Exercise Central (Aortic) Blood Pressure Is Predominantly Driven by Forward Traveling Waves, Not Wave Reflection
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 reservoir and excess pressure were calculated. Central systolic BP increased significantly with exercise (Δ=19±12 mm Hg; P<0.001). This was associated with increases in systolic forward compression waves (Δ=12×106±17×106 W·m−2·s−1; P=0.045) and forward decompression waves in late systole (Δ=9×106±6×106 W·m−2·s−1; P<0.001). Despite significant augmentation in BP (Δ=9±6 mm Hg; P=0.002), reflected waves did not increase in magnitude (Δ=−1×106±3×106 W·m−2·s−1; P=0.2). Excess pressure rose significantly with exercise (Δ=16±9 mm Hg; P<0.001), and reservoir pressure integral fell (Δ=−5×105±5×105 Pa·s; P=0.010). Change in reflection coefficient negatively correlated with change in central systolic BP (r=−0.68; P=0.03). We conclude that elevation of exercise central BP is principally because of increases in aortic forward traveling waves generated by left ventricular ejection. These findings have relevance to understanding central BP waveform morphology and pathophysiology of exercise hypertension.
- Received November 5, 2012.
- Revision received April 24, 2013.
- Accepted April 25, 2013.
- © 2013 American Heart Association, Inc.