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2008a). Left ventricular fractional shortening was not different between groups in the pre-HDBR tests and was not affected by the HDBR period in either group (Table 1). In each of the pre- and post-HDBR tests, isoprenaline infusion decreased the PEPi delay in a dose-dependent manner (Fig. 3). This effect of reducing the PEPi delay was present in both groups, but a group �� time interaction (P Idelalisib chemical structure in PEPi for the Control group following HDBR. In contrast, infusion of noradrenaline increased the PEPi delay in a dose-dependent manner that was similar for the Control and Exercise groups (Fig. 3; P Small molecule library research buy 0.05) and is probably explained by the elevated blood pressure and, therefore, afterload. Isoprenaline infusions did not affect either diastolic blood pressure or cardiac afterload (Table 2). The impact of noradrenaline on the increase in diastolic blood pressure (P Ficain Together, these findings suggest the following: (1) there is an effect of HDBR on systolic timing that is difficult to minimize with exercise countermeasures; (2) the mechanism of the prolonged PEPi lies within the inotropic properties of the left ventricle that can be modified by ��-adrenoceptor activation; and (3) the change in PEPi can occur independently from myocardial contractile function (e.g. fractional shortening) or left ventricular wall thinning. The PEPi is the time the ventricles spend in isovolumetric contraction, the cumulative effect of the time required for ventricular electrical activation, electrical�Cmechanical coupling and the initiation of the rise in left ventricular pressure. In addition to electrical delays reflected in the ECG, the PEPi may be sensitive to changes in preload and in afterload, as well as intracardiac inotropic levels (Weissler, 1977; Mattar et al. 1991). Our analysis excluded any role of altered electrical patterns in the prolonged PEPi. Furthermore, it is unlikely that cardiac preload affected the PEPi with HDBR.