Is cycling bad for the heart??

[Ajax Bay]

The “Extreme Exercise Hypothesis”: Recent Findings and Cardiovascular Health Implications
Caveat: Please read the paper - the precis below with my emboldening is my effort - you may read it differently.
BLUF
There is circumstantial evidence that supports the “Extreme Exercise Hypothesis: .” Subclinical and atherosclerotic coronary artery disease (CAD) as well as structural cardiovascular abnormalities and arrhythmias are present in some of the most active veteran endurance athletes and need appropriate clinical follow-up to reduce the risk for adverse cardiovascular outcomes. Future studies are warranted to establish the long-term cardiovascular health effects of these findings in veteran endurance athletes.

WHO recommends that adults engage in at least 150 min/week of moderate intensity aerobic activities: regular aerobic exercise associated with a reduced risk for cardiovascular morbidity and mortality and that more exercise is better, and it is estimated that maximal cardiovascular health benefits are obtained at an exercise volume that approximates up to 600 mins. The health effects of exercise volumes beyond the “optimal dose” are currently under debate.

Some studies reported an increased risk of disease and/or mortality from highest exercise volumes suggesting that health benefits may plateau or even decline in extreme exercisers. Studies have reported that the most active veteran endurance runners have an increased risk for myocardial fibrosis, coronary artery calcification, and atrial fibrillation (AF). These observations imply that high volumes of chronic endurance exercise training may be detrimental for the heart, hence, the “Extreme Exercise Hypothesis” characterized by a reverse J-shaped curve.

Conclusion
Extreme volumes and/or intensities of long-term exercise are associated with several possible cardiac maladaptations.
There is no clear threshold for an upper limit of the exercise-induced health benefits.
The most active older athletes often demonstrate a higher coronary artery calcification score but the associated cardiovascular risk implications of these observations are currently unknown.
Elevations of biomarkers for cardiomyocyte damage and myocardial fibrosis are common following intense exercise but normalize soon after exercise cessation.
Fibrosis is found in a small subgroup of veteran athletes, but again, the significance of this finding is unknown.
A reversed J-shaped association is found between exercise volumes and AF, with an increased risk at high volumes.
These data suggest:
(1) there is limited evidence that supports the “Extreme exercise hypothesis,” the most compelling relating to the increased risk of AF at high volumes of exercise;
(2) cardiac anomalies may be present in a small proportion of the most active veteran athletes;
(3) High-intensity exercise can acutely, albeit transiently, increase the risk for sudden cardiac arrest (SCA) or sudden cardiac death (SCD) in individuals with underlying cardiac disease.

 

[YellowV2]

I have no tiff, as I've said some forum members here literally know it all .

So you keep saying, do you have anything else informative to add as Ming is asking for?

 

[Ajax Bay]

@gzoom is not going to 'argue' with you boys and girls. They clickbait entitle a thread , post a video (note sub-titled "Is TOO MUCH cycling bad for your heart" with minimal comment (define 'too much' and 'bad'), and when asked for more say 'I'm a very bust person and shall not say what my take is on the video, will add no value, BHF are sponsoring more research - for what's known so far: go and look it up yourself, you guys all obviously know it all' and 11 pages on . . .

 

[FishFright]

@gzoom is not going to 'argue' with you boys and girls. They clickbait entitle a thread , post a video (note sub-titled "Is TOO MUCH cycling bad for your heart" with minimal comment (define 'too much' and 'bad'), and when asked for more say 'I'm a very bust person and shall not say what my take is on the video, will add no value, BHF are sponsoring more research - for what's known so far: go and look it up yourself, you guys all obviously know it all' and 11 pages on . . .

He posted a video with an interesting subject and then there was a huge pile on started by a poster that never even watched the video . After that why should anyone take the thread seriously?

 

[Ajax Bay]

'Cos it's a serious and interesting topic? And 'is cycling bad for your heart' may deter the short attention span viewer from getting out and riding their bike. Ming has a passion for accuracy: you should see their routesheets!

