Klinkenberg Lieke J J, Luyten Peter, van der Linden Noreen, Urgel Kim, Snijders Daniëlle P C, Knackstedt Christian, Dennert Robert, Kietselaer Bastiaan L J H, Mingels Alma M A, Cardinaels Eline P M, Peeters Frederique E C M, van Suijlen Jeroen D E, Ten Kate Joop, Marsch Elke, Theelen Thomas L, Sluimer Judith C, Wouters Kristiaan, Bekers Otto, Bekkers Sebastiaan C A M, van Loon Luc J C, van Dieijen-Visser Marja P, Meex Steven J R
Department of Clinical Chemistry, Maastricht University Medical Center, Maastricht, the Netherlands; Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, the Netherlands.
Department of Cardiology, Maastricht University Medical Center, Maastricht, the Netherlands.
Am J Cardiol. 2016 Jul 15;118(2):281-7. doi: 10.1016/j.amjcard.2016.04.030. Epub 2016 May 4.
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 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 × 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.
在无症状的业余运动员中，长时间耐力型运动与心脏肌钙蛋白（cTn）水平升高有关。目前尚不清楚运动诱导的cTn释放反映的是生理过程还是病理过程。本研究的目的是直接比较耐力型运动后高敏肌钙蛋白I（hs-cTnI）和肌钙蛋白T（hs-cTnT）的释放动力学。此外，还以随机对照交叉方式研究了远程缺血预处理（RIPC）（一种限制缺血再灌注损伤的心脏保护策略）的效果。25名健康志愿者完成了一次30公里的户外跑步试验，试验前进行了RIPC（4×5分钟220毫米汞柱单侧阻断）或对照干预。在试验前、试验后即刻、试验后2小时和5小时检测hs-cTnT、hs-cTnI和敏感肌钙蛋白I（s-cTnI）浓度。完成30公里跑步后，循环cTn显著增加（时间：所有p<0.001），hs-cTnT、hs-cTnI和s-cTnI的最高水平分别为47±27、69±62和82±64纳克/升（平均值±标准差）。60%的参与者在运动后2小时测量到hs-cTnT的最高浓度，而84%和80%参与者在运动后5小时测量到hs-cTnI和s-cTnI的最高浓度。应用RIPC刺激并未减少运动诱导的cTn释放（时间×试验：所有p>0.5）。总之，与急性心肌梗死不同，运动后hs-cTnT的最高水平先于hs-cTnI的最高水平。hs-cTnT和hs-cTnI不同的释放动力学以及RIPC无效应支持了运动诱导的cTn释放可能在机制上与急性心肌梗死中的cTn释放不同的观点。
