Effect of thoracic deafferentation on load-compensating mechanisms in humans

First-breath responses to graded elastic (delta E) and resistive (delta R) loads in 29 cervical cord-injured and 80 normal men were compared with those predicted assuming identical respiratory muscle pressure (Pmus) wave forms in the unloaded and loaded states. The cord-injured group's mean actual and predicted inspiratory duration (TI) responses were equal, indicating that the average duration of their phrenic discharge remained constant during both delta E and delta R. Their mean expiratory duration (TE) responses fell short of predictions with delta E but exceeded predictions with delta R, signifying that a neural mechanism hastened inspiration following delta E but postponed it following delta R. TE/(pred TE) values (an index of phrenic timing) from different loads were proportional to concomitant TI responses but not to indices of diaphragmatic force [peak Pmus, (VT/TI)/(pred VT/TI)], movement (VT, VT/TI), or duration of contraction [TI/(pred TI)]. These findings suggest that oropharyngeal and/or pulmonary receptors signaling airflow duration, rather than diaphragmatic length or tension receptors, adjust phrenic motoneuron timing during mechanical loading. The cord-injured group produced a normal tidal volume (VT) defense coupled with a depressed frequency (f) response to delta E and, conversely, a weak VT defense coupled with a normal f response to delta R. Since both groups' VT/TI responses surpassed predictions equally, the cord-injured group's deficit was attributable entirely to impaired regulation of TE during delta E and TI during delta R. Thus chest wall receptors modulate duration and timing, but probably not average intensity, of the phrenic output during loading. Nearly one-third of the normal, but virtually none of the cord-injured, samples prolonged TI against large delta R and shortened TI agaist large delta E, suggesting that thoracic deafferentation impairs human ability to distinguish large delta R from delta E. These latter findings support the hypothesis that chest wall afferents subserve perception of respiratory force or position in humans.