Increasing inspiratory flow () has been shown to shorten neural inspiratory time (TI_n) in normal subjects breathing on a mechanical ventilator, but the effect of on respiratory motor output before inspiratory termination has not previously been studied in humans. While breathing spontaneously on a mechanical ventilator, eight normal subjects were intermittently exposed to 200-ms-duration positive pressure pulses of different amplitudes at the onset of inspiration. Based on the increase in above control breaths (), trials were grouped into small, medium, and large groups (mean : 0.51, 1.11, and 1.65 l/s, respectively). We measured TI_n, transdiaphragmatic pressure (Pdi), and electrical activity (electromyogram) of the diaphragm (EMGdi). Transient increases in caused shortening of TI_n from 1.34 to 1.10 (not significant), 1.55 to 1.11 (P < 0.005), and 1.58 to 1.17 s (P < 0.005) in the small, medium, and large groups, respectively. EMGdi measured at end TI_n of the pulse breaths was 131 (P < 0.05), 142, and 155% (P < 0.05) of the EMGdi of the control breaths at an identical time point in the small, medium, and large trials, respectively. The latency of the excitation was 126 ± 42 (SD) ms, consistent with a reflex effect. Increasing had two countervailing effects on Pdi: 1) a depressant mechanical effect due primarily to the force-length (11.2 cmH₂O/l) relation of the diaphragm, and 2) an increase in diaphragm activation. For the eight subjects, mean peak Pdi did not change significantly, but there was significant intersubject variability, reflecting variability in the strength of the excitation reflex. We conclude that increasing inspiratory causes a graded facilitation of EMGdi, which serves to counteract the negative effect of the force-length relation on Pdi.