 

[FishFright]

'Cos it's a serious and interesting topic? And 'is cycling bad for your heart' may deter the short attention span viewer from getting out and riding their bike. Ming has a passion for accuracy: you should see their routesheets!

Oh great, the "in a hole with a owl" hypothesis .

 

[MontyVeda]

The other day i noticed this on the wall outside a local shop...

...probably not the best advert for running

 

[fossyant]

The other day i noticed this on the wall outside a local shop...
View attachment 684431
...probably not the best advert for running

It's no worse than the 'black run' signs at a trail centre - i.e. "Serious risk of injury or death, here is the local hospital number !"

 

[tom73]

You are better keeping pretty fit generally as you go into old age Big advantages having a good cardio system as you age. I've two mates that died young of heart attaks. One ex high level racer - died 55, other regular marathon runner, mid 45's. Alot of it is genetics and you can't change that. You can mitigate it by keeping fit.

I shan't worry about it, I'm going to keep smshing out the miles and keep trying to keep up with a couple of very speedy mates from here ! We're all of the no chance getting a leccy bike and we are in our 50's.

You've more chance of kicking it being hit by a car.

Same with my dad he lost a mate in his early 20's from a heart attack. He was a national , international champion hurdler went on to be part of the GB olympic team.

 

[Mr Celine]

Cycling bad for the heart? Possibly, though I haven't seen any robust evidence of that, either on this thread or anywhere else.

On the other hand learning to swim increases your risk of drowning.

I'm going to try to forget how to swim and keep on cycling.

 

[HLaB]

Post #134 in this thread

Well done for keeping up with it all

 

[notmyrealnamebutclose]

60% of the time cycling is 100% deadly

 

[presta]

Since you’re all such fans of evidence, let’s have a look at the newest, largest, and most comprehensive study there’s ever been.

Garcia et al published a new meta-study as recently as 3 months ago, and it’s huge: 196 articles, 94 cohorts with >30 million participants, 163 million person-years of data, and 810,000 deaths. That’s 17 times as many person-years, and 7 times as many deaths as the previous biggest study, which has for the first time enabled them to sub-divide by disease, and produce dose-response curves. Any studies with fewer than 10,000 participants were excluded to reduce the risk of them degrading the accuracy. (A meta-study is a collation of all the relevant studies so that the results can be pooled to increase statistical significance, and avoid cherry-picking.)

Taking at the all-cause mortality for example, their results look like this:

As you can see, as exercise level increases, the risk of death drops markedly at first, and then begins to level off. The zone shaded in dark is the lowest 75% of person-years of data, and the vertical dotted lines mark the 37.5th and 75th centiles. The paler region beyond has been presumed, and constrained, to be linear at the same slope as the 75th centile.

Exercise dose is measured in marginal MET hours per week. METs are a unit for measuring metabolic rate in kcals per hour per kg of bodyweight, so MET hours per week are effectively kcals per week per kg. Marginal means that they are measuring activity over and above sedentary levels: that is, the increase imposed by activity.

In more familiar terms of cycling rather than marginal METhr/wk, if we take a typical cycling speed of 12mph, the metabolic rate from the ACSM Compendium is about 7.4METs. So as the rate for sedentary behaviour is 1MET, the marginal rate is 6.4METs, therefore in one hour you complete 12 miles for 6.4 mMET hours. That gives a ratio of 12/6.4 = 1.875 miles/mMEThr, or for the sake of round numbers, say about two.

We can then calibrate the same graph above in terms of weekly mileage on the bike assuming 12mph (Scale appended in red):

So as you can see, anyone cycling more than about 25 miles a week is off the end of the region for which the data is reliable, and at 60 miles/wk you’re beyond the point where there’s any data at all. I’ve included (in blue) a marker indicating my average exercise level for the 20 year period from 1992-2011. My average for 2009 was twice that again.

Looking at individual conditions separately, you can see that even within the limited range for which there’s reliable data, the risk of some is starting to rise as exercise levels increase:

The paper also comes with an interactive calculator website, so you can amuse yourself playing around with individual conditions, but AF in particular is too specific to appear as a separate graph.

