Effects of prolonged exercise on left ventricular mechanical synchrony in long-distance runners: importance of previous exposure to endurance races.
BACKGROUND
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.


METHODS
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.


RESULTS
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).


CONCLUSIONS
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.
Sahlén
Anders
A
Karolinska Institutet, Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden. anders.sahlen@karolinska.se
Shahgaldi
Kambiz
K
Aminoff
Anna
A
Aagaard
Philip
P
Manouras
Aristomenis
A
Winter
Reidar
R
Ehrenborg
Ewa
E
Braunschweig
Frieder
F
D000483:Alleles; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D015150:Echocardiography, Doppler; D006329:Heart Conduction System / Q000502:physiology*; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System / Q000235:genetics; D012420:Running / Q000502:physiology*; D018709:Statistics, Nonparametric; D014336:Troponin / Q000097:blood; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000235:genetics
D015415:Biomarkers; D014336:Troponin; D007703:Peptidyl-Dipeptidase A