The neural mechanisms causing the airway dilation evoked by exercise are not understood. Three candidates are central command, a reflex arising from contracting skeletal muscle, and the Hering-Breuer reflex. Activation of the latter two mechanisms has been shown to dilate the airways. In contrast, the role played by central command in the control of airway caliber is not known. We, therefore, tested the hypothesis that stimulation of the mesencephalic locomotor region (MLR) in paralyzed decerebrate cats decreased total lung resistance (TLR). Electrical stimulation (20-80 μA) of the MLR increased TLR from 28.2 ± 1.9 to 38.1 ± 2.4 cmH2O L-1 sec-1 (24 sites in 19 cats; p < 0.001). Similarly, microinjection of picrotoxin, a GABA antagonist, (8 mM, 100-400 nl) increased TLR from 26.1 ± 3.3 to 36.3 ± 5.4 cmH2O L-1 sec-1 (9 sites in 9 cats; p < 0.02). All of the changes evoked by electrical and chemical stimulation of the MLR were accompanied by increases in arterial pressure, heart rate, and ventral root motoneuron discharge. In contrast, electrical stimulation of the tibial nerve at intensities that recruited C-fibers reflexly decreased TLR (12 cats; p < 0.001). Our findings provide little evidence for the central command signal originating from the MLR in causing the airway dilation evoked by exercise.
- airways, dilatation, central command
- brainstem, motor command, airway dilatation
- control of breathing, exercise, airway innervation
- exercise, airway dilatation
- mammals, cat
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine