in 1994.
The average age of the fatalities was 41 years. 81% (21) of those who died were men. 5 deaths occurred in people who had completed a marathon before.
There were autopsy results on 24; 21 had coronary artery disease. Coronary anomalies were noted in 2. Electrolyte abnormalities were thought to be significant in 4 and heat stroke in 1. Most died within a mile of the finish line (Figures 1a and 1b).
The overall risk of a fatality, as estimated by this paper was 0.79/100,000 or 1 death for every 126,626 finishers.
Figure 1a. Location of Fatalities, Redelmeier et al. 2007
Figure 1b. Location of Fatalities, Redelmeier et al. 2007
Mathews et al. 20122
Using publically available racing (MarathonGuide.com, Athlinks, and The Association of Road Racing Statisticians) and news (Google, LexisNexis) databases and by directly contacting race organisers, the authors collected statistics on marathon finishers and deaths between 2000 and 2009. Data was cross-referenced with MarathonGuide.com.
The denominator – the numbers completing marathons during the 10-year period – was 3,718,336. There were 2,255,060 men who completed a marathon and 1,463,276 women.
They identified 28 people who died during the race or within 24 hours of finishing. 6 women and 22 men died. The male death rate was 0.98/100,000 and the female death rate was 0.41/100,000. The overall death rate was 0.75/100,000.
The median age of death was 41.5 years (IQR 25.5, range 22-68).
14 deaths occurred in people over the age of 45. 13 of those deaths were caused by atherosclerosis (Table 1). In younger racers, none of the deaths were caused by cardiovascular disease.
The median distance travelled before dying was 22.5 miles (IQR 10.6). 7 completed the marathon before dying. 18 deaths occurred after mile 20. Cardiac and cardiovascular aetiologies accounted for 24/28 deaths.
People were more likely to die in October marathons (n=11); 27% of marathon participants raced in October. This was of no consolation to myself when I ran the Dublin Marathon, in October, aged 47.
Table 1. Cause of Death, Mathews et al. 2012
Kim et al. 20123
In 2012, a study by Kim et al was published in the New England Journal of Medicine. They looked at cardiac arrests that occurred whilst running or within an hour of running a marathon or half marathon. I have not reported the ½ marathon data.
The database of cardiac arrests was compiled prospectively from Jan 1st 2000 to 31st May 2010 – a slightly different time period to Mathews et al. The arrests were cross referenced using LexisNexis and Google. Further searches were performed directed at particular race events and their local newspapers. Contact was also made with race officials. Cases of cardiac arrest were retained for the final analysis if they were identified in 3 separate data sources or confirmed with race staff. The next of kin of those who died were written to asking for further data about exercise history and family history and asking for consent to access medical data.
Running USA compiled statistics for participation (not finishers) rates in marathons or half-marathons in the USA. It was estimated that 3,949,000 people participated in a marathon, and 6,922,000 participated in a half marathon.
59 cardiac arrests were identified, 40 in marathons and 19 in half marathons. The incidence of cardiac arrest was 1.01/100,000 in marathons. 51 of the 59 people who arrested were male. 34 of the 40 arrests in marathons were in men. Male marathon participants had a rate of cardiac arrest of 1.41/100,000. The mean age of those who arrested was 42±13 years.
42 of the 59 died. The mean age of those who died was 39±9 years. The death rate was 0.63/100,000 during marathons (n=25) and 0.25/100,000 (n=17) during half-marathons. Overall men were more likely to die than women (0.62/100,000 vs. 0.14/100,000) during marathons and half-marathons.
Most arrests occurred in the latter quartile of the race (Figure 2). The data was not separated by race type or by mortality.
Hypertrophic cardiomyopathy was the most common underlying diagnosis overall. In those who survived, coronary disease was more common.
It was recognised that the method of ascertainment of cardiac arrests may have missed some cases, and therefore, the true rates of cardiac arrest and death may be higher. Complete clinical data was missing on approximately 50% of the cases. It was also recognised that the participants may have run multiple marathons, and therefore the total number of unique participants, would have been lower.
