We assessed the time delay from the onset of QRS (Q) to peak systolic (S') and diastolic (E') tissue velocities in the left (LV) and right ventricle (RV) before and after prolonged exercise. Nineteen well-trained runners (mean +/- SD age, 41 +/- 9 years) had tissue-Doppler echocardiography performed before and after an 89 km ultra-marathon race. Longitudinal tissue motion was analysed in LV basal and mid-wall segments and RV free wall. Electromechanical coupling was assessed by the delay between Q and S' as well as E' tissue velocities. Average data for all segments were adjusted for the R-R interval. Comparisons were made by paired t-tests. An increase in electro-mechanical delay (EMD) was reported post-exercise in systole (Q-S' LV: 131 +/- 20 vs. 175 +/- 27 ms; RV: 171 +/- 34 vs. 258 +/- 35 ms; P < 0.05) and diastole (Q-E' LV: 486 +/- 51 vs. 647 +/- 44 ms; RV: 500 +/- 80 vs. 690 +/- 75 ms; P < 0.05). Further, post-race peak tissue velocities in basal LV and RV wall segments were reduced (P < 0.05). Recovery from prolonged running was associated with an increased "EMD", and reduced peak tissue velocities, in both ventricles.

We assessed myocardial deformation in sub-endocardial and sub-epicardial layers of the left ventricle (LV) wall before and after running a marathon. Echocardiography scans were performed on 14 male, non-elite runners (mean +/- SD; age 32 +/- 10 years) who completed the 42.2-km London marathon. Para-sternal short axis and apical four-chamber views were recorded for off-line analysis. Peak longitudinal, radial and circumferential strains, peak systolic and early diastolic strain rates were recorded. Circumferential rotation in basal and apical LV scans was used to calculate torsion. Pre-race strain and strain rates were generally greater in the sub-endocardial layer of the LV wall. After race completion, a mixed pattern of change was observed with a reduction in sub-epicardial radial strain (32.6 +/- 12.5 to 20.3 +/- 9.6%; P < 0.01) and sub-endocardial circumferential strain (-26.9 +/- 3.6 to -23.7 +/- 4.1%; P < 0.01) at the apex. Rotation was not altered at either the apical or basal levels and thus torsion was not changed in either the sub-endocardium (6.72 +/- 3.46 degrees to 5.67 +/- 4.98 degrees) or the sub-epicardium (3.48 +/- 2.68 degrees to 3.01 +/- 3.23 degrees). Strain rates and rotation rates were only sporadically altered post-race. There are differences in deformation characteristics between the sub-endocardium and sub-epicardium at baseline, and the limited changes observed post-race were not specific to any region or depth of the LV wall.

Cardiac electrical-mechanical delay (cEMD), left ventricular (LV) function, and cardiac troponin I (cTnI) were assessed after 40 km cycle time trials completed at high (HIGH) and moderate (MOD) intensities in 12 cyclists. Echocardiograms and blood samples were collected before, 10, and 60 min after cycling. cEMD as assessed by time from QRS onset to peak systolic (S') tissue velocity was lengthened after both bouts of cycling but was not mediated by cycling intensity (HIGH: 174 ± 52 vs 198 ± 26 ms; MOD: 151 ± 40 vs 178 ± 52 ms, P < 0.05). Global LV systolic function was unaltered by exercise. cEMD from QRS to peak early (E') diastolic tissue velocity was also increased post-exercise (HIGH: 524 ± 95 vs 664 ± 68 ms; MOD: 495 ± 62 vs 604 ± 91 ms, P < 0.05). Indices of LV diastolic function was reduced after cycling but were not mediated by exercise intensity. cTnI was elevated in two participants after HIGH trial (0.06 ug/L; 0.04 ug/L) and one participant after MOD trial (0.02 ug/L). While cEMD is lengthened and LV diastolic function was reduced post-cycling, altering time-trial intensity had little impact upon cEMD, LV function, and cTnI release.

No abstract

Twelve healthy participants performed two identical high-intensity 40 km cycling trials (morning and evening) under controlled laboratory conditions. Echocardiograms and venous blood samples were collected before and after each exercise bout. Cardiac electro-mechanical-delay (cEMD) was measured as QRS-complex onset to peak systolic (S') and early diastolic (E') tissue velocities. Myocardial strain and strain rates were assessed in longitudinal, circumferential and radial planes at the left ventricular apex and base. Cardiac troponin I (cTnI) and N-terminal Pro-Brain Natriuretic Peptide (NT-proBNP) were assessed as biomarkers of cardiomyocyte damage and wall stress. cEMD was lengthened after both morning (S': 160 ± 30 vs. 193 ± 27; E': 478 ± 60 vs. 620 ± 87, P < 0.05) and evening (S': 155 ± 29 vs. 195 ± 31; E': 488 ± 42 vs. 614 ± 61, P < 0.05) trials. A reduction in peak S' (morning: 6.96 ± 1.12 vs. 6.66 ± 0.89; evening: 7.09 ± 0.94 vs. 7.02 ± 0.76) was correlated with cEMD (r = -0.335, P < 0.05). Peak longitudinal strain was reduced, atrial strain rates were sporadically increased in both trials post-cycling. cTnI was elevated in only two participants (0.04 µg · L(-1), 0.03 µg · L(-1)), whilst NT-proBNP was below the clinical cut-off point in all participants. Prolonged-cycling resulted in a lengthening of cEMD, small changes in aspects of left ventricular deformation and sporadic increases in cardiac biomarkers. None of these effects were moderated by time-of-day.