Exercise markedly influences pulse wave morphology, but the mechanism is unknown. We investigated whether effects of exercise on the arterial pulse result from alterations in stroke volume or pulse wave velocity (PWV)/large artery stiffness or reduction of pressure wave reflection. Healthy subjects (n = 25) performed bicycle ergometry. with workload increasing from 25 to 150 W for 12 min. Digital arterial pressure waveforms were recorded using a servo-controlled finger cuff. Radial arterial pressure waveforms and carotid-femoral PWV were determined by applanation tonometry. Stroke volume was measured by echocardiography, and brachial and femoral artery blood flows and diameters were measured by ultrasound. Digital waveforms were recorded continuously. Other measurements were made before and after exercise. Exercise markedly reduced late systolic and diastolic augmentation of the peripheral pressure pulse. At 15 min into recovery, stroke volume and PWV were similar to baseline values, but changes in pulse wave morphology persisted. Late systolic augmentation index (radial pulse) was reduced from 54 +/- 3.9% at baseline to 42 +/- 3.7% (P < 0.01), and diastolic augmentation index (radial pulse) was reduced from 37 +/- 1.8% to 25 +/- 2.9% (P < 0.001). These changes were accompanied by an increase in femoral blood flow (from 409 +/- 44 to 773 +/- 48 ml/min, P < 0.05) and an increase in femoral artery diameter (from 8.2 +/- 0.4 to 8.6 +/- 0.4 mm, P < 0.05). In conclusion, exercise dilates muscular arteries and reduces arterial pressure augmentation, an effect that will enhance ventricular-vascular coupling and reduce load on the left ventricle.

Abstract-Peripheral systolic blood pressure is amplified above central aortic systolic pressure, but the late systolic shoulder of the peripheral pulse may approximate central systolic pressure. Because late systolic pressure also determines the peripheral augmentation index, a measure of pressure wave reflection within the systemic circulation, this implies a direct relationship between amplification and augmentation. We compared the late systolic shoulder of the peripheral pressure waveform with estimates of central systolic pressure obtained using a transfer function in 391 subjects undergoing diagnostic coronary angiography and/or elective angioplasty (30% with insignificant coronary artery disease). In a subset (nϭ12) Key Words: aorta Ⅲ augmentation index Ⅲ central blood pressure Ⅲ pulse pressure Ⅲ pulse wave analysis P ropagation of the pressure pulse from the left ventricle to the systemic circulation is accompanied by reflections from sites of impedance mismatch. These reflections result in backward traveling pressure waves, which augment pressure at the aortic root, this being quantified by the aortic or "central" augmentation index (AI; cAI; Figure 1). 1-3 At the same time, pulse pressure propagation and reflection within the upper limb results in peripheral amplification of the pressure pulse, so that peripheral systolic pressure (pSBP) measured at the brachial artery, radial artery, or digital artery exceeds central systolic blood pressure (cSBP) at the aortic root. 1,4 Because of the slow rate of change of pressure during diastole, diastolic blood pressure (DBP) is similar at central and peripheral sites (as is mean arterial pressure), 5 but central pulse pressure (cPP) differs from peripheral pulse pressure (pPP). The potential importance of cSBP and cPP was demonstrated in the Conduit Artery Function Evaluation Study, where the difference in outcome between hypertensive regimes was explained by differing central but not peripheral blood pressures, and cPP was predictive of overall outcome. 6 Augmentation of central arterial pressure and peripheral amplification have been regarded as largely unrelated phenomena, with the former being determined by characteristics of wave propagation in the aorta and by reflections from the head and lower body and the latter by reflections from the upper limb. However, cAI is closely related to the peripheral AI (pAI), a measurement taken direct from the late systolic shoulder (pSBP 2 ) of the peripheral arterial waveform (Figure 1), which, in turn, may approximate cSBP. 7 This implies a direct relationship between amplification and augmentation. The purpose of this study was to investigate how closely pSBP 2 equates to cSBP and to define the relationship between AI and cSBP. We first investigated the relationship between pSBP 2 and cSBP estimated noninvasively using a transfer function. We then examined the relationship of pSBP 2 to cSBP measured invasively at the time of cardiac catheterization. The relationship between central and peripheral pressure is critica...

Background-The mechanisms of reduced angina on second exertion in patients with coronary arterial disease, also known as the warm-up angina phenomenon, are poorly understood. Adaptations within the coronary and systemic circulations have been suggested but never demonstrated in vivo. In this study we measured central and coronary hemodynamics during serial exercise. Methods and Results-Sixteen patients (15 male, 61Ϯ4.3 years) with a positive exercise ECG and exertional angina completed the protocol. During cardiac catheterization via radial access, they performed 2 consecutive exertions (Ex1, Ex2) using a supine cycle ergometer. Throughout exertions, distal coronary pressure and flow velocity were recorded in the culprit vessel using a dual sensor wire while central aortic pressure was recorded using a second wire. Patients achieved a similar workload in Ex2 but with less ischemia than in Ex1 (PϽ0.01). A 33% decline in aortic pressure augmentation in Ex2 (PϽ0.0001) coincided with a reduction in tension time index, a major determinant of left ventricular afterload (PϽ0.001). Coronary stenosis resistance was unchanged. A sustained reduction in coronary microvascular resistance resulted in augmented coronary flow velocity on second exertion (both PϽ0.001). These changes were accompanied by a 21% increase in the energy of the early diastolic coronary backward-traveling expansion, or suction, wave on second exercise (PϽ0.05), indicating improved microvascular conductance and enhanced left ventricular relaxation. Conclusions-On repeat exercise in patients with effort angina, synergistic changes in the systemic and coronary circulations combine to improve vascular-ventricular coupling and enhance myocardial perfusion, thereby potentially contributing to the warm-up angina phenomenon. (Circulation. 2012;126:2565-2574.)