Effect of respiratory muscle weakness on P_0.1 induced by partial curarization

Mouth occlusion pressure 0.1 s after onset of inspiration (P_0.1) 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 ΔP_0.1/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 ΔP_0.1/DV̇E (381 ± 46%) during HCVR was significantly increased (P<0.01), 4) the P_0.1 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 P_0.1, unlike V̇E, did not decrease with even severe respiratory muscle weakness. Indeed P_0.1 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 P_0.1 may at least qualitatively reflect CRD up to the level of severe respiratory muscle weakness attained in this study.