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Raised troponin T and echocardiographic abnormalities after prolonged strenuous exercise—the Australian Ironman Triathlon

TLDR
Participation in ironman triathlon often resulted in persistently raised cTnT levels, and the troponin rise was associated with echocardiographic evidence of abnormal left ventricular function.
Abstract
Background: There is concern about whether cardiac damage occurs as a result of prolonged strenuous exercise. Objective: To investigate whether competing in a triathlon is associated with cardiac damage based on a sustained increase in cardiac troponin T (cTnT), and whether such an increase correlates with echocardiographic changes Methods: cTnT and echocardiographic measurements were made in 38 participants in the 2001 Australian ironman triathlon. cTnT was measured the day before, immediately after, and the day following the race. Echocardiography was done the day before, immediately after, and two to six weeks later for measurement of ejection fraction, stroke volume, cardiac output, wall motion analysis, and global left ventricular function (LVF). Results: No subject had detectable cTnT in the pre-race sample. Following the race, 32 subjects (86.5%) had detectable levels of cTnT (>0.01 ng/ml), with six (16.2%) having >0.10 ng/ml. The day after the race, nine subjects (23.7%) still had detectable cTnT, with two recording a level >0.10 ng/ml. Previously described echocardiographic changes of “cardiac fatigue” were observed in the whole cohort. There was a modest but significant correlation between change in ejection fraction and peak cTnT level (p = 0.02, r  = 0.39). Athletes with a post-race cTnT >0.10 ng/ml had a greater decrease in global LVF (p = 0.02) and a trend toward a greater fall in ejection fraction and stroke volume than athletes with cTnT levels 0.10 ng/ml (p>0.05). Conclusions: Participation in ironman triathlon often resulted in persistently raised cTnT levels, and the troponin rise was associated with echocardiographic evidence of abnormal left ventricular function. The clinical significance and long term sequelae of such damage remains to be determined.

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Exercise-Induced Cardiac Troponin Elevation: Evidence, Mechanisms, and Implications

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References
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Cardiac Troponin T Levels for Risk Stratification in Acute Myocardial Ischemia

TL;DR: The usefulness of base-line levels of cardiac troponin T and CK-MB and the electrocardiographic category assigned at admission and the presence of confounding factors that impair the detection of ischemia were assessed to assess the usefulness of outcome.
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Exercise-Induced Muscle Damage and Adaptation

TL;DR: Physical conditioning results in an adaptation such that all indicators of damage are reduced following repeated bouts of exercise, and investigators have suggested that the prophylactic effect of training may be due to performance of a single initial exercise bout.
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It’s Time for a Change to a Troponin Standard

TL;DR: Issues related to the biochemical diagnosis of acute myocardial infarction are emphasized, and new and improved plasma biomarkers with better sensitivity and specificity will be emphasized in preference to markers such as total creatine kinase (CK), CK-MB, lactate dehydrogenase, and aspartate aminotransferase.
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Improved troponin T ELISA specific for cardiac troponin T isoform: assay development and analytical and clinical validation

TL;DR: A cardiac-specific second-generation troponin T ELISA (TnT 2) was developed, in which the cross-reactive antibody 1B10 has been replaced by a high-affinity cardiac- specific antibody M11, which shows promising results in patients with severe skeletal muscle injury.
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Muscle Fiber Necrosis Associated With Human Marathon Runners

TL;DR: It is concluded that both the intensive training for, and the marathon itself, induce inflammation and fiber necrosis which are manifested in the clinical symptoms for rhabdomyolysis and myoglobinuria.
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