Figure 2. Location of Cardiac Arrests, Kim et al. 2012
Webner et al. 20124
In 2009 this group sent 33 item surveys to 400 race directors of US Marathons to ask about the number of marathon participants and associated deaths. 88 (22%) returned the surveys. The marathons were run between 1976 and 2009.
There were a total of 1,710,052 runners. Races had between 30 and 30,000 participants. 30 arrests and 10 deaths were reported. The risk of death was therefore 1 in 171,005, or 0.58/100,000. The cause of death was coronary artery disease in 7. One person had an anomalous coronary artery. The cause of death was not established in 2 cases. 28 of the 30 runners who arrested were male. The mean age of those who arrested was 49.7 years. The mean age and sex distribution of those who died was not specified in the paper.
The location of the arrests was again skewed towards the final miles of the marathon (Figure 3).
There were more participants in this paper, and one less death, than reported when the abstract was presented in abstract form in 2011. Discrepancies between abstracts and final papers are common as the peer review process often picks up errors.
Figure 3. Location of Cardiac Arrests, Webner et al. 2012
These papers can be brought together. It is clear that the typical person who arrests is a middle-aged male around 40 years old. The cause of death is often considered to be coronary artery disease. Typically, cardiac arrest and death occurs in the latter quartile of the race.
The risk of death estimated by these studies was approximately 0.70 per 100,000 finishers, that is 1 death per 142,000 participants (Table 2).
Table 2. Risk of Death During Marathons
Of the two studies that reported marathon deaths by sex, that is Redelmeier et al. and Mathews et al, there were 43 males (80%) who died and 11 females (20%). Mathews et al. reported the breakdown of participants by sex in addition. In that study there were 22 men who died and 6 women. The rate of male deaths was 0.98/100,000 (1 per 102,503) vs. 0.41/100,000 (1 per 243,879) in females (Table 3).
Table 3. Risk of Death by Sex
If further data was available from the papers, more accurate estimates could be made.
The Marine Corps Marathon and the Twin Cities Marathons
A number of papers have been published by the medical team associated with two marathons in the USA: The Marine Corps Marathon (MCM), held in Washington DC and the Twin Cities Marathon (TCM) in Minneapolis. Three papers have been published over the years, looking at data from these two marathons. All are freely available online.
Maron et al. 19965
This paper focused on the MCM from 1976-1994 and the TCM from 1982-1994. All deaths were included. The data is reproduced in table 4.
215,413 runners successfully completed the marathons during this time. 4 sudden deaths occurred during (n=3) or shortly after (15 minutes, n=1) completion of the marathon. 3 were male and 1 was female. The 3 men had coronary disease, the 1 woman an anomalous coronary artery. The one woman died in 1990 in the MCM, aged 19. One man died in the TCM in 1989, aged 40. Two men died in 1986 and 1993 in the MCM, aged 32 and 58 respectively.
Table 4. Maron et al. 1996
Roberts et al. 20006
This paper looked at the 81,277 entrants in the TCM from 1982 to 1994. It therefore contains no new information over and above that of Maron et al. 1996 with regards to deaths.
Its focus was describing all medical issues experienced by marathon runners. For interest medical encounter rates were 25.3/1,000.
Of note, it was stated that 60,757 finished the course – slightly different to the 60,379 from the 1996 paper. There were 48,330 male finishers and 12,427 females. There appears to be a further typographical error in the text, and this number is derived from the table reproduced below (Table 5).
Table 5. Roberts et al. 2000
Updating the data from 1996 yields the following (Table 6):
Table 6. Combination of Maron et al. 1996 and Roberts et al. 2000
Roberts et al. 20137
This paper used data from the two marathons between 1982 and 2009. 1982 was chosen, as data was reported by sex from that year onwards.
The paper reported that there were 540,892 finishers during the study period. 379,863 were male and 168,227 were female.
In total 14 runners collapsed suddenly. 7 were successfully resuscitated. There were 7 sudden cardiac deaths. There was still only 1 female fatality (age 19, anomalous coronary artery, 1990, MCM). The rest who died were male. The underlying diagnosis for all men was coronary artery disease. The mean age of the men was 48 years. The location of the collapse was on average at 16 miles.
