Original research
Predictors of cardiac troponin release after a marathon

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Abstract

Objectives

Exercise leads to an increase in cardiac troponin I in healthy, asymptomatic athletes after a marathon. Previous studies revealed single factors to relate to post-race cardiac troponin I levels. Integrating these factors into our study, we aimed to identify independent predictors for the exercise-induced cardiac troponin I release.

Design

Observational study.

Methods

Ninety-two participants participated in a marathon at a self-selected speed. Demographic data, health status, physical activity levels and marathon experience were obtained. Before and immediately after the marathon fluid intake was recorded, body mass changes were measured to determine fluid balance and venous blood was drawn for analysis of high-sensitive cardiac troponin I. Exercise intensity was examined by recording heart rate. We included age, participation in previous marathons, exercise duration, exercise intensity and hydration status (relative weight change) in our model as potential determinants to predict post-exercise cardiac troponin I level.

Results

Cardiac troponin I increased significantly from 14 ± 12 ng/L at baseline to 94 ± 102 ng/L post-race, with 69% of the participants demonstrating cardiac troponin I levels above the clinical cut-off value (40 ng/L) for an acute myocardial infarction. Linear backward regression analysis identified younger age (β = −0.27) and longer exercise duration (β = 0.23) as significant predictors of higher post-race cardiac troponin I levels (total r = 0.31, p < 0.05), but not participation in previous marathons, relative weight change and exercise intensity.

Conclusions

We found that cardiac troponin I levels significantly increased in a large heterogeneous group of athletes after completing a marathon. The magnitude of this response could only be partially explained, with a lower age and longer exercise duration being related to higher post-race cardiac troponin I levels.

Introduction

The presence of the cardiac troponin I (cTnI) in blood is a highly sensitive and specific biomarker for cardiac injury and serves as a central marker in the diagnosis of acute coronary syndromes.1, 2, 3 Many studies have demonstrated an increase in cTnI after prolonged endurance exercise, in the absence of clinical symptoms of a myocardial infarction.4, 5, 6 Relatively little is known, however, about factors that may be associated with, and thus potentially predict, the degree of elevation in cTnI after strenuous running exercise. This important information may help clinicians and laboratories with the challenging interpretation of elevated cTnI levels in athletes.

Studies examining factors that relate to the exercise-induced increase in cTnI have predominantly included small and homogeneous groups of athletes. These studies demonstrated that subject characteristics (i.e. age and running experience),7 exercise characteristics (i.e. exercise duration and intensity),5, 8, 9 and hydration status10 may relate to the exercise-induced increase in cTnI. These studies typically focused on a single factor only, thereby being unable to assess multiple parameters which may relate to post-race cTnI levels. As an exception to this rule, Fortescue et al. studied cardiac troponin responses in >400 Boston marathon runners.6 Although age and running inexperience were identified as factors contributing to post-exercise increases in cTnT, they did not correct for important confounders, such as exercise intensity.11, 12 Therefore, current studies provide only a limited insight into factors that could independently, or in combination, predict the magnitude of the exercise-induced increase in cTnI.

Therefore, the aim of this study was to identify parameters that predict the elevation in cTnI after a marathon in a large and heterogeneous group of athletes, and to explore the interaction of the identified parameters using regression analysis. The novel aspect of our study is that we examined the potential independent predictive capacity of parameters that have previously been related to the exercise-induced cTnI release. We hypothesized that exercise intensity, exercise duration, age, loss of body mass and running experience independently predict post-race cTnI levels.

Section snippets

Methods

A total of 92 moderately to highly trained runners (26–71 years of age) of the Eindhoven Marathon 2010 (The Netherlands) were recruited to the study. An advertisement was placed on the Eindhoven Marathons website to recruit participants. Before participation all participants provided written informed consent. The medical ethical committee of the Radboud University Nijmegen Medical Centre approved the study which was conducted in line with the Declaration of Helsinki.

All participants completed

Results

During the race mean wet bulb globe temperature (WBGT) was 18.8 °C, with a relative humidity of 52%. Of the 92 participants who started the race, 9 participants did not finish the race, because of exhaustion (n = 2), acute knee problems (n = 1), heat (n = 1), dyspnoea (n = 1), hip problems (n = 1), headache (n = 1) or another sport-related injury (n = 2) and were therefore not included in the analysis. One participant was excluded afterwards because of missing multiple data-points. Therefore, 82 participants

Discussion

This study confirmed the presence of exercise-induced release of cTnI in asymptomatic, healthy athletes competing in a marathon. In accordance with previous studies, cTnI levels increased significantly in our post-race blood sample, with 69% of the participants showing cTnI levels above the clinical cut-off point used for the diagnosis of an acute myocardial infarction.6, 7, 19 The novel aspect of our study is that we examined the potential independent predictive capacity of parameters that

Conclusion

In conclusion, we found that cTnI levels increased in a large heterogeneous group of athletes after completing a marathon. Including previously identified factors that relate to the exercise-induced release of cTnI into a statistical model, we found that the presence of this response was inversely correlated to the age of participants, whilst longer exercise duration also resulted in higher exercise induced troponin levels. Other factors that have previously been demonstrated to relate to

Practical implications

  • Cardiac troponin levels elevate in all athletes after running a marathon.

  • 69% of marathon athletes exceed the clinical threshold of cardiac troponin levels directly post-race.

  • Age and exercise duration can partially predict the post-race cardiac troponin levels.

  • Exercise-induced cardiac troponin elevations are more likely to reflect a physiological rather than a pathological response.

Acknowledgements

T.M.H.E. is financially supported by the Netherlands Organization for Scientific Research (Rubicon Grant 825.12.016), and D.H.J.T. received an E. Dekker stipend of the Dutch Heart Foundation (2009T064). We recognize the excellent help of Sports and Technology, the organization of the Eindhoven Marathon, Siemens Medical Solutions Diagnostics B.V. (Breda, The Netherlands), Kjille Melis, Susanne Haasbroek, Rianne van Brenk, Tom de Bont, Linda Pardoel, Jochem Slikboer, Stan van Dijk, Inge Bakker,

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