A mathematical model demonstrates that an increase in the baroreflex set point and local vasodilatation can explain cardiovascular changes at the onset of moderate exercise.
Model supports baroreflex reset plus vasodilatation as dominant early-exercise drivers; leaves open prospective validation before any clinical application.
We have tested whether the cardiovascular changes at the onset of exercise could be simulated only by an increase in the baroreflex set point and locally induced vasodilatation in the exercising muscles. The mathematical model consists of a heart, a linear elastic arterial reservoir and two parallel resistive vascular beds. The arterial baroreflex loop is modelled by three separate time domain processing objects, each with its own gain, time constant and delay. These are intended to simulate the action of a sympathetic signal to the peripheral vascular bed, a parasympathetic signal to the heart and a sympathetic signal to the heart. We used this model with previously published experimental data to estimate the unknown parameters in the reflex control loop. In all 10 subjects and in the global averaged response, the short-term cardiovascular responses were adequately simulated by using individual sets of parameters in the model. An increase in the baroreflex set point and locally induced vasodilatation in the exercising muscles can explain almost all of the cardiovascular changes in the recorded variables (mean arterial pressure, RR interval and stroke volume) at the onset of exercise.
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Elstad et al. (2002) studied this question.
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