Moderate amounts of exercise produce a multitude of health benefits. Both the American Heart Association (AHA) and World Health Association (WHO) now recommend 150 min per week of moderate intensity exercise for adults.
Some recent observations, though, have raised the question: when it comes to exercise, can there be too much of a good thing? And, more specifically, can too much exercise somehow be harmful to the heart. With the increased popularity of adult recreational and competitive sports–particularly in cycling, running, and triathlon–there is a growing number of adults who are pursuing exercise far in excess of the AHA and WHO recommendations. The questions surrounding the issue of “too much exercise” are very pertinent.
A few recent articles in the popular press summarize some of the findings and frame the debate:
- Can Too Much Extreme Exercise Damage Your Heart?–at Cleveland Clinic online
- Can Too Much Exercise Harm the Heart?–by Gretchen Reynolds at NY Times Well Blog
- Is Too Much Exercise BAD for the Heart?–by Anna Hodgekiss at The Daily Mail
- Extreme Exercise and the Heart–by Lisa Rosenbaum at The New Yorker
The worrisome observations have generally been made in small numbers of symptomatic athletes, in groups of athletes whose athletic history–or “dose” of exercise is poorly characterized, or in studies that were designed for some purpose other than determining the effects of “too much exercise” on the heart.
I’ve said previously that these observations deserve our attention, but that we really need more targeted investigation into this issue. In a study just released online (ahead of print) in the medical journal, Circulation, Philipp Bohm and colleagues from the Institute of Sports and Preventive Medicine at Saarland University in Germany bring us an important new look at “extreme” exercisers.
This new study focuses on a group of 33 healthy, male, Caucasian competitive elite master endurance athletes. This group of athletes was selected so that it included only athletes with a 10+ year continuous training history of 10+ hours per week; the average training was 16.7 hours per week and the average training history was 29 +/- 8 years. These athletes had an average age of 47 years (range, 30-60 years). This group of athletes included:
- Sixteen were former elite professional athletes
- One Ironman world champion and several 2nd and 3rd place finishers
- The world record holder at the long distance triathlon
- A 2nd ranked cyclist of the Vuelta a Espana (Tour of Spain)
- Six Olympic athletes in the sports of triathlon and rowing
- A former winner of the Munich Marathon.
A control group consisted of 33 healthy Caucasian men who were pair-matched for age, height, and weight. This control group was selected to include only individuals who exercised <3 hours per week.
All of the subjects underwent a comprehensive evaluation that included:
- History and physical examination (to exclude any athlete with a history of overt heart disease, high blood pressure, smoking history, or other risk factor for heart disease)
- Resting EKG
- Cardiopulmonary exercise testing
- Echocardiography, including tissue-Doppler imaging and speckle tracking
- Contrast-enhanced cardiovascular magnetic resonance imaging (CMR).
Interestingly, none of the athletes presented with, or reported a history of, atrial fibrillation.
There were several unsurprising, and expected differences between the athletes and the controls. First, the resting heart rate (HR) for the athletes (48 +/- 7 beats per minute) was slower than for the controls (65 +/- 11 beats per minute). Second, the size of the athletes’ hearts was significantly greater. The left ventricular (LV) mass for the athletes’ hearts (188 +/- 26 g) was significantly greater than the controls (124 +/- 23 g). Similarly, the right ventricular (RV) mass for the athletes’ hearts (70 +/- 13 g) was significantly greater than the controls (49 +/- 11 g). Among the 33 athletes, 22 met a traditional definition of “athlete’s heart,” with a heart volume of 13+ mL/kg of body weight. As expected, the VO2 max of the athletes (60 +/-5 ml/kg/min) was significantly greater than controls (37 +/- 6 ml/kg/min).
The important results of the study were those that showed no difference between the athletes and the controls. With echocardiography, there was no difference between athletes and controls in LV longitudinal strain or RV longitudinal strain–measures of the strength of contraction. Using CMR, there was no difference between athletes and controls in LV ejection fraction (EF) or RV EF–again, measures of the strength of contraction. One athlete (3%) had a LV EF slightly less than normal, at 45%. No athletes or control subjects had abnormalities of the RV that could be suggestive of the potentially life-threatening problem of arrhythmogenic right ventricular cardiomyopathy (ARVC). One athlete (3%) had late gadolinium enhancement (LGE) on CMR that suggested previous, asymptomatic inflammation of the pericardium, the sac in which the heart sits. LGE analysis showed no evidence of unusual fibrosis or scarring in either athletes or controls.