The rate of death overall was 1/78,299 finishers or 1.28/100,000. In men the rate was 1/63,311 finishers (1.58/100,000) whereas in women it was lower at 1/68,227 (0.59/100,000).
Details of the deaths are as follows (Table 7).
Table 7. Details of Deaths. Roberts et al. 2013
The Marine Corps Marathon have now published data on their website of the number of finishers since the race began in 1976. It can be found here, and is reproduced in table 8.
Table 8. Marine Corps Marathon Finishers
This allows for a combination of all of the papers, leading to a final estimate of risk:
Between 1982 and 2009 there were 540,892 finishers. From 1976 to 1981 a further 26,387 completed the MCM. The total finishers of the two races from their inception (MCM 1976, TCM 1982) to 2009 was therefore 567,279. There were 7 deaths in that time. The rate of death, therefore, was 1.23/100,000 finishers, or 1 death for every 81,039 finishers.
The London Marathon
Dan Tunstall-Pedoe was the London Marathon Medical Director between 1981 and 2006. He presented data on the first 26 London Marathons in 2007.7
In the paper, data was obtained from St John’s ambulance, receiving hospitals and the coroner. The paper stated that there were a total of 650,000 finishers. A total of 8 deaths were recorded in this time.
The first death was in 1990, and ascribed to hypertrophic cardiomyopathy (HCM). In 2001 and 2005 there were two further deaths from HCM. Deaths in 1993, 1995, 1996, 1997 and 2003 were ascribed to ischaemic heart disease.
This yielded a crude rate of death of 1/81,250 (1.23/100,000).
There is also corroborative data online, written by him and published at Peak Performance with data up to and including 2003. The data there is slightly different. HCM deaths were reported as occurring in 1990 and 2001 – as above. 5 deaths from ischaemic heart disease were reported as occurring in 1991, 1994, 1995, 1997 and 2003. This was the same number of deaths as in the published paper over the same timeframe. Data was published on the number of finishers up until 2003. This yielded a death rate of 1/67,414 (1.48/100,000).
An online search to determine the number of finishers yielded data from additional sites. There are race reports, hosted on the London Marathon website, which mention the number of finishers in the very early races. Wikipedia provides data on the first London Marathon. Marathonguide.com has data on the number of London Marathon finishers. I also searched the London Evening Standard and BBC News Websites. Combining the data from these sources yields the following table (Table 9). All the data is from marathonguide.com unless otherwise specified.
I also emailed Professor Sanjay Sharma, the current director of the London Marathon, who was kind enough to respond directly. He stated that there have been 14 deaths.
As of 2017 over 1,000,000 people had completed the London Marathon (1,038,733). This yields a death rate of 1/74,105 or 1.35/100,000. I look forward to seeing a more detailed paper from Professor Sharma with confirmed finishing statistics and further medical details, including the age and sex, of those who died.
Table 9 summarises the data as far as is possible.
4 Tunstall-Pedoe D. Marathon Cardiac Deaths. Sports Med 2007;37:448-50.
HCM Death from hypertrophic cardiomyopathy
IHD Death from ischaemic heart disease
These two sets of data can be drawn together, yielding a death rate of 1/76,477 finishers or 1.31 deaths/100,000 finishers. The two separate marathons have strikingly similar results (Table 10). The rates of death are higher than those ascertained by more general surveys, as would be predicted as the authors were directly linked with providing medical support to the marathons over many years.
Table 10. Mortality During Specific Marathons
Men around the age of 40 are the most likely to die participating in a marathon. Death typically occurs in the latter stages of the marathon, and is often caused by previously undiagnosed ischaemic heart disease, although hypertrophic cardiomyopathy and increasingly heat stroke are also concerns.
Different methodologies have yielded conflicting estimates of the death rates during marathons. Large surveys of multiple marathons have suggested that the death rate is 0.70/100,000 finishers. Detailed studies of a small number of events has suggested the rate is higher at 1.31/100,000 finishers.
As always, the truth is somewhere in between. But what is clear is that the chances of dying during a marathon are very low.
The data are frustrating. The authors of the papers almost certainly have some further data, not included in the publications that could facilitate a more formal meta-analysis.
