Cardiac electromechanical delay is increased during recovery from 40 km cycling but is not mediated by exercise intensity.

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.

Do the effects of high intensity 40 km cycling upon left ventricular function and cardiac biomarker during recovery vary with time of day?

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.