CORRESPONDENCE: LETTER TO THE EDITOR
Post-Exercise Release of Cardiac Troponins
Arnold Koller, PhD* and
Wolfgang Schobersberger, MD
* Institute for Sportsmedicine, Alpine Medicine and Health Tourism, LKH Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria (Email: arnold.koller{at}uki.at).
Post-exercise release of cardiac troponin (cTn)T and cTnI has been previously reported after prolonged strenuous exercise (1). Up to now, it has been unclear whether post-exercise release of cTn represents necrosis of cardiac myocytes and thus irreversible damage or a transient and reversible change in membrane permeability of the myocyte (1). Similarly, whether the substrate for post-exercise release of cTn is physiologic or pathologic has not been determined (1).
Middleton et al. (2) examined the kinetics of cTnT during and after completion of a marathon on a motorized treadmill. They suggest that the consistent elevation and pattern of cTnT observed in all participants during and after exercise likely reflects a physiologic as opposed to pathologic substrate. It seems unlikely that minor elevations in cTnT subsequent to endurance exercise are due to myocardial necrosis (2). Rather, it is possible that post-exercise cTn release represents reversible cardiomyocyte membrane damage that might reflect part of a remodeling process (2).
To test the effects of reversible myocardial ischemia, Kurz et al. (3) used a pre-commercial high-sensitivity cardiac troponin T (hsTnT) assay with a 5-fold lower detection limit than the standard assay. Single-photon emission computed tomography was performed to objectively document transient reversible ischemia. The finding that hsTnT does not increase after reversible myocardial ischemia supports the experimental results of Fishbein et al. (4), demonstrating that troponin release was restricted to irreversible myocyte necrosis. Moreover, intact cTnI and degradation products were detectable by Western blot-direct serum assay (WB-DSA) in patients with acute ST-segment elevation myocardial infarction (5). Metabolic inhibition of cardiomyocytes induces parallel release of intact cTnT and cTnI and their degradation products, starting only after onset of irreversible cardiomyocyte damage (6). By contrast a recent study demonstrates that viable cardiomyocytes release cTnI as an intact protein by a stretch-related mechanism mediated by integrins (7). Integrin stimulation in cardiomyocytes does not result in degradation of cTnI into its fragments (7). Accordingly, if post-exercise release of cTn represents reversible cardiomyocyte membrane damage, it is due to a stretch-related mechanism (7) as opposed to metabolic stress or ischemia (3,4,6). However, it has been previously demonstrated that no relationship exists between post-exercise cTn release and a stretch-related mechanism (8).
Therefore, it is possible that release of cTn represents irreversible damage that has been proposed either as pathognomic of cardiac necrosis or might reflect part of a remodeling process (physiologic substrate) (1,9). To further understand exercise-induced cTn release, future work should use WB-DSA (5) to demonstrate degradation products representing irreversible cardiomyocyte damage (3,4,6,7).
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1. Koller A. Exercise-induced increases in cardiac troponins and prothrombotic markers Med Sci Sports Exerc 2003;35:444-448.[CrossRef][Web of Science][Medline]2. Middleton N, George K, Whyte G, Gaze D, Collinson P, Shave R. Cardiac troponin T release is stimulated by endurance exercise in healthy humans J Am Coll Cardiol 2008;52:1813-1816.[Free Full Text] 3. Kurz K, Giannitsis E, Zehelein J, Kattus HA. Highly sensitive cardiac troponin T values remain constant after brief exercise- or pharmacologic-induced reversible myocardial ischemia Clin Chem 2008;54:1234-1238.[Abstract/Free Full Text] 4. Fishbein MC, Wang T, Matijasevic M, Hong L, Apple FS. Myocardial tissue troponins T and I. An immunohistochemical study in experimental models of myocardial ischemia. Cardiovasc Pathol 2003;12:65-71.[CrossRef][Web of Science][Medline] 5. Madsen LH, Christensen G, Lund T, et al. Time course of degradation of cardiac troponin I in patients with acute ST-elevation myocardial infarction. The ASSENT-2 troponin substudy. Circ Res 2006;99:1141-1147.[Abstract/Free Full Text] 6. Hessel MHM, Michielsen ECHJ, Atsma DE, et al. Release kinetics of intact and degraded troponin I and T after irreversible cell damage Exp Mol Pathol 2008;85:90-95.[CrossRef][Web of Science][Medline] 7. Hessel MH, Atsma DE, van der Valk EJ, Bax WH, Schalij MJ, van der Laarse A. Release of cardiac troponin I from viable cardiomyocytes is mediated by integrins Pflugers Arch 2008;455:979-986.[CrossRef][Web of Science][Medline] 8. Koller A, Sumann G, Griesmacher A, et al. Cardiac troponins after a downhill marathon Int J Cardiol 2008;129:449-452.[CrossRef][Web of Science] 9. Anversa P, Leri A, Kajstura J. Cardiac regeneration J Am Coll Cardiol 2006;47:1769-1776Correspondence.[Abstract/Free Full Text]
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