What is needed, however, is a prospective registry of entrants / finishers and medical events from race directors. It would help understand what the true extent of the problems are. It would help concentrate medical expertise and help train event professionals to deal with the most common scenarios.
How to screen for these problems in advance? An ECG can be helpful and is often advised, but does not reliably pick up either ischaemic heart disease or hypertrophic cardiomyopathy. An echocardiogram can diagnose hypertrophic cardiomyopathy reliably. A cardiac CT can pick up asymptomatic coronary disease. Judging from the lack of symptoms and training, an exercise tolerance test or stress-echocardiogram is likely to be falsely reassuring. But that is a lot of testing to prevent a rare event. It’s not cost effective, and can probably not be supported by the NHS in the UK, at least.
There is no doubt there is a big difference between myself and Ian. He will be going off to Italy to cycle up a hill in October on a very nice bike. It will be sunny and there will be wine and olives. Later in the month, I am off to run a marathon in Dublin. I won’t bother checking the weather. It will be cold and wet. And there will be no wine at all, although hopefully some Guinness, so not all bad. There are times when I wish I had put a bit more effort into maths at school.
I do worry about running “long” distances, and what strain it puts upon the heart. But what are the risks of dying during a marathon? You can’t rely on newspaper headlines. They only report the bad events. They don’t write headlines along the lines of “Marathon run today, nobody died”. It’s therefore important to look at studies where it has been planned to study the outcomes, or where outcomes are tracked over a long period. But finding raw data is harder than you might think.
I thought I would start with the Berlin marathon. It’s on soon – typically taking place at the end of September. And it’s fast – a place to set world records. More importantly it’s run by a lot of people – 46,950 people in 2016. When there are big numbers there can be good data. Unfortunately, after emailing them, they don’t keep statistics. So that’s no good.
What about London? In 2001, I “ran” the marathon. It turns out that not running at all in the previous month because of a knee injury and drinking wine each night doesn’t make for a good marathon. Being overtaken by a tree is pretty galling.
The first London marathon was staged in 1981, and since then over 1,000,000 people have completed the race. There have (probably) been 14 deaths since then, although it depends on how things are counted, and there are discrepancies between reports.
From 2007, race statistics and details of deaths are pretty secure. David Rogers, aged 22, died that year from hyponatraemia (water intoxication). In 2011 Claire Squires, aged 30, died of heart failure in front of Buckingham palace. It was felt that DMAA, a now banned amphetamine stimulant, contributed (it wasn’t banned at the time). In 2014 Robert Berry, aged 42, died from heat stroke. In 2016 David Seath died from heat stroke (probably) aged 30.
258,911 men have completed the race since 2007 (including 2007 and 2017) and 140,271 women. So, the death rates are 1.2/100,000 for men and 0.71/100,000 for women.
If you accept that 14 have died over the course of the race, and that 1,039,225 people have completed it (a combination of race reports from the London Marathon website, marathonguide.com, and a page on peakendurance sport.com) then the overall risk rises to 1.5/100,000 for both sexes.
Boston is another famous city with a famous marathon, unfortunately for sad reasons at present. I’ll be looking out for Stronger when it is released in the UK. There is a professor at Harvard who has collated some data. When it arrives in the post, I will update the blog with the key points.
The New York Marathon is the world’s largest. It started in 1970. They have a great analytics page (http://www.tcsnycmarathon.org/analytics). Tata Steel aren’t popular in the UK, but Tata Consultancy Services are my new friend. 1,070,784 people have participated in the NY Marathon since 1970 – 764,609 men and 306,175 women. The average man aged 40-49 completes the distance in 04:15:57. Finding the deaths is a little harder. 3 died in 2008. They don’t keep those stats on the website, and more data trawling is required. I have emailed them, but won’t hold my breath.
What have I learned? Finding out accurate data is hard. I still have more stones to look under. And marathon organisers don’t want to hear about deaths or advertise them (odd that…). If you have access to any data please let me know. But one thing is certain: deaths running a marathon are mercifully rare. It’s about the same risk as spending an hour on a plane (http://www.besthealthdegrees.com/health-risks/).
