Respiratory neuromuscular response to CO2 rebreathing with inspiratory flow resistance in humans.

The effects of inspiratory flow resistance on mouth occlusion pressure (P0.15) and diaphragmatic EMG (EMGdi) responses to CO2 rebreathing were studied in normal subjects. Occlusion pressures were measured 150 msec after onset of an inspiratory effect; EMGdi was analyzed as a moving time average and quantified in terms of peak activity and rate of rise of activity. After a control CO2 response was obtained in each subject, rebreathing was repeated 30 min later with either of two inspiratory flow resistive loads, 5 cm H2O/L/sec (IR5) and 14 cm H2O/L/sec (IR14). With IR5 (6 subjects), the P0.15 response was decreased in two subjects, unchanged in two, and increased in two; peak EMGdi was unchanged in all, while rate of rise of EMGdi response decreased in 4 of the 6 subjects. With IR14 (6 subjects, 9 runs), the P0.15 response was not decreased in any subject, remained unchanged in 4, and increased in 5; peak EMGdi response to rebreathing in all runs was, again, unchanged by this load, but rate of rise of EMGdi was decreased in 3 and unchanged in 6. The inspiratory off-switch threshold as reflected by peak diaphragmatic activity was not changed by inspiratory flow resistance, whereas inspiratory neural drive as reflected by the the rate of rise of activity was decreased in some subjects. The decrease in inspiratory drive without change in inspiratory off-switch threshold resulted in prolongation of inspiration in an attempt to effect efficient lung expansion. However, the defense of ventilation during rebreathing with both resistances appeared to mainly depend on the response of inspiratory muscle force (P0.15), since in 7 of the 7 runs in which the P0.15 response was significantly increased from control, the ventilatory response was not decreased.