Myocardial Stress After Competitive Exercise in Professional Road Cyclists

Dear Editor-in-Chief: We read with interest the article by König et al. (3) and applaud the authors for tackling an exciting and rapidly changing area. However, we believe a number of points need to be clarified. Two details initially need to be addressed: 1) our article (5) did not examine myocardial damage after extreme endurance exercise; rather, it examined short-term exercise and markers of myocardial damage, and 2) the second article referenced from our group (6), examined a 2-d mountain marathon (running), not cycling as suggested by König et al. (3). Clarification should also be made with regard to the cardiospecificity of the first- and second-generation cTnT assays. While our study (5) suggested that concern over the cardiospecificity of the first- and second-generation assays had been raised, König et al. (3) reiterate and expand this point to suggest that both assays “show considerable cross-reactivity with skeletal TnT.” This is not true; rather the first-generation cTnT assay demonstrated cross-reactivity with skeletal TnT, however, the second-generation assay employed completely cardiospecific antibodies. The second-generation assay did, however, possess poor linearity due to the use of bovine cTnT as the standard material. Accordingly, the third-generation assay was developed with recombinant human cTnT as the standard material to address the linearity problem. Collinson et al. (1) present a thorough discussion of the development of the cTnT assay. It should also be noted that the cTnT values observed within our study (6) were below the 0.1 μg·L−1 cutoff for myocardial infarction (MI) and not “beyond the threshold indicating substantial myocardial damage” suggested by König et al. (3). Clarification with regard to clinical cutoff levels for cTnT should also be made. Presently a cTnT concentration of 0.1 μg·L−1 is the cutoff for MI. The detection limit, however, of the third-generation assay is 0.01 μg·L−1, and due to the cardiospecificity of the antibodies now employed it is accepted that any elevation in cTnT provides evidence of cardiac insult (1). König et al. (3) report baseline cTnT as 0.01 ± 0 μg·L−1. We assume that <0.01 μg·L−1 is meant as this is the detection limit of the assay. While a mean rise in cTnT from <0.01 μg·L−1 to 0.02 μg·L−1 may not be statistically significant, an elevated cTnT value of 0.1 μg·L−1 observed in one subject is worthy of comment and is certainly not within the “normal range” given that the 99th percentile is 0.01 μg·L−1 (Roche Diagnostics). The precise origin of cTnT observed following prolonged exercise (cytosolic or myofibrilar), is presently not known, although our group and others (4) have suggested that it is likely cytosolic. Similarly the long-term implications of such cTnT release are yet to be elucidated. This coupled with recent discussion regarding stratification of cTnT cutoffs (2) suggest the phenomenon of exercise induced cardiac troponin release should not be dismissed. Additionally, recent work from our group suggests that cTnT release (both below and above the 0.1 μg·L−1 MI cutoff) following prolonged exercise (London Marathon) in less trained individuals is more widespread than previously thought and therefore warrants further investigation.