I’ll book a return ticket back from Dublin. The flight is quite short.
We’ve put lights on #DougWaymark at 2000 on last feed. Sun is setting. Calais is lit up as we head down with the tide. Wind has dropped.
Enduroman Events @EnduromanEvents Aug 7
2030 water taken. Moon is rising behind a cloud over Calais. Air temp dropping, light fading. #DougWaymark swims on. #Arch2Arc
Enduroman Events @EnduromanEvents Aug 8
Our friend Douglas Waymark sadly passed away during his Solo Arch to Arc. Enduroman community miss him. Short tribute http://www.enduroman.com”
It’s impossible not to be moved by this series of tweets.
Many of you will have read of the sad death of Doug Waymark this week, as he attempted to complete the Arch to Arc challenge. This is a run from Marble Arch in London to Dover (87 miles) followed by a swim across the channel (21 miles) followed by a cycle to Paris (180 miles). Only 25 people have completed it. The record is 59 hours and 56 minutes.
Doug got into trouble during the swim, 12 miles off the coast of Dover. He could not be resuscitated. He was an able athlete who had completed ultra-events before. It’s impossible to know at this stage exactly what happened.
Phidippides is said to have run from Marathon to Athens to deliver news of a military victory at the Battle of Marathon. On delivering the news he died suddenly. Death during exertion is mercifully rare, but always shocking. How can it be that someone who is fit and well can die so suddenly?
The most common cause of death during exercise in men over 40 is coronary artery disease – a blockage of one of the coronary arteries. These arteries supply your heart with blood. When one blocks, an area of the heart can’t function any more. If it is a branch of a small artery you may not notice. If it is one of the larger arteries you will typically die very rapidly. What people don’t understand is that an artery can go from open to blocked very quickly. And therefore, you can have no symptoms at the start of a race. As you get older you build up deposits of fat, covered over with a thin layer, in the arteries. This thin covering can rupture and then a clot can rapidly form, blocking the artery. Furthermore, because the human body is amazing, it is possible for the body to compensate for quite significant problems in the coronary arteries before symptoms arise.
An alternative (there are many) is that he could have torn one of the coronary arteries – coronary artery dissection – or the aorta itself. This can happen under periods of intense strain, although it is less common. Some people have coronary arteries that arise from slightly different locations (anomalous coronary arteries) and these seem to be the cause of sudden death during exercise in some people.
In younger people, hypertrophic cardiomyopathy seems to be the most common underlying condition which causes sudden death during exercise. This is a disorder of the heart muscle. Normally the heart muscles are laid down in neat sheets – the muscle cells are aligned. In hypertrophic cardiomyopathy (HCM) the muscle cells look like they have been scattered and the term used is disarray. People suffering from HCM are more prone to heart failure and heart rhythm problems.
There are other possibilities too – such as problems with the right ventricle (arrhythmogenic right ventricular cardiomyopathy) and problems with the electrical systems (Long QT syndrome, catecholaminergic polymorphic ventricular tachycardia – they all have obscure names). More on these in future articles.
But the reality is that death during sport is rare. About 1 in 1,000,000 young people die during exercise each year and about 6 per 100,000 middle aged people. And that is why Doug Waymark made the news.
More lives are saved by exercising than caused by it. But as with all things in life, nothing is completely safe. Reading the news suggests that Doug was someone who helped and inspired others to achieve their goals. He will have saved many lives, although tragically lost his own.
On Tuesday night, I ran 10K. It took just under an hour. My heart rate went no higher than about 130bpm. I stepped off the treadmill, had a quick shower and carried on with the day. I didn’t have any pain. It felt good.
Perhaps this shouldn’t be a cause for celebration. It’s not an exceptional time and I am firmly middle of the pack at my local Park Run on Saturdays. But it was for me. 16 years ago, I stopped running. A year ago, or so I started again on holiday. It was awful and I could barely run a mile with the kids.
Since then there has been a battle with iliotibial band syndrome, Achilles tendonitis, shin splints and a slipped disc. I have had physio and after several insoles, I am now on my third pair of shoes (Mizuno Running Solution selected – it worked!). I am best friends with a foam roller. I am also 20Kg lighter.
