Mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) reflects central respiratory drive (CRD), but its dependence on respiratory muscle strength is unknown. To clarify this relationship, we produced progressive levels of respiratory muscle weakness by infusion of d-tubocurarine in eight supine spontaneously breathing normal subjects. Hypercapnic ventilatory response (HCVR) was measured before curarization and at mild (mean inspiratory effort 62 ± 3% of control), moderate (42 ± 3%), and severe (23 ± 1%) weakness. At the severe level of weakness 1) supine functional residual capacity was not significantly changed from base line, 2) the percent of base-line slope of ΔP0.1/ΔP(CO2) (122 ± 27%) was significantly greater (P<0.01) than that for change in expired minute ventilation (ΔV̇E)/ΔP(CO2) (39 ± 10%), 3) the percent of base-line ΔP0.1/DV̇E (381 ± 46%) during HCVR was significantly increased (P<0.01), 4) the P0.1 response was significantly increased from base line at two out of three specific levels of PCO2 while the V̇E was unchanged or significantly decreased, and 5) peak inspiratory resistance did not significantly change. Thus P0.1, unlike V̇E, did not decrease with even severe respiratory muscle weakness. Indeed P0.1 increased at two out of three levels of P(CO2) under circumstances when higher CRD is expected. One potential explanation for the results is that P0.1 may at least qualitatively reflect CRD up to the level of severe respiratory muscle weakness attained in this study.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Applied Physiology Respiratory Environmental and Exercise Physiology|
|State||Published - 1984|
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