It’s common knowledge that exercise is good for the heart. But does this apply equally to everyone who keeps fit, regardless of the volume of training?
Sadly not. Many doctors and scientists now believe that, as far as the heart is concerned, there may be such a thing as too much.
I have a personal interest in this subject: since 2014, my heart has been misbehaving during exercise, leaping to rates as high as 230bpm, usually early on during a ride or run, often refusing to fall until I stop or slow down.
It happens frequently, though usually settles into its normal rhythm within about 10 minutes.
I’ve undergone many tests but so far with no firm diagnosis. My background: I’m 35, have been running and cycling for around a decade, and until recently racked up seven to 10 hours, including two or three hard sessions, nearly every week.
Could it be that I’ve overdone it and damaged my heart?
Evidence that endurance exercise can damage the heart has been mounting for years, and much of it is cited in an excellent new book from across the pond, The Haywire Heart, co-written by journalist Chris Chase, heart doctor John Mandrola and former pro cyclist Lennard Zinn.
The book’s introduction highlights that it is very difficult to establish definitive conclusions about the long-term effects of exercise among athletes. For example, a 2011 study observed that among 834 former Tour de France riders average longevity was 17 per cent higher than in the general population.
This may seem reassuring, but it cannot be ruled out that these riders were innately invulnerable to the ardours of high-volume training — a likely characteristic among pro cyclists.
Non-elites like me may need to be more cautious.
The most common form of heart rhythm problem is atrial fibrillation (AF), where the top chambers of the heart (atria) intermittently contract too fast — thankfully the heart’s atrioventricular node acts like an electronic resistor and prevents the lower chambers (ventricles) from joining in the chaos.
A 2009 meta-analysis of six case-controlled studies on athletes concluded that being an endurance athlete makes you five times more likely to develop AF — one in four of us ends up with the condition.
Men are considerably more prone to arrhythmia than women — exactly why is unclear — and tall men are the most susceptible of all.
The biggest concern about AF is that it increases stroke risk, as fibrillating atria do not contract or empty fully, which can allow blood clots to form.
Of course, stroke risk is also influenced by a whole host of other factors (high blood pressure, diabetes, etc.) — many of which are mitigated by regular exercise. The question is, how best to balance the risks and benefits of exercise?
Watch now: Five ultimate foods for cyclists
Moderation not cessation
One thing’s for certain with heart rhythm problems: prevention is very much better than cure.
Once you have a condition such as AF, it is unlikely to resolve itself, as Michael Papadakis, a specialist in sports cardiology at St George’s, University of London, explains:
“In an athlete who experiences occasional episodes of AF and continues to exercise at the same intensity, it is likely that the frequency of the episodes will increase and eventually the heart will stay most of the time in AF… In most cases we would recommend that they take their foot off the throttle and try and moderate but not stop exercising.”
In other words, developing arrhythmia is likely to force you to seriously cut back your training; far better to make smaller pre-emptive changes before harm is done.
Why are athletes’ hearts more prone to rhythm problems? There is not yet a definitive answer, but AF does not occur in normal hearts: it begins with a trigger, an out-of-sync beat, via an abnormality in the atrial muscle, and there are good grounds for suspecting such abnormalities commonly result from years of endurance exercise.
Athletic hearts have to tolerate extremes. In training, heart rate is raised by adrenaline (sympathetic nervous system), while low heart rates are dictated by the vagus nerve (parasympathetic nervous system).
Athletes’ hearts experience very high and very low (resting) rates on a daily basis. “This back and forth,” writes John Mandrola, “may create the milieu that triggers premature beats, which could then induce AF.”
Just like a cyclist’s leg muscles, their heart is forced to get stronger, adapt to the demands placed on it, and may sustain inflammation and injury resulting in scarring — studies have observed raised markers of inflammation in endurance athletes.
It is known that scarring can disrupt the flow of electrical signals in the heart, creating another potential trigger point for arrhythmic beats.
One particular condition is so strongly linked with endurance exercise that it has been named Phidippides cardiomyopathy — after the Greek messenger who, circa 490 BC, died after having run the 26.2 miles from Marathon to Athens.
It is thought that this hazardous condition, characterised by patches of cardiac fibrosis (scarring), is caused by prolonged, relatively intense exercise that keeps the heart in a state of volume overload for several hours at a time.
Scarring is not the only risk; it is also understood that endurance exercise can cause the heart muscle to grow larger (hypertrophy), or heart tissue to stretch (dilation).
The related structural changes may be implicated in arrhythmia, though this area is not yet fully investigated or understood.
One of the biggest challenges for scientists is trying to separate out exercise-related risk factors from pre-existing conditions and factors unrelated to athletic adaptations.
Taking up sport after years of heart-unhealthy living, for instance, is unlikely to reverse the damage — if problems ensue, it’s difficult to single out the cause.
“Most studies look at athletes at a particular point in time, e.g. middle age,” explains Papadakis.
“It can be difficult to decipher what is due to prolonged exercise and what is due to other life events. The ideal study would assess [markers or heart damage] from adolescence or even childhood over a number of decades, and that’s difficult.”
There are many different types of arrhythmia aside from AF, and the most serious types — thankfully rare — affect the larger lower chambers of the heart (ventricles).
In cases of ventricular fibrillation (VF), the heart cannot function, resulting in cardiac arrest and, in the worst case scenario, sudden cardiac death (SCD).
The most common cause of VF in those aged over 35 is the blockage of an artery caused by heart disease unrelated to exercise; somewhat reassuringly, there is scant evidence linking life-threatening ventricular arrhythmia and endurance exercise.