I am now edging towards 50K a week. Most of it is pretty low intensity and in Zone 2/Zone 3. But, what also went through my mind in what was a pretty boring hour on the treadmill was the nagging question as to whether what I was doing was healthy and good for me.
Coronary heart disease – the narrowing of the coronary arteries which supply the heart muscle – is bad. When the narrowings reach a certain point, then on exercise not enough blood can get to parts of the heart. This typically (but not always, nothing is ever always in medicine – some people get breathlessness or undue fatigue) causes pains in the chest. The pains are usually described as an ache or pressure – angina. If an artery blocks suddenly then part of the heart muscle can die – a heart attack (myocardial infarction). This is usually painful – people get severe and prolonged pain, they are often pale and sweaty. They can feel nauseated and vomit.
Coronary heart disease is more common as you get older, if you are a man, or if you have high blood pressure, diabetes or a high cholesterol. It runs in families too. If you want to get an idea of your risk then follow this link: https://www.qrisk.org/2017/.
A marker of coronary artery disease and risk is coronary calcium. This gets deposited with age, along with cholesterol. You can see it on CT scans particularly clearly. Typically, if you take a group of ordinary individuals, the more calcium that is there, the more likely you are to have a heart attack.
Athletes have more calcium in their coronary arteries than non-athletes. And coronary artery disease is the most common cause of sudden death in athletes. I can recall a couple of people on the ward recently who “died” and were then resuscitated during exercise. It’s not uncommon.
Not so fast. In fact, generally, the more exercise you do, the less likely you are to have a heart attack. Some articles suggest your risk is about 50% less (but NOT zero). This is one of those annoying paradoxes that crops up in medicine all the time. It is probably down to the composition of the plaques that are seen – the plaques in athletes are more “stable” – less likely to rupture and cause a heart attack. More work is required to understand this though.
So, keep exercising – but listen to your body. If you are doing the same route and you are struggling more than you would expect then be careful, although everyone has good and bad days, and everyone ages. If you are getting chest tightness when you exert yourself which eases off with rest, then seek medical attention.
Post Script: I ran 24K on Saturday. It felt good. But, of course, the jump was too much and now my knee is sore and swollen. I really should know better…
So, I’m intending that this blog should be a basic course in the heart and how it adapts to exercise. It’s fair to say that this is something of a complex topic, and there is much controversy and debate. We have not got it all worked out by a long way, and I reserve the right to completely change my mind about things over time. That is the nature of medicine.
The heart is only one part of the cardiovascular system which helps you exercise. It includes the heart, the lungs, the blood, the muscles and of course the brain. My PhD touched on how the nerves and brain react to exercise. It was 3 years of pure frustration, as it turned out to be quite hard.
The first thing to understand are some basics of the heart itself. You can skip this if you already know all about it, but I will assume some sort of basic knowledge in future posts. You will have covered this in GCSE biology, or for those of us who are old and decrepit enough, O level biology.
Blood comes back from the body having been “used” into the right atrium via the superior vena cava (from the arms, chest and head) and the inferior vena cava (from the rest of the body). It’s important to realise that there is vast variation in the precise distribution. The right atrium is a thin walled chamber which discharges its blood into the right ventricle via the tricuspid valve. Valves are thin-walled structures that are elegantly complex pieces of engineering that keep blood going in one direction through the heart. People write entire books on valve structure and function. Valve disease can be important when considering exercise. 1-2% of the population have a “bicuspid” aortic valve, and exercise can accelerate it narrowing – it then usually requires replacement which is a major operation.
The right ventricle is the pumping chamber that forces blood into the lungs. The system is at low pressure, and the muscles of the right ventricle aren’t as well developed as those on the left side of the heart – the right ventricle is a bit thinner, and probably a bit more vulnerable to stress. This is thought to be important in the development of conditions such as ARVC (arrhythmogenic right ventricular cardiomyopathy) – more on this later. Blood flows out of the right ventricle and into the pulmonary arteries and the lungs themselves.