It’s easy to see why the reliable data ends where it does when you compare the risk plot against the distribution of exercise dose among the study subjects:

The most common level of exercise is the equivalent of just 7miles of cycling a week, and half the population are doing less than 20m/wk. So, yes, exercise is very good for you, but the only evidence for that is at levels far below what a typical cycling enthusiast is likely to be doing. In short, Garcia shows good evidence that moderate exercise is better than none, but not any evidence that a lot of exercise is better still, or even that it isn’t worse.

That distribution doesn’t bode well for the prospect of getting any large scale studies into AF when large volumes of exercise are the very thing you need to be able to test, and especially as there’s a 20-30 year latency period from exposure to developing the arrhythmia. One reason that existing studies are of limited accuracy is that they’re mostly retrospective, with difficulties in retrospectively quantifying exercise dose, and all the confounding variables you need to control for. On the other hand, if you want a prospective study, not only are you likely to have to wait decades for the result, but you have the job of recruiting a huge number of people willing to keep accurate exercise records for that length of time. I think those who demand more statistical rigour have a choice: make a timely decision using the best information available, or wait until it’s too late in the hope of getting what you want. Even recent meta-studies are still using quite old data, because there isn’t much new stuff coming through yet.

There are those on here who concede that cycling increases the risk of AF, but insist that it only applies to athletes, so what’s the definition of an athlete? Well, perhaps unsurprisingly, there isn’t one, or at least not a standardised one.

Pelliccia et al in the 2020 guidelines from the ESC (European Society of Cardiology) for cardio patients participating in sport have the most to say on the matter:

“The ESC defines an athlete as ‘an individual of young or adult age, either amateur or professional, who is engaged in regular exercise training and participates in official sports competition’. Similarly, the American Heart Association (AHA) and others define a competitive athlete as an individual involved in regular (usually intense) training in organized individual or team sports, with an emphasis on competition and performance.”

In essence, a competitive cyclist, on the grounds that they’re the ones most likely to be motivated to train hard, but they then go on to say:

“In a proposed classification of athletes based on the minimum volume of exercise, ‘elite’ athletes…generally exercise ≥10h/week; ‘competitive’ athletes…exercise ≥6h/week; and ‘recreational’ athletes exercise ≥4h/week.”

And then finally, they finish with:

“This distinction is somewhat arbitrary since some recreational athletes, such as long-distance cyclists and runners, engage in exercise at higher volumes than some professional athletes”

No sh!t? I was averaging over 14 hours a week in 2009.

In Recommendations For Participation In Leisure-Time Physical Activity And Competitive Sports (2006) Heidbuchel et al said:

"It needs to be stressed, however, that there is no clear division between recreational and (semi)-competitive sports. Some patients may engage in high intensity exercise during leisure time activities”

In AF In Athletes And The Interplay Between Exercise And Health (2013) La Gerche et al said:

“..what is seen as vigorous exertion in cardiovascular epidemiology studies would not even be considered warm up tempo in sports science parlance”

It’s the same with the definition of ‘vigorous’ or ‘high intensity’. Pelliccia above defines:

Moderate Intensity as 55-74% MHR and
High intensity as 75-90% MHR, (70-85% HRR)

(But beware that Verdicchio says that %HRR is not a valid measure of intensity in AF patients because its correlation as a proxy for %VO2 doesn’t hold true.)

On the other hand, Garcia defines vigorous exercise as 7METs, which is about 12mph cycling, and in the 2013 Guidelines for Exercise Testing and Prescription, the ACSM define vigorous as 6METs, which is only 10mph.

As LaGerche et al says: “The non-standardised gradations of exercise intensity complicate interpretation of exercise studies.”

So you have a catch-22, without a clear definition of the difference between the control and study group it’s difficult to avoid cross-contamination of the two groups, and with cross-contamination the effect of the exercise becomes diluted in the test results. Some on here are quoting data for all cardiac conditions, but that will also mask the data for AF in particular.

