The world literature reports that among young individuals subjected to strenuous exertion, sometimes competing at high altitudes, there may be an increase in the levels of cardiac troponin I and also of cardiac troponin T [4].
In some cases, physical exertion is accompanied not only by an increase in troponin but also by cardiac functional manifestations. Some athletes presented dyspnea, reversible pulmonary hypertension, and increased levels of cardiac troponin I associated with right ventricle dysfunction, as proven by echocardiography [9].
However, some alterations in the cardiovascular system of elderly individuals can promote higher risk for myocardial injuries. The increase of ventricle wall thickness, the increase of tension in the ventricle wall, and prolonged myocardial contraction may result in impaired perfusion of the endocardial cells [8].
It seems that the coronary flow does not change with age, but there are no studies to measure it in elderly individuals without coronary artery disease [4]; this opens the perspective that, under intense physical exertion, small changes in this flow may promote injuries in asymptomatic myocardial cells.
In the single study found in the world literature about myocardial injury in the elderly after long-distance runs, Lucía et al. [10], by analyzing the troponin I levels in elderly people participating in the Madrid Marathon, did not find any evidence of myocardial injury . It is worth noting that the number of participants of both sexes in that single study of an elderly population was ten.
We found significant differences between CPK 1 and CPK 2 samples, showing that although the initial value was high, the test contributed to increase that value. However, when we compared CPK 2 and CPK 3 samples as well as CPK 1 and CPK 2 samples, no statistical differences were observed. This phenomenon may be attributed to the reduced number of subjects participating in the present study, associated to a few disagreeing CPK values, which may have contaminated the sample.
The samples collected before the marathon run showed an increase in the CPK and CK-MB levels. The average of these values and the fact that almost half the athletes presented high CPK and CK-MB levels disagree with the findings published in the literature, where such levels are normal in most samples collected before the marathon run [3, 13]. Most probably this is because, as reported by the athletes themselves, they had been intensely training until the day before the marathon run. The studies mentioned above estimate that the athletes had reduced their training rhythm 1 week before the marathon run and practiced maintenance exercises only.
We found a pattern of CK-MB increase compared to the initial sample, although the high values were maintained after the run. We believe that the high value found in sample 2 and the maintenance of the result in sample 3 are due to the release of the marker of the myocardial musculature injured during the marathon run, proving the findings shown in the literature.
With such high levels of CPK and CK-MB levels, it is impossible to detect the presence or absence of concomitant myocardial injury by just analyzing these substances; thus, the analysis of cardiac troponin I levels is particularly important to detect myocardial injury in these athletes.
The cardiac troponin I level of the runners admitted in this study did not change in any of the samples and was maintained always below 0.50 ng/ml.
Our findings are close to those reported by Lucía et al. [10]. We observed an expressive increase in the CPK and CK-MB values in the elderly runners, although they ran a shorter distance (15 km). The cardiac troponin I value was found to be within the normal range, showing that up to the distance they ran the athletes did not present myocardial injury.