Regulation of Respiration During Induced Muscular Work in Decerebrate Dogs

Abstract

Ventilatory responses to induced exercise were studied in 15 decerebrate dogs. In control experiments (without exercise) it was found that ventilation, O2 consumption, ventilatory equivalent for O2 and arterial pCO2 and H+ con-centration showed no significant change over a period of 500 minutes after decerebration at the level of the midbrain. During induced exercise in decerebrate dogs both ventilation and O2 consumption increased gradually to attain a steady state; in contrast to this nembutalized dogs showed an overshoot in ventilation. The difference is interpreted as being due to quickly accommodated reactions mediated through the cerebral cortex. During the steady state of exercise the relationship between ventilation and O2 consumption is expressed by the equation: Ventilation (1/min. body temp, ambient barometric pressure saturated (BTPS)) = 0.0333 ([plus or minus] 0.0016) O2 consumption (ml./min. standard temp, and pressure perfectly dry (STPD)) = 0.154, with r = 0.9526. As functions of O2 consumption (40-362 ml/min. STPD), the arterial H+ concentration remained constant during exercise (r = -0.1863; p> 0.50) but the arterial pCO2 decreased (r = -0.3818; p<0.05). The relationship between pCO2 and H+ concentration follows a respiratory pathway. It is concluded that the sensitivity of the respiratory centers to exercise in decerebrate dogs is the same as in nembutalized dogs and in un-anesthetized trained dogs and that cortical irradiation probably is not responsible for the normal regulation of exercise hyperpnea.