With all that in mind, Calvo et al have produced the first ever dose-response curve similar to the Garcia ones for exercise-induced AF. They found that the most powerful predictor was lifetime-accumulated hours of high-intensity endurance training. AF cases had a history of nearly 5 times the training hours of the controls, and those with a history of more than 2000 hours had nearly four times the odds of developing AF. Endurance sports like cycling were much more risky than team sports.

What I found particularly interesting is that after controlling for exercise hours, competitive athletes were less likely to develop AF than non-athletes. So it’s the exercise hours that were the determinant of risk, not whether you’re a competitive athlete! My guess is that this might be because athletes benefit from organised coaching, which would put them in a better position to avoid overtraining.

So from this plot, 1000 hours is about optimum for maximising health benefit, and by the time you reach 2000hr all that benefit is lost.

As ever, the intensity is not objectively defined, Calvo uses four subjective levels assessed with questionnaire:
1. Sedentary: no physical effort, minimal walking
2. Light: minimal effort, eg. slow walking, no increase in HR, no perspiration
3. Moderate:, not exhausting, slightly increase HR, some light perspiration
4. High-intensity: vigorous, intense sweating and deep-breathing

For my own part, I can account for over 8,000 hours, with more still that went unaccounted, so if even a quarter of that was high intensity that puts me into the risk zone, especially as I’m 6’5”, and height is another major risk factor which exacerbates the effect of training (see below).

Crump et al is an interesting paper, not only because it’s huge like Garcia, with over 1.5m male participants, but it also uses objectively measured data harvested from military conscription records. They’re measuring aerobic fitness at age 18 though, which is a poor substitute for lifetime exercise hours, so it doesn’t show such a strong effect.

The purpose of it, however, was to explore the interaction of other risk factors like height and weight, and what they found was that not only were height weight and fitness risks for AF, but fitness magnified the effect of height and weight. Tall stature and high aerobic fitness was the highest risk of all, and fitness is actually protective for short men. If other studies aren’t controlling for height and weight, this may explain a lot of the variation in past results.

It occurs to me that the lower risk for athletes compared to non-athletes, and the lower risk by fitness rather than by exercise hours might be indicating that the root cause of AF risk is overtraining rather than either fitness or exercise hours per se.

So what’s the current advice?

Well, the 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation say:

“Physical activity should be considered to help prevent AF incidence or recurrence, with the exception of excessive endurance exercise, which may promote AF.”

This is categorised as

Class IIa: Weight of evidence/opinion is in favour of usefulness/efficacy. Should be considered

and

Level C: Consensus of opinion of the experts and/or small studies, retrospective studies, registries.

The supplementary data to the above guide lists all the risk factors for incident AF:

Nobody would argue that eating as much as you can is healthy on the grounds that starving is unhealthy, I think it’s bizarre to suggest that exercise is any different.

 

[All uphill]

Since you’re all such fans of evidence, let’s have a look at the newest, largest, and most comprehensive study there’s ever been.

Garcia et al published a new meta-study as recently as 3 months ago, and it’s huge: 196 articles, 94 cohorts with >30 million participants, 163 million person-years of data, and 810,000 deaths. That’s 17 times as many person-years, and 7 times as many deaths as the previous biggest study, which has for the first time enabled them to sub-divide by disease, and produce dose-response curves. Any studies with fewer than 10,000 participants were excluded to reduce the risk of them degrading the accuracy. (A meta-study is a collation of all the relevant studies so that the results can be pooled to increase statistical significance, and avoid cherry-picking.)

Taking at the all-cause mortality for example, their results look like this:

View attachment 685106

As you can see, as exercise level increases, the risk of death drops markedly at first, and then begins to level off. The zone shaded in dark is the lowest 75% of person-years of data, and the vertical dotted lines mark the 37.5th and 75th centiles. The paler region beyond has been presumed, and constrained, to be linear at the same slope as the 75th centile.

Exercise dose is measured in marginal MET hours per week. METs are a unit for measuring metabolic rate in kcals per hour per kg of bodyweight, so MET hours per week are effectively kcals per week per kg. Marginal means that they are measuring activity over and above sedentary levels: that is, the increase imposed by activity.