Once all the business of gas exchange has been done in the lungs (oxygen in, carbon dioxide out) then the blood comes back via the pulmonary veins into the left atrium. During most of my training the pulmonary veins were possibly one of the least exciting anatomical structures you had to learn about, but then it was discovered that AF starts there quite often, and now many people spend entire lives studying them.
The left ventricle is considered to be the main structure of the heart. Blood enters this from the left atrium via the mitral valve. It leaves the left ventricle via the aortic valve and passes into the aorta and from there around the body. Cardiology has traditionally focused on the left ventricle and its function.
One of the key concepts when understanding how the left ventricle works is the “ejection fraction”. This is the proportion of blood ejected from the ventricle each time it beats. Cardiologists, and patients, get very hung up on this measure, and it is important, but there are important limitations. The normal volume of the left ventricle is about 140ml in a typically sized person. Typically, around 2/3rds of the blood is ejected each time the heart beats (about 90ml). Anything over 55% or so is considered normal. But really, what the body needs is not for the left ventricle to have a particular ejection fraction, what the body needs is enough oxygen delivered to the tissues. That depends on how much blood is pumped around the system each minute and how much oxygen it is carrying. Doctors often forget this. I’ll talk more about this in another post. Disease of the heart muscle is termed cardiomyopathy. When people talk about “heart failure” they are usually referring to disease affecting the muscle of the left ventricle. Exercise, particularly endurance exercise can affect the heart muscle in both good and bad ways.
The aorta branches many times when passing blood around the body. The first are the coronary arteries. In most people, there is a right coronary artery and a left coronary artery – the first part of the left coronary artery (the left main stem) branches early into the left anterior descending artery and the circumflex. Narrowings in these arteries cause angina – a pressure or discomfort on exertion (usually) felt across the chest. A sudden blockage can cause a heart attack. There is a lot of debate about whether or not exercise causes changes in the arteries, and whether or not those changes are harmful. Again, a subject for a future post.
So that is the whirlwind tour of the heart structure. In future posts I will touch on valve disease, diseases of the heart muscle and coronary artery disease. Then having finished with the plumbing I will move onto the electrics. It will become clear that in fact as doctors we probably know less than you think. The world of sports medicine is in its infancy really.
Unlike many on Crickles I am a long way from being a professional athlete. I ran the London Marathon in 2001 and was overtaken by a tree. At last year’s Porlock Hill Climb (which I went to, but failed to enter in time) I would not have been last. But 31 minutes is not great. Most of my sporting activity is to help my kids. My youngest likes to run – typically about 10K. My middle one loves cycling and triathlons. As they are young (11&13) I do most of their training with them. It’s getting harder, and I can see a time in the not too distant future when I won’t be able to keep up.
My day job involves many things, but I specialise in sudden cardiac death. All too often I am dealing with families who have lost someone out of the blue. Sometimes they are athletes, probably more often than chance would predict, sometimes not.
Around 1 in 50,000 athletes <35 years old die suddenly each year.
So I wonder about whether or not I should get my kids screened. Many conditions which lead to sudden cardiac death can be picked up by quite simple tests, such as electrocardiograms (ECGs). It takes 5 minutes. In countries such as Italy and France there are widespread screening programmes. I sometimes see people from the UK who have abnormalities picked up when they have been to Europe to participate in an event, and had their mandatory ECG.
There has been a limited study in the UK, run by Sanjay Sharma, probably the best known Sports Cardiologist in the UK. They screened almost 5000 athletes between 14-35. 1 in 300 had a potentially serious underlying conditions after more complete evaluation. ECG screening seems to work. A large study in Italy demonstrated that it reduced the risk of sudden death in athletes by 90%.
But it’s not quite so easy. Athlete’s ECGs are “abnormal” anyway, and knowing what is normal for an athlete takes training. Furthermore, many people with abnormal ECGs don’t have problems after more detailed testing.
As some will know, identifying something potentially serious doesn’t mean that something serious will happen. In fact for some diagnoses, such as long QT syndrome, it is often more likely that nothing serious will happen. And then they may be banned from sporting participation, and struggle to enter certain careers. A diagnosis, which may never cause harm, can be life changing. I have all too often been unable to help families, who want to know what the future holds. I see people desperately grasping for certainty where none exists.
