Remember my post “X+Y = Wellness?” In it, I asked:
When did this become our dominant paradigm?
cardiovascular capacity = fitness = wellness
And, I concluded:
I’m not saying people shouldn’t run, or cycle, or do things to enjoy their bodies. What I am saying is that what we need is a profound, profound paradigm shift away from athletic-based performance measures as indicators of health and wellness and towards the things that truly allow human beings to live fulfilling, rich, long lives.
I read an abstract* of a journal article this week that reminded me, yet again, of the dangers (and I don’t use that term lightly) of conflating “athletic performance” and “wellness.”
The article is titled “Predictors of cardiac troponin release after a marathon,” and it can be found online here in the Journal of Science and Medicine in Sport.
It was an observational study and it’s objective was articulated as follows:
Exercise leads to an increase in cardiac troponin I (cTnI) in healthy, asymptomatic athletes after a marathon. Previous studies revealed single factors to relate to post-race cTnI levels. Integrating these factors into our study, we aimed to identify independent predictors for the exercise-induced cTnI release.
So let’s back up. What’s troponin and why do we care about independent predictors of its release?
Troponin is a regulatory protein and it comes in three forms: C, I and T. Troponin is involved in muscle contraction for cardiac and skeletal muscles, but not smooth muscles. There is a lot more that can be said on the topic of troponin, but for our purposes it’s not necessary to go further.
The thing that we do need to know about it is that increased levels of troponin circulating in the blood can indicate damage to the heart muscles and such measurements can be a diagnostic tool for acute myocardial infarction, a/k/a a “heart attack.”
Now, back to the study.
It has been previously established – that is, as established as things get in this realm – that marathon running can elevate troponin levels in the blood. Here’s a link to a 2010 meta-analysis and literature review concluding:
The available data demonstrate that cTn levels are frequently elevated after a marathon with unclear cardiovascular significance. This elevation of cTn appears to be consistent among a diverse patient population.
(cTn = cardiac troponin)
So the authors of this newly published research wanted to figure out whether there were any predictors that might influence these elevated levels. Specifically, they considered:
- participation in previous marathons
- exercise duration
- exercise intensity
- hydration status (as measured by relative weight change pre- and post- race)
They measured only the troponin I (cTnI) but according to their results:
cTnI increased significantly from 14 ± 12 ng/L at baseline to 94 ± 102 ng/L post-race, with 69% of the participants demonstrating cTnI levels above the clinical cut-off value (40 ng/L) for an acute myocardial infarction.
I just want to underscore the second part of that sentence: Nearly seventy percent of the marathoners sampled had levels of troponin, an indication of damage to the heart muscle, ABOVE the clinical cut-off value for a heart attack.
Using “linear backward regression analysis,” they found two factors that predicted higher post-race levels of troponin I:
- younger age
- longer exercise duration
(“Longer exercise duration.” That would include the slow marathoners. Like yours truly, who completed the Chicago marathon in 2005.)
Now, whether this post-race damage translates into a health risk has not been established. I’ve culled a few articles on the subject for you to review here**. One could argue that the destruction of heart tissue causes muscle growth and development leading to a stronger, healthier heart.
But, it does not necessarily follow from that destroy and rebuild premise that more is better. The danger or the salvation is in the dose, and this was the idea explored in an article published in June 2012 in the Mayo Clinic Proceedings.
Lead author, James H. O’Keefe, states:
… a safe upper dose limit potentially exists, beyond which the adverse effects of physical exercise, such as musculoskeletal trauma and cardiovascular stress, may outweigh its benefits.
In essence, O’Keefe and his colleagues argue that the repeated injuries to the heart that occur in training for and competing in endurance events can cause structural changes and adaptations to the heart.
So my takeaway from the new article on predictors of cardiac troponin release is pretty simple:
I’m not going to be running any more marathons in this lifetime.
That’s where I come down. I just don’t see terrific longitudinal data that these repeated insults to the heart muscle are not problematic. And remember, you have to consider the amount of training that is required to run a marathon. We’re not talking about a one-time troponin release. We’re talking about repeated, weekly insults to the heart muscle culminating in the final event.
If endurance events are your bread-and-butter, then take a gander through the information I’ve offered you and make up your own mind on the matter. I will absolutely keep my eyes and ears open for developments on this issue.
My other takeaway is a re-affirmation of my contention before, that we need to start assessing wellness by a means other than athletic performance. Our go harder, faster, longer societal impulse, be damned.
* Apologies that I did not read the full study. I know that unless I read the full study, I cannot offer the most credible conclusions. But the institution through which I get access to academic journals does not offer access to this one, and I just can’t afford or justify the $37 price tag.
** There are nine articles listed and there are some very compelling findings in some of them. Give them a peek.
You can find this and other gems at Thank Goodness It’s Monday here!