Most cases of sudden death in sport result from an undetected pre-existing condition — exercise is the trigger rather than the underlying cause. Here, the challenge is effective screening.
How much exercise is too much?
It’s a key question but difficult to answer: how much exercise is too much?
Far more research is needed to establish useful upper limits, but it should not be assumed that the more exercise you do, the healthier you will be; already studies have shown a plateau effect.
“The take-home message from these findings,” writes Mandrola, “is that if health is your goal, you need not exercise more than 30-60 minutes per day.”
There is compelling evidence that racking up year after year of hard training increases the likelihood of heart glitches, as Mandrola explains:
“Years of endurance training inevitably cause inflammation, scarring and stretching.
“These changes to the fundamental structure of the heart can irrevocably alter how it operates… it becomes easier to see how [such training] probably leads to AF.
“The fact that detraining often fixes the problem only bolsters this hypothesis.”
This does not mean that everyone who trains hard for years will experience rhythm problems, but it does underscore the importance of avoiding overtraining, heeding warning signs and giving your heart plenty of rest and recovery time, especially as you grow older.
“In our 50s and 60s, we need more rest after hard exertion,” confirms Mandrola.
“Ageing muscles are more susceptible to exercise-induced damage and are slower to adapt and repair.”
Exercise v longevity
Still pursuing a diagnosis for my own erratic heart, I attend a follow-up appointment with heart rhythm specialist John Silberbauer.
He explains to me that, having been unable to record my irregular rhythm on an ECG, diagnosis is impossible.
But there is some good news: because I’ve not had any ominous symptoms and have undergone tests including echocardiogram and MRI, the most serious conditions are ruled out:
“Effectively you have been screened.”
Nonetheless, Silberbauer is determined to nail down the cause: “You’re young and this issue doesn’t look like it’s going away. It is well worth diagnosing it, as there is a very good chance of being able to treat and get rid of it.”
What’s the most likely diagnosis, I ask. “I would have thought AF or SVT [supraventricular tachycardia], both of which are benign.”
I suggest to Silberbauer that I could try to get hold of an AliveCor app and attempt to capture an ECG of my racing heart while out on a ride or run. He agrees: it’s well worth a try.
Before leaving, I ask Silberbauer his opinion on the link between heart rhythm problems and endurance exercise.
“My own view — though I’ve no hard evidence to support it — is that a proportion of people have a genetic weakness which, if they don’t exercise, lies dormant; whereas, if they take up endurance exercise, the weakness is activated and becomes a problem.
“Too much of anything is probably a bad thing, but obviously doing some exercise is better than doing none.”
Cardiac screening: should you get tested?
Sudden death from cardiac arrest among young athletes is rare, affecting only around one in 50,000. Ninety per cent of victims are male.
The most common cause of sudden cardiac death (SCD) is hypertrophic cardiomyopathy — disease of the heart muscle — most forms of which are detectable by screening.
Unfortunately, screening is not routinely carried out in the UK, owing to concerns over high rates of false positives and related cost implications.
However, recent research published in the British Journal of Cardiology suggests that refining the screening can reduce the need for follow-up investigations by more than 50 per cent, thereby slashing costs by 21 per cent.
It has been argued that funds are better spent on defibrillators at sporting venues — potentially life-saving, but only if your cardiac event occurs at an equipped venue.
For us cyclists, who spend much of our time riding alone on country lanes in the middle of nowhere, screening is our best bet.
According to Dr Steven Cox, CEO of Cardiac Risk in the Young (CRY), his organisation’s research, led by Professor Sanjay Sharma, has established new international screening guidelines that have slashed the level of false positives to four per cent.
“This represents a massive saving for the NHS,” Cox told CW.
“Minimising unnecessary tests, especially in the current climate, is very important. However, this lower level of false positives relies on being seen by a trained sports cardiologist who is using the latest criteria.”
His advice for making sure you’re seen by a suitably qualified specialist is to go through the CRY screening programme (testmyheart.org) — free for anyone aged 14 to 35.
It is well worth getting tested, says Cox, because one in 300 people have an undiagnosed heart condition that it would be to their benefit to have picked up.
“The most common condition affects at least one in 700 people and can be cured with an ablation procedure… The vast majority of conditions we detect result in lifestyle modifications that do not stop people from competing.”
What about the most serious conditions; what proportion of those are picked up by screening?
“The vast majority, about 80 to 90 per cent,” says Cox. “Research has shown a 90 per cent reduction in cardiac deaths as a result of screening.”
For young cyclists, there is clearly a strong case for screening — though some cardiologists remain ambivalent.
“There are two sides to the argument,” says consultant cardiologist Dr Mark Dayer. “I’ve seen people have their life upended by getting tested — being diagnosed is far more likely to complicate than to save your life.
“Would I get my own children screened? It’s a decision I’m currently agonising over.”
What about screening for older riders, I ask Cox.
“Over the age of 35, standard screening will not discount that there could be other potential causes of, for instance, a heart attack.”
In veteran athletes, the biggest risk factors are not underlying inherited conditions but other forms of heart disease, often lifestyle-related.
“A 40 or 50-year-old is more likely to benefit from other assessments such as exercise testing and a different form of screening that takes into account their lifestyle factors — more than just an ECG.”
So, if you’re over 35, new to endurance sport and/or have any reason to suspect you’re at an increased risk of heart problems, it’s well worth visiting getting checked by a doctor who is clued-up on sports cardiology.
This article was originally published in June 2017.