Effect of the “Race Across The Alps” in elite cyclists on plasma cardiac troponins I and T

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  • Myocardial fatigue in recreational marathon runners: A speckle-tracking echocardiography study

    2018, Indian Heart Journal
    Citation Excerpt :

    Studies have reported biochemical and functional cardiac changes, including elevation in cardiac troponin I and B-type natriuretic peptide (BNP) as well as left ventricular (LV) wall motion abnormalities on echocardiography, soon after completion of endurance races of various sporting disciplines.3–5 Also, effects of acute dysfunction have been recently reported post-marathon in elite runners.5 A number of case reports and cohort descriptions have shown that supraphysiological exercise causes changes in the left ventricle in elite athletes and may even predispose them to ventricular tachycardia and sudden cardiac death.6,7

  • Troponin and exercise

    2016, International Journal of Cardiology
    Citation Excerpt :

    One exception is the group of cardiologists who cycled 1580 km in 8 days, but they did not take pre-exercise blood samples to document small increases of cTn [71]. However, there are several examples of troponin elevation in professional or “highly trained” cyclists [72–75], as when all volunteers had elevation of cTn at some point during Tour de France 2007 [76]. Ultramarathons are races covering a distance more than 42,2 km and troponin has been assessed in multiple ultramarathons since the 90's [6,52,53,77–93].

  • Cardiac troponin in ischemic cardiomyocytes: Intracellular decrease before onset of cell death

    2014, Experimental and Molecular Pathology
    Citation Excerpt :

    Nevertheless, the cardiac troponins (cTns) have been reported to be elevated in the absence of AMI, in situations where irreversible cardiomyocyte damage is unlikely to play an important role (Hamm et al., 2002; Kelley et al., 2009), such as seen in subjects after strenuous exercise (Fortescue et al., 2007; Michielsen et al., 2008; Mingels et al., 2009). It has been hypothesized that the elevated levels of cTn seen after exercise are the result of a transient increase in the cardiomyocyte membrane permeability, resulting in the release of cTn from the cytosolic cTn pool of cardiomyocytes (Neumayr et al., 2002, 2005; Remppis et al., 1995; Shave et al., 2007). In contrast, irreversible cellular damage, as observed after AMI or myocardial ischemia, will result in the release of both cytosolic and structurally bound cTn (and its complexes) from disintegrating myofibrils.

  • The association between cortisol response to mental stress and high-sensitivity cardiac troponin T plasma concentration in healthy adults

    2013, Journal of the American College of Cardiology
    Citation Excerpt :

    It is possible that the cortisol response to stress contributes to the increased levels of troponin T observed here by several indirect mechanisms. First, oxidative stress could play a role in cortisol-induced troponin release (42,43). Supporting this hypothesis, the temporal change in serum troponin levels matches the increase in the concentration of myocardial malondialdehyde, a marker of free radical lipid peroxidation (44).

  • Cardiac troponins in young marathon runners

    2012, American Journal of Cardiology
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