Cardiac Troponin T and I Release After a 30-km Run
Lieke J.J. Klinkenberg, Peter Luyten, Noreen van der Linden, Kim Urgel, Daniëlle P.C. Snijders, Christian Knackstedt, Robert Dennert, Bastiaan L.J.H. Kietselaer, Alma M.A. Mingels, Eline P.M. Cardinaels, Frederique E.C.M. Peeters, Jeroen D.E. van Suijlen
(+10 others)
2016
American Journal of Cardiology
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
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... 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 3 5 min 220 mm 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 -64 ng/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 3 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 exerciseinduced cTn release may be mechanistically distinct from cTn release in acute myocardial infarction. Ó 2016 Elsevier Inc. All rights reserved. (Am J Cardiol 2016;118:281e287) Insight into the (patho)physiology of exercise-induced cardiac troponin (cTn) release is an active and relevant topic of discussion. 1 The recent advent of both a high-sensitivity (hs-) assay for cTnI (cTnI) and T (cTnT) with similar analytical characteristics enables to directly compare the kinetics of both diagnostic equivalent molecules. For example in acute myocardial infarction (AMI), where cTn release results from the breakdown of the contractile apparatus after ischemic myocardial injury, peak levels of hs-cTnI and hs-cTnT are reached at similar levels after admission. 2,3 A direct comparison of exercise-induced hs-cTnI and hs-cTnT release could provide more insight into the underlying (patho)physiology. In addition, remote ischemic preconditioning (RIPC), a powerful noninvasive cardioprotective strategy, can be applied to study the contribution of an imbalance between oxygen supply and demand in exercise-induced cTn release. RIPC describes the application of brief episodes of nonlethal ischemia and reperfusion to a tissue or an organ, resulting in protection of the same or another visceral organ against an injurious ischemic insult in the future. 4 In line with the cardioprotective effect of RIPC in various settings of tissue ischemia, we hypothesize that if an oxygen demand-supply imbalance contributes to exercise-induced cTn release, application of an RIPC stimulus would result in reduced postexercise cTn levels. The aim of this study was a headto-head comparison of the release kinetics of hs-cTnT and hs-cTnI after prolonged endurance-type exercise. In
doi:10.1016/j.amjcard.2016.04.030
pmid:27282835
fatcat:uhnscddmanatricnedpr6b2kha