On the basis that I haven’t dropped dead yet, and neither has my wife, and on the basis that my kids are still amateur and have no symptoms, I think I’ll leave it a bit longer. But as data mounts, and if they become more serious, I will probably err towards organising some testing for them. Like most parents, I worry far more about them than I do myself. In the meantime I’ll be cycling with one son on Sunday on Exmoor.
Last week there was a letter in cycling weekly by a chap called Barry Jones. He had developed atrial fibrillation during a ride. It had been blamed by him and by the medics on coffee. I think it’s an example of “attribution bias”. This is when you look for the reason you want, rather than the real reason, to explain away a problem
For many years, doctors were taught that caffeine led to heart rhythm problems. Doctors have been counselling patients to avoid caffeine when they present with palpitations. There is no doubt that in overdose, caffeine can indeed cause heart problems.
But, “normal” caffeine consumption and the risk of heart rhythm problems has now been looked at in several large populations. The bottom line is that, for most people who drink only moderate amounts of coffee, caffeine intake is not related to heart rhythm problems, including atrial fibrillation (AF). Caffeine can also improve performance. As a cardiologist with an interest in heart rhythm problems and exercise, I have had to change what I advise over time.
Sadly, there is growing evidence that AF is related to exercise. The risks of developing the condition are many times higher in athletes, and there is an apparent relationship between exercise volume and intensity, particularly in men. I see many cyclists and triathletes who develop this problem in middle age. It is incredibly frustrating for them. The story of an athlete’s heart rate monitor showing high heart rates for long periods of time (not just the brief spikes we all see) along with a drop off in performance is classic.
It is possible, as with everything in life, to have too much of a good thing. Overall, exercise appears to be beneficial to health, at least in moderation; the upper limits aren’t well defined yet. I keep exercising (moderately) with adequate recovery. Life is all about balancing risks. But don’t blame the coffee when your heart rhythm goes haywire. It’s probably a consequence of your epic suffer score. And do seek medical attention – there is lots we can do, and lots you need to know.
There is little doubt that some exercise is good for you. Many studies have suggested that exercise improves many aspects of our lives, including delaying ageing, living longer and improving quality of life.
Exercise causes the heart to change. The heart rate slows, the right side of the heart enlarges and the left side of the heart thickens. Medicine doesn’t quite understand all the changes yet, and the limits of what is normal and what is not are gradually being worked out.
In recent years, there has been a vogue for more extreme exertion – look at the popularity of ironman events and ultramarathons. As a doctor, it’s a bit odd. Either patients seem to do nothing, or want to run the Sahara. There is no in-between.
As with everything in life, exercise brings its own issues, not only aching legs and torn muscles. There is little doubt that, like everything else, extremes carry their own risks. And, I don’t think we know precisely what those risks are, or the level of exercise at which those risks occur.
As a cardiologist, I see problems frequently. The most common situation is the middle-aged man who sometimes can’t keep up on the hills any more, and who has noticed his heart rate is off the scale at those times. Atrial fibrillation is a common heart rhythm problem which hits performance and appears to be associated with endurance exercise.
Pheidippides (Phidippides) was the famed courier who inspired marathon running (and died). His name lives on in cardiology. Phidippides cardiomyopathy describes a pattern of scarring in the ventricle which occurs after extreme exertion in some. The scarring can affect heart function and cause heart rhythm problems. The last definite case I saw was a man who completed the Paris-Brest-Paris randonneur event. 1200Km in 90 hours.
Chris Case (athlete), John Mandrola (cardiologist) and Lennard Zinn (athlete) have written a book – the Haywire Heart. The title is alarming, but get beyond this, and the book is good. It presents a balanced (well, reasonably) view of the pros and cons of more extreme exertion. It explains how the heart works, the problems that can occur and puts them into context. It doesn’t quite deliver on its promise on telling you how to protect your heart though. But I don’t think anyone knows how to do this yet.
Any endurance athlete who is interested in their heart should read this.
I’m still working (slowly) towards the Exmoor 70.3.