Increasing inspiratory flow (V) over dot has been shown to shorten neural i
nspiratory time (TIn) in normal subjects breathing on a mechanical ventilat
or, but the effect of (V) over dot on respiratory motor output before inspi
ratory termination has not previously been studied in humans. While breathi
ng spontaneously on a mechanical ventilator, eight normal subjects were int
ermittently exposed to 200-ms-duration positive pressure pulses of differen
t amplitudes at the onset of inspiration. Based on the increase in (V) over
dot above control breaths (Delta(V) over dot), trials were grouped into sm
all, medium, and large groups (mean Delta(V) over dot: 0.51, 1.11, and 1.65
l/s, respectively). We measured TIn, transdiaphragmatic pressure (Pdi), an
d electrical activity (electromyogram) of the diaphragm (EMGdi). Transient
increases in (V) over dot caused shortening of TIn from 1.34 to 1.10 (not s
ignificant), 1.55 to 1.11 (P < 0.005), and 1.58 to 1.17 s (P < 0.005) in th
e small, medium, and large Delta(V) over dot groups, respectively. EMGdi me
asured at end TIn 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 excit
ation was 126 +/- 42 (SD) ms, consistent with a reflex effect. Increasing (
V) over dot had two countervailing effects on Pdi: 1) a depressant mechanic
al effect due primarily to the force-length (11.2 cmH(2)O/l) relation of th
e diaphragm, and 2) an increase in diaphragm activation. For the eight subj
ects, mean peak Pdi did not change significantly, but there was significant
intersubject variability, reflecting variability in the strength of the ex
citation reflex. We conclude that increasing inspiratory (V) over dot cause
s a graded facilitation of EMGdi, which serves to counteract the negative e
ffect of the force-length relation on Pdi.