Cardiology/original researchCardiac Troponin Increases Among Runners in the Boston Marathon
Introduction
Marathon running has surged in popularity in the last quarter century, with more than 400,000 runners participating annually in the United States and millions more worldwide.1 Studies indicate that a small percentage of endurance athletes develop increases of myocardial-specific markers with exercise, with increases in some cases in the range diagnostic for acute myocardial infarction.2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 Although the significance of these increases in the setting of prolonged physical activity remains uncertain, a small but growing published literature suggests these increases may actually be well tolerated and are not clearly associated with significant cardiovascular morbidity,7, 11 which presents a substantial challenge to medical personnel who must interpret troponin increases in the setting of prolonged exertion.
Epidemiologic factors associated with troponin increases among marathon runners have not been well characterized, in large part because previous study cohorts have been small and have lacked sufficient clinical and demographic heterogeneity to identify statistically robust factors. A greater understanding of the profile of runners experiencing troponin increases may shed light on the clinical significance of these increases after prolonged exercise. In addition, improved awareness of the background population of runners with increases may provide a useful context in which to interpret troponin increases in specific athletes after prolonged exertion and to assist medical personnel to respond to such increases with appropriate urgency. The purpose of this study was to determine the incidence of troponin increases in a large and heterogeneous population of marathon runners, including elite and nonelite runners, and to identify a population of runners most likely to develop troponin increases after prolonged physical activity.
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Study Design, Setting, and Selection of Participants
Runners participating in the 2002 Boston Marathon were recruited at an exposition event 1 to 2 days before the race. All runners were required to attend this event to pick up their official race number and ChampionChip electronic athlete tracking device (Champion Chip, Nijmegen, The Netherlands). Runners were invited to participate regardless of whether they registered for the Boston Marathon on the basis of a competitive qualifying time or on behalf of a recognized charitable organization for
Results
Table 1 summarizes the baseline demographic and training characteristics of the study population. In all, 766 runners enrolled in the study, of 16,936 total 2002 marathon registrants (5%). Of the 766 runners enrolled, 482 (63%) completed both the pre- and postrace surveys and had laboratory results analyzed after completing the run. Of the 482 runners with complete data collection, 66% were men, and mean age was 39 years. Sex and age distributions were similar between the study cohort and the
Limitations
Our findings must be interpreted within the limitations of the study. First, follow-up in our study population was 64%, which could skew results if differential follow-up occurred. However, runners with less marathon experience were less likely to follow up at the end of the race, suggesting that our findings may in fact underestimate the true prevalence of troponin increases in this population. That the Boston Marathon is a qualifying marathon may also skew our data set towards fitter runners
Discussion
In this large and heterogeneous cohort of marathon runners, we found that troponin increases were relatively common after completion of a marathon and that levels frequently entered the reference range diagnostic for acute myocardial infarction. Younger age and marathon inexperience were the factors most strongly associated with troponin increases in our cohort, irrespective of the cutoff used to define troponin increase. By contrast, runner performance and the presence of traditional
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Supervising editors: Rita K. Cydulka, MD, MS; David L. Schriger, MD, MPH
Author contributions: EBF and AYS contributed equally to this article as co-first authors. EBF, AYS, DSG, RCM, SA, BJF, MIS, MJL, JWN, and CSDA contributed to the study design. EBF, AYS, DSG, RCM, SA, BJF, MIS, and CSDA collected the data. EBF, AYS, DSG, and CSDA did the statistical analysis and article preparation. NR provided laboratory expertise and processing. All authors reviewed the article. EBF takes responsibility for the paper as a whole.
Funding and support: This study was supported in part by grant MO1-RR-02172 from NIH NCRR to the Children’s Hospital Boston General Clinical Research Center; and the Kobrun Family Fund through the Department of Cardiology, Children’s Hospital Boston.
Reprints not available from the authors.