Left ventricular mechanics and arterial-ventricular coupling following high-intensity interval exercise

High-intensity exercise induces marked physiological stress affecting the secretion of catecholamines. Sustained elevations in catecholamines are thought to desensitize cardiac beta receptors and may be a possible mechanism in impaired cardiac function following strenuous exercise. In addition, attenuated arterial-ventricular coupling may identify vascular mechanisms in connection with postexercise attenuations in ventricular function. Thirty-nine normally active (NA) and endurance-trained (ET) men and women completed an echocardiographic evaluation of left ventricular function before and after an acute bout of high-intensity interval exercise (15 bouts of 1:2 min work:recovery cycling: 100% peak power output and 50 W, respectively). Following exercise, time to peak twist and peak untwisting velocity were delayed (P < 0.01) but did not differ by sex or training status. Interactions for sex and condition (rest vs. exercise) were found for longitudinal diastolic strain rate (men, 1.46 ± 0.19 to 1.28 ± 0.23 s(-1) vs. women, 1.62 ± 0.25 to 1.63 ± 0.26 s(-1); P = 0.01) and arterial elastance (men 2.20 ± 0.65 to 3.24 ± 1.02 mmHg · ml(-1) · m(-2) vs. women 2.51 ± 0.61 to 2.93 ± 0.68 mmHg · ml(-1) · m(-2); P = 0.04). No cardiac variables were found associated with catecholamine levels. The change in twist mechanics was associated with baseline aortic pulse-wave velocity (r(2) = 0.27, P = 0.001). We conclude that males display greater reductions in contractility in response to high-intensity interval exercise, independent of catecholamine concentrations. Furthermore, a novel association of arterial stiffness and twist mechanics following high-intensity acute exercise illustrates the influence of vascular integrity on cardiac mechanics.