In normal humans during quiet breathing, expiration is mostly driven by elastic recoil of the lungs. Expiration becomes active when ventilation must be increased to meet augmented metabolic demands, or in response to expiratory loading, be it experimental or disease-related. The response to expiratory loading is considered to be mediated by both reflex and cortical mechanisms, but the latter phenomenon have not been neurophysiologically characterized. We recorded the EEG in 20 healthy volunteers (9 men, 11 women, age: 22 to 50 yr) during unloaded breathing, voluntary expirations, and in response to 50 cmH2O·l(-1)·s expiratory resistive load (ERL), 20 cmH2O expiratory threshold load (high ETL), and 10 cmH2O expiratory threshold load (low ETL). EEGs were processed by ensemble averaging expiratory time-locked segments and examined for pre-expiratory potentials, defined as a slow negative shift from the baseline signal preceding expiration, and suggestive of cortical preparation of expiration involving the supplementary motor area. Four subjects were excluded because of technical EEG problems. Pre-expiratory potentials were present in one subject at baseline and in all subjects during voluntary expirations. They were present in eight subjects during low ETL, in 15 subjects during high ETL, and in 13 subjets during ERL (control vs. low ETL, P = 0.008; control vs. high ETL, P < 0.001; and control vs. ERL, P < 0.001). Respiratory discomfort was more intense in the presence of pre-expiratory potentials (P < 0.001). These results provide a neurophysiological substrate to a cortical component of the physiological response to experimental expiratory loads in humans.
Keywords: cerebral cortex; control of breathing; dyspnea; expiration; expiratory loading; supplementary motor area.
Copyright © 2015 the American Physiological Society.