Several studies have observed increases in the concentration of cTnI and cTnT in highly trained athletes during training and after athletic competition (51-63). The majority of reports have addressed marathon runners and triathletes. The early literature confused the presence of increased CK-MB in athletes with myocardial injury. This hypothesis was dispelled with the evidence that CK-MB-enriched skeletal muscle, injured during intense exercise, was responsible for the increased serum CK-MB values (62,63). Substantial

JiSSiSiTij 3.5S 5S

Fig. 9. Serum cTnT alterations in rats exposed to 3-5 h of intense exercise;p < 0.01 vs controls; p < 0.01 between groups. (Reproduced from ref. 55.)

increases in cardiac troponin have been reported as follows: ultracyclists with increase in cTnl in 34% of 38 participants (59); 6 of 23 Ironman triathletes, along with abnormalities in their ECG (51); 10% of marathon runners with increases in cTnT and cTnl, evaluated in at least five different studies (6-24 h post race) (56-58,60,62,63); military recruits in arduous training with increases in cTnT (62). Extreme exercise using 3-5 h of forced swimming in a rat model showed substantial increases in cTnT that corresponded with histological evidence of localized myocyte damage (Figs. 9 and 10) (55). However, in human subjects, studies have demonstrated normal postrace quantitative antimyosin myocardial imaging in asymptomatic marathon runners (excluding silent myocardial cell necrosis by imaging), even in the presence of increased cardiac troponin evidence of myocardial cell death (56). Possible mechanisms for the release of cardiac troponin may be global ischemia injury or a more natural turnover of myocardial cells following the stress of running, an issue currently under debate. Long-term risk stratification or outcome studies in these apparently healthy endurance athletes have not been performed.

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