Kudos to the investigators here. The study is apparently self-funded. It’s expensive to perform this kind of testing; in the United States, the costs of this study would easily run into the many hundreds of thousands of dollars. Kudos, too, to the editors at Circulation. There is a tremendous bias against publishing so-called “negative” studies, where no important differences are found between study and control groups. Many “negative” studies are left on the editing room floor–and we never hear about them.
This is an important study because it is the first to gather and study a group of long-term endurance athletes with a substantial, and defined, training load over an extended period of time. The results deserve our attention. At nearly 17 hours per week of exercise or training, these athletes obviously far exceeded the contemporary recommendations for 150 minutes of moderate exercise per week. Just doing some quick math, the average cumulative exercise “dose” is more than 25,000 hours. As I’ve said many times before, it’s worth asking the question if such an exercise pattern can be harmful to the heart over the long term. This is a terrific group of athletes to study in order to help answer that question.
We must keep in mind that, with just 33 athletes, this is a small study. With only 33 athletes, it’s obviously possible to miss something that would be found in the 34th athlete. We must also keep in mind that the study only involves male athletes. Female athletes are not immune from heart problems and deserve study, too.
It is a striking finding that no athlete was found to have atrial fibrillation–either now, or in the past. Moreover, no athletes experienced arrhythmias during the cardiopulmonary exercise test. A number of previous studies have reported a 2- to 5-fold increase in atrial arrhythmias among long-term endurance athletes. Like the current study, all of those previous studies have involved small number of athletes. None, though, have focused on athletes like these, with such extensive exercise and training histories. In my opinion, endurance athletes broadly can take some comfort from the findings of this new study with regard to the potential risk of atrial arrhythmias.
It’s noteworthy that the LV and RV function of the athletes was no different than the controls. One athlete had mildly depressed LV function, for reasons that are not clear. In short, though, the study found no evidence of cardiac damage–at least, in terms of the pumping function–that accrued over the long term. We know that there is some depression of LV and RV function immediately after an intense bout of exercise (eg, marathon, long-distance triathlon, long-distance cycling event), but we also know that these changes resolve within days to weeks afterward. The current study argues against the hypothesis that repeated episodes of intense exercise (ie, many marathons or triathlons over a lifetime) might result in a decrease in LV or RV function. Again, this is encouraging news for endurance athletes.
Finally, the CMR and LGE results are important. Aside from the 1 athlete with possible previous pericarditis, there were no worrisome findings of fibrosis or scarring that might be attributable to injury from repeated episodes of intense, strenuous exercise. These LGE findings are at odds with some observations of unexplained fibrosis in other cohorts of long-time runners, even if the consequences of such findings remain uncertain. This area of investigation deserves further attention. For now, I’d say that long-time participation in endurance sports does not necessarily result in unexplained fibrosis in the heart.
- Thoughts on the recent VeloNews article
- PRO/CON: Prolonged intense exercise leads to heart damage
- Do elite athletes live longer?
Lars Andrews says
They studied the wrong people. They need to study cardiac athletes.
Larry Creswell, MD says
Thanks, Lars. It’s hard to argue against further study.
What would you propose in terms of a study? Perhaps the right person (investigator) might be reading here….and welcome your suggestions.
Lars Andrews says
I do believe that we need to be looking at an athletes history of training and competing whilst having a cough, cold, fever, injury … because we know that cytokines released into the blood stream can paralyse and damage heart cells and that repeated micro-injuries to myocytes must eventually result in non-viable and scarred heart muscle and conductive cells ?
And was there any differencies in IVS thickness? Was it something like 1.2-1.3 ?
Larry Creswell, MD says
The interventricular septum thickness was 11.7 +/- 0.7 mm in the athletes and 10.3 +/- 0.8 mm in the controls, a significant difference.
So 12.4 is < 13.0 and that means "athlete's heart" not "dangerous hypertrophy"?
I'd like to add the following idea: athletes training 8, 10, 15 and more hours tend to lead a more healthy lifestyle than non-athletes – no smoking, no alcohol and a low-fat and high-carb diet, sometimes lack of sleep.
So when we look at the results, we see the cumulative effect, not only the effect of doing endurance sports.
This is super interesting and thank you for sharing.
For sure, n=33 is really small for detecting rare conditions. With the danish studies on AF in XC skiers, it’s right that one would expect that someone in this small cohort has encountered AF. (Nearly 13% in the danish cohort). Maybe they were too young ? Do the also give the LA volumes in their paper (can’t find it today) ?
The interesting part is the huge volume of hours with a high intensity work.
