Responses of cat's internal intercostal motor units to hypercapnia and lung inflation

Single motor unit potentials from the eighth internal intercostal (IIC) muscle were recorded along with tracheal pressure and end-tidal CO2 (PETCO2) in spontaneously breathing, Dial-urethane anesthetized cats during hypercapnia (3, 5, or 7% CO2) and during lung inflation (LI, 100 ml above functional residual capacity) before and after vagotomy. Hypercapnia depressed IIC activity in 5 of 7 cats; the higher the PETCO2, the lower was the firing rate and the fewer the number of spikes per breath. LI evoked an initial silent phase (ISP) in 6 of 10 cats followed by a prolonged IIC burst. Hypercapnia combined with LI abolished or diminished the ISP and shortened the prolonged burst with an increase in firing rate and a recruitment of new units. Vagotomy silenced IIC activity in 7 of 10 cats, but LI after vagotomy activated IIC activity in 10 of 10 cats, though neither an ISP nor prolonged activity occurred. Our data suggest that major factors in controlling IIC activity are reciprocal inhibition from bulbospinal inspiratory neurons, excitatory and inhibitory inputs mediated by vagal afferents, and a modulation of IIC activity via gamma-loop. Hypercapnia affects the former two factors.