SBR Utopia - OPEN (Page 112)

Thought I'd post the attached (it's from a site that requires membership so I can't just post the link). . The Annual Meeting of The American College of Cardiology was this past week in San Francisco. I was not in attendance but have been reading the news synopses. I'm not trying to start a debate on risks of endurance sports, but I did find some of the comments below to be interesting - specifically phenotype/genotype/gender risk. While not stated below, gender risk might be negated by onset of menopause. Fred, if he pops over, could add more to this. I would not call any of this groundbreaking but it is contemporary. The author references data presented in live sessions at the meeting...fyi this does not mean that the data are yet peer reviewed. The commentary below is purely discussion. I don't know the author but note that he has identified himself as a competitive cyclist. Anyhow, found it interesting. 

Kim

Does exercise cause myocardial fibrosis? Please don't say exercise can cause heart disease

MAR 11, 2013 10:10 

What one treatment in the practice of medicine are you most sure of?

For me, it is absolutely clear: Regular exercise promotes and sustains wellness. Don't call it exercise; that's too clinical. Just say using your body on a regular basis.

Not all, but a large share, of this American College of Cardiology (ACC) 2013 meeting addresses diagnostic tests for and treatments of diseases that could have been prevented or delayed. Excluding genetic disorders and flukes of nature (paroxysmal supraventricular tachycardia and idiopathic cardiomyopathy, for example), much of what a heart doctor treats is avoidable. We can all agree that the human race is suffering through a period of severe underexercise.

This is why it hurts me to even bring up the idea that too much exercise could cause problems. You don't want anything down in print about exercise being bad for the heart.

But why wouldn't exercise have a dose-response curve? Everything does, except, perhaps, love. (Whoa, did I just type that?)

Endurance exercise and its potential to cause heart disease is a compelling narrative. All good stories feature conflict.

On the one hand, exercise is good and vital. But . . . on the other is the endurance-athlete mindset (I know them well). These folks have studied the training modules: You load the muscle with stress. Although this induces short-term inflammation, with adequate rest, the muscle adapts and comes back stronger. Our competitors train like crazy, so to win we must outwork our adversaries. Alas, the problem is that training like Lance does not mean riding like Lance. (That simile is less apropos these days, but you understand.)

There were a number of notable sessions at the 2013 ACC meeting that shed light on this intriguing topic. In the next few paragraphs, I will offer my completely biased views on the matter of chronically inflaming oneself over a lifetime.

Endurance athletics and AF

During a session entitled Turn the beat around: Atrial fibrillation in the active patient and athlete, Dr Brian Olshansky (University of Iowa) made clear that long-term endurance athletics (definitely) increases the risk of atrial fibrillation. There can be no debate on this. He also pointed out that female gender might be protective. Women endurance athletes seem not to have the association with AF. That was interesting. (Are women smarter about training?)

What is the mechanism of AF in athletes?

The short answer is we do not know. In the same session, Dr Rachel Lampert (Yale) offered evidence that there might be something to the interaction between high vagal tone interspersed with bursts of adrenaline. It makes sense because we know both milieus are arrhythmogenic: vagal stimulation decreases action potential duration and enhances electrical heterogeneity, while norepinephrine increases automaticity and ectopy. Add to this the possibility of structural remodeling and inflammation, and you have a good theory of why athletes are susceptible to AF.

The only thing I would add to this story is the possible role of genetics. Clearly, the phenotype of slow-twitch athletes with AF is repetitive—tall, Northern Euro, detail-oriented, measured, determined, etc. Why wouldn't their genotypes be similar as well? We know that AF has a strong genetic basis; it's a good bet that susceptibility to the effects of exercise is, too. What's more, might the same genes that make one think riding six hours in the rain is fun also make one susceptible to AF?

Is there such a thing as the Phidippides cardiomyopathy? It's a relevant question for electrophysiologists, because fibrosis increases the susceptibility to arrhythmia and sudden death. A great deal of observational data suggest that a small but not insignificant minority of endurance exercisers develop myocardial scar, predominantly in the right ventricle and septum. One theory is that short-term inflammation induces injury, and if the heart is never allowed to rest and heal, inflammation leads to scar. Postmarathon and -triathlon studies confirm transient rises in cardiac enzymes and RV dysfunction. And some studies show a correlation between exercise chronicity/intensity with fibrosis. (The above hyperlink takes you to a thorough review article on the subject.)

Not everyone agrees. Dr Kyler Barkley from the University of Texas presented this series of 93 healthy senior citizens for whom an extensive 20-year bank of demographic data were available. They grouped subjects into four strata of exercise ranging from sedentary to competitive athletes. Fitness tests along with MRIs were done in each of the subjects. Their findings were both simple and elegant. Cardiopulmonary fitness, measured by VO₂ max tests, correlated well with training, which isn't surprising, but confirms the validity of the self-reported exercise dose. Most importantly, none of the competitive-level seniors had evidence of scar on MRI scans. The conclusion: long-term endurance exercise does not cause fibrosis.

Two points were raised in the Q and A. The first addressed this study's differences from prior observational data on fibrosis. Dr Barkley hinted at the possibility that occult heart diseases might have accounted for the discordance. Their cohort was well measured and followed closely over two decades. The second issue was whether his study's subjects represented a survivor cohort. Were they just a self-selected group that tolerated the chronic exercise? The answer here is unknown.

My take

Please don't ask where the upper limit of exercise is. I don't think there is just one threshold. Individuals differ in their tolerance for stress. As physicians, though, we can emphasize to our patients what we know:

It is possible to exercise enough to harbor an increased risk of arrhythmia and maybe even induce fibrosis. It's worth noting that "superfitness" does not inoculate against heart disease. Do not judge a book by its cover. The engine should not be assumed healthy because the chassis looks sleek.

A final note: Good luck getting this cohort to modify their lifestyle.

JMM