In more familiar terms of cycling rather than marginal METhr/wk, if we take a typical cycling speed of 12mph, the metabolic rate from the ACSM Compendium is about 7.4METs. So as the rate for sedentary behaviour is 1MET, the marginal rate is 6.4METs, therefore in one hour you complete 12 miles for 6.4 mMET hours. That gives a ratio of 12/6.4 = 1.875 miles/mMEThr, or for the sake of round numbers, say about two.

We can then calibrate the same graph above in terms of weekly mileage on the bike assuming 12mph (Scale appended in red):

View attachment 685107

So as you can see, anyone cycling more than about 25 miles a week is off the end of the region for which the data is reliable, and at 60 miles/wk you’re beyond the point where there’s any data at all. I’ve included (in blue) a marker indicating my average exercise level for the 20 year period from 1992-2011. My average for 2009 was twice that again.

Looking at individual conditions separately, you can see that even within the limited range for which there’s reliable data, the risk of some is starting to rise as exercise levels increase:

View attachment 685108

The paper also comes with an interactive calculator website, so you can amuse yourself playing around with individual conditions, but AF in particular is too specific to appear as a separate graph.

It’s easy to see why the reliable data ends where it does when you compare the risk plot against the distribution of exercise dose among the study subjects:

View attachment 685109

The most common level of exercise is the equivalent of just 7miles of cycling a week, and half the population are doing less than 20m/wk. So, yes, exercise is very good for you, but the only evidence for that is at levels far below what a typical cycling enthusiast is likely to be doing. In short, Garcia shows good evidence that moderate exercise is better than none, but not any evidence that a lot of exercise is better still, or even that it isn’t worse.

That distribution doesn’t bode well for the prospect of getting any large scale studies into AF when large volumes of exercise are the very thing you need to be able to test, and especially as there’s a 20-30 year latency period from exposure to developing the arrhythmia. One reason that existing studies are of limited accuracy is that they’re mostly retrospective, with difficulties in retrospectively quantifying exercise dose, and all the confounding variables you need to control for. On the other hand, if you want a prospective study, not only are you likely to have to wait decades for the result, but you have the job of recruiting a huge number of people willing to keep accurate exercise records for that length of time. I think those who demand more statistical rigour have a choice: make a timely decision using the best information available, or wait until it’s too late in the hope of getting what you want. Even recent meta-studies are still using quite old data, because there isn’t much new stuff coming through yet.

There are those on here who concede that cycling increases the risk of AF, but insist that it only applies to athletes, so what’s the definition of an athlete? Well, perhaps unsurprisingly, there isn’t one, or at least not a standardised one.

Pelliccia et al in the 2020 guidelines from the ESC (European Society of Cardiology) for cardio patients participating in sport have the most to say on the matter:

“The ESC defines an athlete as ‘an individual of young or adult age, either amateur or professional, who is engaged in regular exercise training and participates in official sports competition’. Similarly, the American Heart Association (AHA) and others define a competitive athlete as an individual involved in regular (usually intense) training in organized individual or team sports, with an emphasis on competition and performance.”

In essence, a competitive cyclist, on the grounds that they’re the ones most likely to be motivated to train hard, but they then go on to say:

“In a proposed classification of athletes based on the minimum volume of exercise, ‘elite’ athletes…generally exercise ≥10h/week; ‘competitive’ athletes…exercise ≥6h/week; and ‘recreational’ athletes exercise ≥4h/week.”

And then finally, they finish with:

“This distinction is somewhat arbitrary since some recreational athletes, such as long-distance cyclists and runners, engage in exercise at higher volumes than some professional athletes”

No sh!t? I was averaging over 14 hours a week in 2009.

