Diaphragmatic EMG response to isocapnic hypoxia and hyperoxic hypercapnia in humans.
The EMGdi response to both isocapnic hypoxia and hyperoxic hypercapnia was studied in the same sitting in six normal subjects. Rebreathing methods achieving "open loop" conditions were used. EMGdi was quantified as a moving time average. In almost all subjects, during hypoxia changes in EMGdi were inversely and hyperbolically related to changes in PAO2. When EMGdi was plotted against extrapolated O2 saturation, the relationship was linear in all subjects. The EMGdi response to hypoxia was qualitatively similar to the concurrent responses VI and P.15. EMGdi was linearly related to PACO2 during CO2 rebreathing. The slopes of the EMGdi response to decreasing O2 saturation were positively correlated to the slopes of the EMGdi response to PACO2, so that subjects with a low hypoxic response also had a low CO2 response and vice versa. The couplings of neural to muscular and muscular to ventilatory events as assessed by the ratio of the slopes of EMGdi to P.15 and P.15 to VI, respectively, were similar for all subjects and were not related to the degree or type of chemostimulation. The following were our conclusions. (1) EMGdi can be used as an index of respiratory motoneuron drive during hypoxic or hypercapnic breathing in normal humans. (2) The relative degree of responsiveness to hypoxic and hypercapnia stimuli (chemosensitivity) appears to be similar in any given individual. (3) In normal subjects, changes in inspiratory muscle pressure and ventilation are proportionate to changes in inspiratory neural drive as assessed by EMGdi.
D000328:Adult; D002245:Carbon Dioxide / Q000378:metabolism; D003964:Diaphragm / Q000294:innervation / Q000503:physiopathology*; D004576:Electromyography; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D010100:Oxygen / Q000378:metabolism; D010791:Phrenic Nerve; D013268:Stimulation, Chemical
D002245:Carbon Dioxide; D010100:Oxygen