Donnellan Eoin, Phelan Dermot
Department of Cardiovascular Medicine, Cleveland Clinic, Desk J1-5, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195, USA.
Curr Heart Fail Rep. 2018 Apr;15(2):116-122. doi: 10.1007/s11897-018-0385-9.
Markers of myocardial stress, including troponin, creatine kinase, and brain natriuretic peptide are frequently elevated after endurance athletic pursuits. Here, we summarize the current literature pertaining to the potential mechanism of cardiac enzyme release in athletes and seek to determine the clinical implications of these findings.
Recent studies have highlighted the potential adverse cardiac effects of long-term extreme endurance exercise. While troponin release occurs in a pattern distinct from ischemic damage, BNP release has been correlated with right ventricular dysfunction and is likely related to wall stress from prolonged increases in cardiac output. Higher intensity pre-race training regimes are associated with lower race-day enzyme release. While the holistic benefits of regular moderate exercise are indisputable, recent studies have raised concerns about the potential risks of extreme endurance exercise. Release of serum biomarkers suggesting myocardial damage was first described in the 1970s, yet our understanding of the implications of these findings remains incomplete. The mechanisms of release are complex but appear to be primarily physiological phenomena rather than pathologic.
耐力运动后，包括肌钙蛋白、肌酸激酶和脑钠肽在内的心肌应激标志物常升高。在此，我们总结了当前有关运动员心脏酶释放潜在机制的文献，并试图确定这些发现的临床意义。
近期研究强调了长期极限耐力运动对心脏的潜在不良影响。虽然肌钙蛋白的释放模式与缺血性损伤不同，但脑钠肽的释放与右心室功能障碍相关，且可能与心输出量长期增加导致的壁应力有关。赛前更高强度的训练方案与比赛日更低的酶释放相关。虽然定期适度运动的整体益处无可争议，但近期研究引发了对极限耐力运动潜在风险的担忧。血清生物标志物提示心肌损伤的释放最早在20世纪70年代被描述，但我们对这些发现的影响的理解仍不完整。释放机制复杂，但似乎主要是生理现象而非病理现象。
