TY - JOUR
T1 - Cardiac Troponin T and I Release After a 30-km Run
AU - Klinkenberg, Lieke J. J.
AU - Luyten, Peter
AU - van der Linden, Noreen
AU - Urgel, Kim
AU - Snijders, Danielle P. C.
AU - Knackstedt, Christian
AU - Dennert, Robert
AU - Kietselaer, Bastiaan L. J. H.
AU - Mingels, Alma
AU - Cardinaels, Eline P. M.
AU - Peeters, Frederique E. C. M.
AU - van Suijlen, Jeroen D. E.
AU - ten Kate, Joop
AU - Marsch, Elke
AU - Theelen, Thomas L.
AU - Sluimer, Judith C.
AU - Wouters, Kristiaan
AU - Bekers, Otto
AU - Bekkers, Bas
AU - van Loon, Lucas
AU - Visser - van Dieijen, Marja
AU - Meex, Steven J. R.
PY - 2016/7/15
Y1 - 2016/7/15
N2 - 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 x 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 (tiine: 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 x 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.
AB - 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 x 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 (tiine: 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 x 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.
U2 - 10.1016/j.amjcard.2016.04.030
DO - 10.1016/j.amjcard.2016.04.030
M3 - Article
C2 - 27282835
SN - 0002-9149
VL - 118
SP - 281
EP - 287
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 2
ER -