In Recommendations For Participation In Leisure-Time Physical Activity And Competitive Sports (2006) Heidbuchel et al said:

"It needs to be stressed, however, that there is no clear division between recreational and (semi)-competitive sports. Some patients may engage in high intensity exercise during leisure time activities”

In AF In Athletes And The Interplay Between Exercise And Health (2013) La Gerche et al said:

“..what is seen as vigorous exertion in cardiovascular epidemiology studies would not even be considered warm up tempo in sports science parlance”

It’s the same with the definition of ‘vigorous’ or ‘high intensity’. Pelliccia above defines:

Moderate Intensity as 55-74% MHR and
High intensity as 75-90% MHR, (70-85% HRR)

(But beware that Verdicchio says that %HRR is not a valid measure of intensity in AF patients because its correlation as a proxy for %VO2 doesn’t hold true.)

On the other hand, Garcia defines vigorous exercise as 7METs, which is about 12mph cycling, and in the 2013 Guidelines for Exercise Testing and Prescription, the ACSM define vigorous as 6METs, which is only 10mph.

As LaGerche et al says: “The non-standardised gradations of exercise intensity complicate interpretation of exercise studies.”

So you have a catch-22, without a clear definition of the difference between the control and study group it’s difficult to avoid cross-contamination of the two groups, and with cross-contamination the effect of the exercise becomes diluted in the test results. Some on here are quoting data for all cardiac conditions, but that will also mask the data for AF in particular.

With all that in mind, Calvo et al have produced the first ever dose-response curve similar to the Garcia ones for exercise-induced AF. They found that the most powerful predictor was lifetime-accumulated hours of high-intensity endurance training. AF cases had a history of nearly 5 times the training hours of the controls, and those with a history of more than 2000 hours had nearly four times the odds of developing AF. Endurance sports like cycling were much more risky than team sports.

What I found particularly interesting is that after controlling for exercise hours, competitive athletes were less likely to develop AF than non-athletes. So it’s the exercise hours that were the determinant of risk, not whether you’re a competitive athlete! My guess is that this might be because athletes benefit from organised coaching, which would put them in a better position to avoid overtraining.

View attachment 685110

So from this plot, 1000 hours is about optimum for maximising health benefit, and by the time you reach 2000hr all that benefit is lost.

As ever, the intensity is not objectively defined, Calvo uses four subjective levels assessed with questionnaire:
1. Sedentary: no physical effort, minimal walking
2. Light: minimal effort, eg. slow walking, no increase in HR, no perspiration
3. Moderate:, not exhausting, slightly increase HR, some light perspiration
4. High-intensity: vigorous, intense sweating and deep-breathing

For my own part, I can account for over 8,000 hours, with more still that went unaccounted, so if even a quarter of that was high intensity that puts me into the risk zone, especially as I’m 6’5”, and height is another major risk factor which exacerbates the effect of training (see below).

Crump et al is an interesting paper, not only because it’s huge like Garcia, with over 1.5m male participants, but it also uses objectively measured data harvested from military conscription records. They’re measuring aerobic fitness at age 18 though, which is a poor substitute for lifetime exercise hours, so it doesn’t show such a strong effect.

The purpose of it, however, was to explore the interaction of other risk factors like height and weight, and what they found was that not only were height weight and fitness risks for AF, but fitness magnified the effect of height and weight. Tall stature and high aerobic fitness was the highest risk of all, and fitness is actually protective for short men. If other studies aren’t controlling for height and weight, this may explain a lot of the variation in past results.

View attachment 685112

View attachment 685114

It occurs to me that the lower risk for athletes compared to non-athletes, and the lower risk by fitness rather than by exercise hours might be indicating that the root cause of AF risk is overtraining rather than either fitness or exercise hours per se.

So what’s the current advice?

Well, the 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation say:

“Physical activity should be considered to help prevent AF incidence or recurrence, with the exception of excessive endurance exercise, which may promote AF.”

This is categorised as

Class IIa: Weight of evidence/opinion is in favour of usefulness/efficacy. Should be considered

and

Level C: Consensus of opinion of the experts and/or small studies, retrospective studies, registries.

The supplementary data to the above guide lists all the risk factors for incident AF:

View attachment 685116

Nobody would argue that eating as much as you can is healthy on the grounds that starving is unhealthy, I think it’s bizarre to suggest that exercise is any different.

Thank you for that. Great work.

 

[Ajax Bay]

Magnum opus. BZ!