Cardiac Troponin T and I Release After a 30-km Run

Lieke J.J Klinkenberg,Alma M.A Mingels,Kim Urgel,Sebastiaan C.A.M Bekkers,Elke Marsch,Jeroen D.E Van Suijlen,Otto Bekers,Daniëlle P.C Snijders,Joop Ten Kate,Judith C Sluimer,Kristiaan Wouters,Christian Knackstedt,Robert Dennert,Eline P.M Cardinaels,Marja P Van Dieijen-Visser,B Kietselaer ,Peter R Luyten ,Thomas Theelen ,Frenk Peeters ,Naomi Van Der Linden ,Luc J C Van Loon ,Steven J R Meex

doi:10.1016/j.amjcard.2016.04.030

Abstract

Prolonged endurance-type exercise is associated with elevated cardiac troponin (cTn) levels in asymptomatic recreational athletes. It is unclear whether exercise-induced cTn release mirrors a physiological or pathological underlying process. The aim of this study was to provide a direct comparison of the release kinetics of high-sensitivity cTnI (hs-cTnI) and T (hs-cTnT) after endurance-type exercise. In addition, the effect of remote ischemic preconditioning (RIPC), a cardioprotective strategy that limits ischemia-reperfusion injury, was investigated in a randomized controlled crossover manner. Twenty-five healthy volunteers completed an outdoor 30-km running trial preceded by RIPC (4× 5 min 220mm Hg unilateral occlusion) or control intervention. hs-cTnT, hs-cTnI, and sensitive cTnI (s-cTnI) concentrations were examined before, immediately after, 2 and 5 hours after the trial. The completion of a 30-km run resulted in a significant increase in circulating cTn (time: all p <0.001), with maximum hs-cTnT, hs-cTnI, and s-cTnI levels of 47 ± 27, 69 ± 62, and 82 ± 64ng/L (mean ± SD), respectively. Maximum hs-cTnT concentrations were measured in 60% of the participants at 2 hours after exercise, compared with maximum hs-cTnI and s-cTnI concentrations at 5 hours in 84% and 80% of the participants. Application of an RIPC stimulus did not reduce exercise-induced cTn release (time× trial: all p >0.5). In conclusion, in contrast to acute myocardial infarction, maximum hs-cTnT levels after exercise precede maximum hs-cTnI levels. Distinct release kinetics of hs-cTnT and hs-cTnI and the absence of an effect of RIPC favors the concept that exercise-induced cTn release may be mechanistically distinct from cTn release in acute myocardial infarction.

Highlights

The present study provides a direct comparison of the release kinetics of hs-cTnT and high-sensitivity cTnI (hs-cTnI) after prolonged endurance-type exercise
We show that remote ischemic preconditioning (RIPC), a powerful noninvasive cardioprotective strategy in the setting of ischemia-induced cardiac troponin (cTn) release, has no effect on exerciseinduced cTn release
This observation is distinct from cTn release resulting from the breakdown of the contractile apparatus after ischemic myocardial injury, where peak levels of hs-cTnT and hs-cTnI are reached within the same time line after hospital admission, followed by cTn elevations for over several days after the onset of myocardial ischemia.[2,3]

Summary

Introduction

Abbott Diagnostics and Beckman Coulter provided troponin I assays to Prof. The sponsors had no role in the design and conduct of the study, in the collection, analysis, and interpretation of the data, or in the preparation, review or approval of the manuscript and the decision to submit the manuscript for publication. The American Journal of Cardiology (www.ajconline.org) addition, we examined the effect of RIPC on exerciseinduced cTn release using a randomized controlled singleblind crossover design

Objectives

Methods

Results

Conclusion