Diaphragmatic EMG and occlusion pressure response to elastic loading during CO2 rebreathing in humans.

The effects of external elastic loading (EL) (19 cmH2O/l), applied continuously (C) and intermittently (I) during CO2 rebreathing, on diaphragmatic electromyogram (EMGdi), mouth occlusion pressure (P0.15), and ventilation (VI) were studied in normal subjects. EMGdi was analyzed as moving time average and quantitated in terms of peak (mean p) and average rate of rise of inspiratory activity (mean p/TI). CEL resulted in an increased mean p/TI response to CO2 in all subjects with P0.15 increasing in proportion to EMGdi. Tidal volume (VT) during rebreathing was decreased in all cases with VI being preserved in four of six runs due to increased breathing frequency (f). Although mean p was increased for a given end-tidal CO2 (PACO2) level during CEL, for a given rate of rise of inspiratory activity mean p was decreased in three of five subjects, indicating a diminished threshold for inspiratory "off-switch." CEL results in an augmented inspiratory drive that serves to increase muscle output and stabilize VT; the increased drive and decrease inspiratory off-switch threshold shorten TI mediating the compensatory increase in f. The first breath IEL resulted in decreased VT and mean p without change in mean p/TI, and all increased with subsequent loaded breaths independent of changes in PCO2. Load compensation for externally applied EL is mediated by neural mechanisms independent of chemical drive.