Methods
We modified a previously published model (Toska et al (1996)) in order to simulate the onset of exercise. The mathematical model consists of a heart, a linear elastic arterial reservoir, and two parallel resistive vascular beds. The arterial baroreflex loop is modeled by two separate time domain processing objects, each with its own gain, time constant, and delay. These objects simulated the action of a sympathetic signal to the peripheral vascular bed and a parasympathetic signal to the heart. In repeated model simulations, the control parameters in the model were systematically adjusted by an automated algorithm that minimized the deviations between the time courses of the cardiovascular variables simulated by the model and the previously recorded responses in each individual.
In order to simulate the locally induced vasodilation in the exercising muscles, the peripheral runoff from the arterial reservoir was increased exponentially after the onset of exercise. The increase in the baroreceptor setpoint was started gradually before the onset of exercise in order to simulate the anticipatory increase in mean arterial pressure and heart rate before exercise. This exponential increase was then continued after the onset of exercise. The increase in the venous return was simulated by adding a fraction of the increasing flow to the exercising muscles to the stroke volume with a time delay.

Results
In each of all 10 subjects, the short-term cardiovascular responses were adequately simulated by using individual sets of parameters in the model. We were also able to simulate the coherently averaged mean responses.

Conclusions
The immediate cardiovascular adjustments at the onset of exercise can be fully explained by an immediate increase in baroreceptor setpoint, a locally induced vasodilation in the exercising muscles and a corresponding increase in the venous return to the heart.