Elastic loads of 9 cmH2O/1 were suddenly applied to the external airways of four normal human subjects during hypercapnic hyperpnea of 20-32 1/min using a closed-circuit breathing apparatus that permitted alveolar carbon dioxide pressure (PACO2) to be held nearly constant in spite of loading induced changes in ventilation. Transient depression of minute ventilation (V) and mean inspiratory flow (VT/TI) was observed immediately on loading; both these variables increased progressively to steady levels less than control without significant changes in alveolar chemistry. Two subjects increased VT (volume compensators) whereas the other two chose to increase f (frequency compensators). The net result in V and VT/TI compensation was not different between these groups. Load removal always resulted in an overshooting response of 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 V-VT in the steady state; in three of the 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.