Short sprints (30s) attenuate post-prandial blood glucose in young healthy males.

AIMS: Low-volume, high-intensity exercise is a time-efficient method of inducing physiological responses and may also improve glucose homeostasis. Therefore, effects of two different volumes of sprint-interval cycling on post-prandial blood glucose were assessed. METHODS: Twenty healthy young males undertook two Wingate anaerobic tests (2WAT), four Wingate anaerobic (4WAT) and without-exercise (CON) 90 min after eating a standard meal. Blood glucose was examined at 60, 90, 105, 120, 135 and 150 min post-prandially. RESULTS: 2WAT and 4WAT both accelerated the decrease of blood glucose compared with CON (P<0.05). There were significant reductions at 120 (4.45 ± 0.64 vs. 4.93 ± 0.9 vs. 5.68 ± 0.69), 135 (4.28 ± 0.50 vs. 4.48 ± 0.75 vs. 5.54 ± 0.6) and 150 min (4.64 ± 0.71 vs. 4.71 ± 0.73 vs. 5.36 ± 0.48, all P<0.05). Blood glucose at 120 min was lower after 2WAT than 4WAT (4.45 ± 0.64 vs. 4.93 ± 0.9, P<0.05), this producing a significant statistical interaction between groups and post-exercise time (P<0.005). CONCLUSIONS: 2WAT and 4WAT tests both accelerate the post-prandial decrease in blood glucose in young healthy males, 2WAT being superior to 4WAT in producing this response, even though 2WAT is easier to perform and less time consuming.

Left ventricular myocardial strain and strain rates in sub-endocardial and sub-epicardial layers before and after a marathon.

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.

Evidence of increased electro-mechanical delay in the left and right ventricle after prolonged exercise.

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.