I think this is a physiological  and normal response to abnormal and pathological ultra-intense exercise. These physiologic processes are a reflection of exercise-induced cardiac or muscle damage. Many studies were demonstrated an influence of a lifetime of endurance or ultra-endurance exercise upon the heart with induction of myocardial fibrosis and late gadolinium enhancement in athletes...

Thank you for the answer Tatiyana Vaikhanskaya

I think this is self-induced pathology!

You should compare the cutoff values, because all biomarkers will rise aftar any continuous exercise

Thanks Noble and Marocolo for your answer

I think it's a very good question and the answer remains unclear.

If we see the detectable Tn seen in high intensity exercise as purely physiological, we could point to the hypothesis that strenuous excercise induces an increase in myocardial sarcolemmal membrane permeability allowing some of cardiac specific troponins detectable on current high sensitivity assays to reach the circulation without any hint of pathological injury.

If we hypothesise that there is an element of low level pathological myocardial injury that can be induced by high intensity exercise, we might see this as a form of very low grade Type II myocardial ischaemia.  This describes myocardial ischaemia that is not driven by coronary flow limitation per se, but rather by a mismatch between metabolic supply and demand of the myocardial substrate.

We frequently see this Type II ischaemia clinically in scenarios where sometimes staggering troponin rise can be seen in instances other than coronary flow limitation-such as in the septic shock patient in ICU or the hypoxic, hypovolaemic patient and in numerous other scenarios.

However, I think one can also look at this question totally differently by critically examining what we mean by the word 'pathological'.

For something to be 'pathological', it really has to be associated with a definable adverse risk or outcome to us.

Exercise training on the other hand is known to decrease cardiovascular risk and increase numerous beneficial health outcomes.  In that regard, it would be hard to sensibly use the word 'pathological' to describe the troponin finding in exercise for most individuals, whatever its mechanism may be at the cellular level.

It is physiologically risen same as the ckmb

Hi,

This subject is compelling and intriguing!

I agree it is still controversial, as well.

As far as I am concern, release of myocardial intracellular proteins into the blood stream is a sign of myocardial damage. Particularly if it is associated with myocardial fibrosis later on, as detected by late gadolinium enhancement.

As observed by Dr. Yu, a type II myocardial ischemia is an objective hypothesis for its pathophysiology, in my opinion. Those intensely trained athlete undergo cardiac remodeling-related ventricular hypertrophy, which will in turn increase myocardial VO2.  Depending on a particular coronary reserve, a supply vs demand mismatch will eventually occur. And type II myocardial ischemia is far from being harmless in other settings (PLoS One. 2014; 9(1): e84285. doi: 10.1371/journal.pone.0084285).

Many of those sports associated with strenuous physical exercise are actually much anew modalities (i.e., ultramarathon, triathlon, iron man, etc). Modern are, as well, sensitive markers of myocardial injury and myocardial scar imaging evaluation (i.e., MRI LGE). Thus, characterization of the cardiovascular risk associated is still to be defined.

Peace and blessings;

Well, this is fruitful discussion.

Exercise will also increase glomerular basement membrane in kidneys and lead to leak of albumin in urine . Up to my knowledge , this goes with hypothesis of increased myocardial sarcolemmal membrane permeability . Measuring serum level of these cardiac markers will categorize this level as physiological due to intense exercise or pathological due to true ischemia .

This is the critical question in relation to exercise-induced cardiac troponin release.  Many authors have documented cTn release following exercise, and it is not always prolonged or highly strenuous in nature.  Elevations in cTn have been documented after 30 minutes of treadmill running, basketball games and prolonged walking.  In the vast majority of cases the cTn release is relatively low in comparison to clinical cut-offs and is normalised within 24-48 hours.  These characteristics have led most to suggest that it is a physiologic release, much the same as the release of skeletal muscle markers after exercise.  However, occasionally the magnitude of release far exceeds clinical thresholds and in these individuals it is likely that the release of cTn is related to subclinical disease.  This field of research has walked hand in hand with the development of assays and so it is difficult to compare between studies, and the newer high sensitive assays are identifying more and more individuals with elevated cTn post-exercise.  There is therefore the risk of clinical confusion.  In one of our previous publications we have suggested an algorithm to deal with this issue (Shave JACC 2010).   Finally, while it is my belief that much of cTn release following exercise is physiologic in nature, I am not sure of the cumulative impact of minor elevations in cTn occurring time and time again over many years in competitive athletes.  Andre La Gerche and colleagues have studied/discussed this issue at length and have posed an intriguing hypothesis of pathological remodelling in response to prolonged exercise.  More work is certainly needed in this area...

If the subject is a fully trained stamina athlete such as a long distance runner, he/she may have cardiac hypertrophy that I regard as a pathological condition, but my colleagues above may consider physiological!