Abstract
Elastic loads of 9 cm H2O/l were suddenly applied to the external airways of 4 normal humans during hypercapnic hyperpnea of 20-32 l/min using a closed-circuit breathing apparatus that permitted alveolar CO2 pressure (PACO2) to be held nearly constant in spite of loading-induced changes in ventilation. Transient depression of minute ventilation (.ovrhdot.V) and mean inspiratory flow (VT/TI) was observed immediately on loading; these variables increased progressively to steady levels less than control without significant changes in alveolar chemistry. Two subjects increased VT (volume compensators); the other two increased f (frequency compensators). The net result in .ovrhdot.V and VT/TI compensation was not different between these groups. Load removal always resulted in an overshooting response of .ovrhdot.V lasting for several breaths and due entirely to an overshoot in VT because f transiently fell to or below control at once. Elastic loading always resulted in a steeper plot of .ovrhdot.V-VT in the steady state; in 3 subjects the transition to this steeper line was immediate. The steady state responses were qualitatively, though not quantitatively, consistent with pattern adaptation appropriate to minimize the work-rate of breathing.