Interaction among humoral and neurogenic mechanisms in ventilation control during exercise

The control of ventilation during exercise is analyzed by a mathematical model. It represents a significant improvement of our previous work, including the effect of potassium on peripheral chemoreceptors, a fast and a slow neurogenic component, and a more accurate description of blood flow control. Moreover, the feedforward contributions (potassium and neurogenic) have been incorporated within a larger model of feedback ventilatory control by central and peripheral chemoreceptors to O2 and CO2 changes, and the interaction among the different mechanisms in ventilation control have been analyzed during moderate (100 W) and severe (300 W) exercise. Results suggest that ventilatory changes during exercise can be mostly ascribed to feedforward neurogenic mechanisms, which ensure quite constant levels of arterial oxygen and CO2 pressure, thus avoiding the involvement of feedback mechanisms. Potassium plays a mild role in ventilation control during steady-state conditions. However, it may have a role in the transient phase after the onset of severe exercise, allowing a faster attainment of the final steady-state ventilation level. In agreement with the physiological literature, the model evidences the presence of three distinct kinetic components in V(E), which ensue from the temporal superimposition (sometimes antagonistic sometimes synergistic) among the several incorporated mechanisms.