A hypertensive response to exercise independently predicts cardiovascular events and mortality.1 However, the physiological mechanisms contributing to elevation in blood pressure (BP) with exercise are poorly understood. Previous studies have focussed on changes to brachial BP during exercise, but little attention has been directed toward understanding central (aortic) BP (the pressure to which organs such as the heart are exposed). Because of variations in pulse pressure amplification, central systolic BP is usually lower than brachial systolic BP and may differ greatly between individuals with the same brachial systolic BP.2-5 Moreover, central to peripheral pressure amplification may be magnified during exercise, 6,7 and we have also reported that individuals with increased cardiovascular risk because of hypercholesterolemia have significantly raised central systolic BP and augmentation index, but not brachial systolic BP, during light to moderate exercise. 8 Thus, risk related to BP may be better assessed by central BP during light to moderate intensity exercise, rather than resting brachial BP. However, despite these observations, little is known of the contributing central hemodynamics.At rest, with each heart beat a pressure wave generated by the left ventricle is propagated along the arteries and is reflected back toward the heart at sites of impedance mismatch. Return of this reflected pressure wave is proposed to be the sole contributor to augmentation (increase) in central BP.3 However, more recently it has been proposed that aortic pressure can be regarded as the sum of a reservoir pressure and an excess pressure, composed of discernibly discrete forward and backward propagating waves.9,10 Moreover, recent work has proposed that such discrete reflected waves make only a minor contribution to augmentation of the central BP under resting conditions.11 Whether the rise in central systolic BP with exercise can be attributed to increases in discrete forward or reflected waves, or the reservoir, has not been determined in humans. Given the large increase in systemic vasodilation that Abstract-Exercise hypertension independently predicts cardiovascular mortality, although little is known about exercise central hemodynamics. This study aimed to determine the contribution of arterial wave travel and aortic reservoir characteristics to central blood pressure (BP) during exercise. We hypothesized that exercise central BP would be principally related to forward wave travel and aortic reservoir function. After routine diagnostic coronary angiography, invasive pressure and flow velocity were recorded in the ascending aorta via sensor-tipped intra-arterial wires in 10 participants (age, 55±10 years; 70% men) free of coronary artery disease with normal left ventricular function. Measures were recorded at baseline and during supine cycle ergometry. Using wave intensity analysis, dominant wave types throughout the cardiac cycle were identified (forward and backward, compression, and decompression), and aortic reservoi...

Wave intensity analysis (WIA) is a technique developed from the field of gas dynamics that is now being applied to assess cardiovascular physiology. It allows quantification of the forces acting to alter flow and pressure within a fluid system, and as such it is highly insightful in ascribing cause to dynamic blood pressure or velocity changes.When co-incident waves arrive at the same spatial location they exert either counteracting or summative effects on flow and pressure. WIA however allows waves of different origins to be measured uninfluenced by other simultaneously arriving waves. It therefore has found particular applicability within the coronary circulation where both proximal (aortic) and distal (myocardial) ends of the coronary artery can markedly influence blood flow. Using these concepts, a repeating pattern of 6 waves has been consistently identified within the coronary arteries, 3 originating proximally and 3 distally. Each has been associated with a particular part of the cardiac cycle.The most clinically relevant wave to date is the backward decompression wave, which causes the marked increase in coronary flow velocity observed at the start of the diastole. It has been proposed that this wave is generated by the elastic re-expansion of the intra-myocardial blood vessels that are compressed during systolic contraction. Particularly by quantifying this wave, WIA has been used to provide mechanistic and prognostic insight into a number of conditions including aortic stenosis, left ventricular hypertrophy, coronary artery disease and heart failure. It has proven itself to be highly sensitive and as such a number of novel research directions are encouraged where further insights would be beneficial.

No abstract