According to the theory of arterial acceleration, the pressure increase at stroke onset elicits stretch induced depolarization of the smooth muscle cells within the conducting arteries of the arterial tree. Smooth muscle cells have been shown sensitive to stretch. They are arranged circularly (not longitudinally as in the gut) and contain gap junctions in abundance, making them an electronic syncytium. A depolarization at the aortic notch with spread along the arterial tree from proximal to distal as a peristaltic wave. Since this depolarization is assumed short lasting and is triggered by the first increase of pressure at stroke onset, it is assumed not to interfere with the ejection phase of the heart.
The timing of the arterial acceleration in the model is dependent on a sufficiently rapid rise of pressure in one of the arterial capacitances at the left side. Its effect is simulated as a brief reduction in the model's capacitances occurring simultaneously in the triggered capacitance and in those further downstream. The model does not simulate the peristaltic wave from proximal to distal that the theory of arterial acceleration assumes.
The amount of capacitance reduction can be set by a slider at the bottom left of the main screen. The minimal reduction is set to 0% and the maximal reduction to 20%. The reduction in capacitance is applied as a sine function over the so-called acceleration time. The acceleration time varies with the strength of the acceleration selected between 60 and 180 ms.