Reflex inputs to the cardiovascular and respiratory centers from dynamically working canine muscles. Some evidence for involvement of group III or IV nerve fibers.

Abstract

Reflex inputs to the circulatory and ventilatory centers from dynamically contracting muscles and their interaction with extramuscular inputs were studied in anesthetized dogs. Dynamic work of hindlimb muscles was evoked by electrical stimulation of sciatic nerve branches (40 tetani/min with square wave pulses: 0.2-1.0 V, 0.3-0.7 ms, 30-100 Hz). These pulses activated group I and II nerve fibers and they affected heart rate (HR), minute ventilation (VE), and mean arterial pressure (MAP) only to a small degree when neuromuscular transmission was blocked by cooling distally from the electrodes. Comparable small changes were obtained if these fibers were excited by their natural stimuli when moving and stretching the legs and muscles, respectively. These responses disappeared when the legs were moved and the muscles stretched after the dogs were immobilized with drugs, indicating that they were caused by increased muscle tension and not movement as such. If neuromuscular transmission was restored, muscular contractions were induced which caused great reflexogenic increases of HR, VE and MAP. Muscular reflex drives to the centers were then eliminated by cold blockade of nervous transmission in both sciatic nerves proximally from the stimulating electrodes while contractions were not interrupted. Blood metabolically enriched in this way entered the systemic circulation, thereby creating humoral extramuscular drives. Muscular reflex inputs accounted for the major and humoral drives for the minor portion of the total cardiovascular and respiratory responses during onset as well as during steady state of dynamic work, although humoral drives increased with time. The time courses of the reflexly induced changes tallied with those of muscular blood flow, indicating a relation with similar metabolic processes. The reflex drives were abolished if a blocking temperature typical for nonmyelinated or small myelinated group IV or III nerve fibers was reached. The main responses were only obtained if electrical stimuli were raised to levels where they activated group III or IV afferents.