The decay rate of inspiratory muscle pressure (Pmus1) was measured during the post-inspiratory period of zero flow (TEz) occuring under a discontinuous inspiratory elastic load with the following tests. (a) Voluntarily changed breathing frequency (f{hook}) at similar end-inspiratory muscle pressure (PmuseI), (b) as above plus dead space, hence greater PmuseI, (c) breathing spontaneously through a dead space or during exercise to obtain different f{hook} at similar PmuseI. The decay rate of PmusI relative to PmuseI (RDRI) at increased f{hook} was similar to the corresponding relative decay rate of transdiaphragmatic pressure. Hence, the increase of f{hook} did not elicit phasic activity of expiratory muscles during TEz. RDRI increased proportionally to f{hook}: i.e. for a given f{hook}, the decay rate of PmusI was proportional to PmuseI. RDRI increased hyperbolically with decrease of expiratory time and was not directly related to inspiratory time. In each subject these relationships were unique for different tests. These findings show that increase of Pmusel alone does not shorten the persistence of PmusI during expiration, whereas a timing factor, by increasing RDRI, allows shortening of expiration without the intervention of expiratory muscles. © 1979.