On the other hand, I’m more concerned about me and my fellows rec-competitive athletes than with great champions with an extraordinary physiology and who benefits from a good follow-up.
So, I hope one day we will see the same kind of study with hundreds of recreationnal athletes with 3+ hours of training per week.
Larry Creswell, MD says
Good points. I do think it’s remarkable that 0/33 athletes had afib. Like you say, though, perhaps they’re not old enough.
I don’t see that LA size was reported in the paper.
Yes, it would be interesting to have a thorough longitudinal study of recreational adult athletes.
Phil Hendry says
It strikes me that these are all truly ‘elite’ athletes… As such, might it not be that there are no arrhythmia sufferers because they have, in effect, been selected simply by ‘surviving’ at that level? In other words, if at some point in their sporting career they had suffered from such a condition, they would not now be in the group – because their condition would prevent the level of training/fitness to allow performance at that level. So, in effect, the sample consists of ‘the lucky ones’? That, then, would make it hard to draw any meaningful conclusions on a ‘general population’ of athletes.
I’m not qualified in any way to comment – I’m merely a retired academic physicist; my interest is because I’ve been a competition swimmer, recently diagnosed with atrial flutter and atrial fibrillation.
It would be interesting to find out the Athlete’s health history ie: did they have a predisposition for health issues or family history of heart disease. We all read about people who appear to be healthy and fit due to rigorous bicycling or endurance training who have a sudden heart issue like a valve blowing out or an enlarged aortic root or a heart attack. I have to ask myself was it from physical activity and pushing ones heart or was there a predisposing factor and it was already there.
A lot of people poo poo getting a physical because they look lean and mean and feel great but what if there’s a genetic component a heart valve that’s had a slight murmur now is pushed into something more than slight,an aneurysm that went undetected but now is becoming larger due to the stress being put upon it. That’s why physicals are so important. Thank you for this article,
Larry Creswell, MD says
Thanks, Charlotte. I do believe there is a role for periodic physical examination.
I am 69 year old fitness cyclist. I was investigated, due a bout of high blood pressure that abated with recovery (possibly after too much high intensity exercise – think massive exercise induces compartment syndrome as a possibility).
My first cardiologist wanted to put in a pacemaker but obtained a 2nd opinion from one who “studies the athletes heart” at UVA in Virginia. After careful stress test (ignoring >3.2mm ST depression on ekg which evened out) to exhaustion with ekg, very careful echo ~2hrs later (I was still in recovery mode) He found the interventricular septum thickness enough to prescribe an MRI with contrast. The result, no fibrosis, LV at max of normal, RV slightly enlarged, and characterized as an “elite athletes heart”!
Funny this is my only significant trophy!
I was released to return to full exercise with come back to see me if you think you need to 🙂
Simon Whyatt says
Interesting indeed, though I wonder whether elite athletes are the best people to study?
They are no doubt genetic outliers. Perhaps they are still in top condition despite all the training they’ve done.
Would be great to see same study with a larger study, with a greater cross section of subjects. Also prospective – surely there’s a high risk of survivorship bias also?
Michel Accad says
Good post, Larry.
For some reason I cannot access the full text, even with my university library account, so I couldn’t read the recruitment method (may be too early for release). I wonder if the absence of atrial fibrillation is not a selection bias effect.
Katja Rietdorf says
Thanks for this well balanced view on the article. I work on atrial fibrillation myself and classify myself as an endurance athlete, training 8-12+ h a week for a 12 h bike race.
I am well aware of the studies linking cardiac problems and endurance exercise, and am glad that not all find an increased cardiovascular risk with the level of exercise done. But there are plenty of other health problems, like cancer, diabetes, neuro-degenerative diseases etc. which are reported to benefit from exercise. Are you aware of any studies for these diseases checking whether the beneficial effects might also be ‘bell shaped’ and ‘too much’ exercise can actually also carry a risk? The cancer study you mentioned shows no such correlation, but are you aware whether any work on endurance athletes has actually been carried out?
Larry Creswell, MD says
Great questions, Katja. Sadly, the truth is that “extreme” exercisers simply haven’t been studied in any detail.
@ everyone who metioned the selection bias: I am a non-scientist, so please explain what could that be? That the athletes are all healthy? The controll group consisted of healthy individuals, too. Could you please elaborate on that? Thanks a lot.
Can everyone read the study for free or do I have to pay for the journal?
Larry Creswell, MD says
I think the article is only available to subscribers (including libraries).
Selection bias can apply to both the study group and the control group. We say there is selection bias when a group is not representative of a larger population for some reason. Any reason.