Mechanical Synchrony in Long-Distance Runners: Importance of Previous Exposure to Endurance Races

Karolinska Institutet, Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.
Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography (Impact Factor: 4.06). 09/2010; 23(9):977-84. DOI: 10.1016/j.echo.2010.06.030
Source: PubMed


Prolonged exercise has been shown to lead to elevated levels of cardiac troponin and altered cardiac function on echocardiography. It is not known if cardiac synchrony is altered by prolonged exercise. The aims of this study were to assess changes in intra-left ventricular mechanical synchrony and circulating levels of cardiac troponin following prolonged exercise and to evaluate the importance of prior exposure to endurance racing.
Forty-three male participants in a 30-km cross-country race (20 new participants at this event [median, 3 previous endurance races] age matched against 23 repeat participants [median, 31 previous endurance events]) were assessed prospectively 1 to 2 days before and 24 hours after the race using troponin T and Doppler tissue imaging analyzing the standard deviation of time to peak myocardial systolic velocity (T(s)-SD) in a six-basal, six-midventricular segment model measuring myocardial synchrony. The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene was also analyzed, as I allele carriers reportedly have superior endurance performance, while the D allele predisposes to renin-angiotensin system-induced cardiac remodeling.
Prerace troponin T was undetectable in all runners, and postrace levels were higher in new runners (median, 0.03 microg/L; interquartile range [IQR], 0.01-0.04 microg/L) than in repeat runners (median, 0.01 microg/L; IQR, 0.01-0.02 microg/L) (P = .03). Although new and repeat runners had similar T(s)-SD at baseline (32 msec [IQR, 22-43 msec] vs 34 msec [IQR, 29-45 msec], P = .13), dyssynchrony increased only in new runners (40 msec [IQR, 31-47 msec], P < .001; in repeat runners, median, 38 msec [IQR, 29-43 msec], P = .30; median relative difference, +13% vs +5%, P = .02). ACE genotype distribution was similar in both groups. Multivariate analysis showed that (1) a lack of prior endurance exposure; (2) more copies of the ACE D allele; and (3) lower peak systolic velocity were independent predictors of postrace dyssynchrony (P < .05 for all).
Prolonged exertion increased ventricular mechanical dyssynchrony in new endurance participants and in ACE D allele carriers. The long-term impact of such changes warrants future study.

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    ABSTRACT: Prolonged endurance exercise in humans has been associated with an acute impairment in diastolic and systolic cardiac function and the release of cardiac troponin. In this chapter, we review recent evidence from studies using novel echocardiographic parameters and highly sensitive cardiac troponin assays. We demonstrate that the mechanics of left and right ventricular functions are acutely impaired after completion of prolonged exercise and that this reduction in function is likely multifactorial in etiology. However, we highlight that exercise-induced cardiac troponin release is not a marker of exercise-induced pathology but likely a physiologic response to exercise. Finally, we discuss the potential link between prolonged exercise and the increased incidence of cardiac pathology in veteran athletes.
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