Static contraction of the hindlimb muscles, induced by electrical stimulation of the ventral roots, reflexly increases arterial blood pressure and heart rate. Although stimulation of groups III and IV muscle afferents is believed to cause these reflex increases, the responses of these afferents to a level of static contraction that increases arterial pressure have not yet been determined. Therefore, in barbiturate-anesthetized cats, afferent impulses arising from endings in the gastrocnemius muscle were recorded from the L7 or S1 dorsal roots, while the cut peripheral end of the L7 ventral root was stimulated. In addition, the effects of capsaicin (100-200 micrograms) and bradykinin (25 micrograms) on the activity of the groups III and IV afferents stimulated by contraction were examined. Contraction of the gastrocnemius muscle to a level equal to or greater than that needed to cause a pressor response stimulated 12 of 19 (63%) group III afferents and 13 of 19 (68%) group IV afferents. However, the discharge patterns of the group III afferents stimulated by contraction were very different from those of the group IV fibers. No relationship was found between those fibers stimulated by contraction and those stimulated by chemicals. Our results suggest that although both groups III and IV muscle afferents contribute to the reflex cardiovascular increases evoked by static exercise, group III fibers were likely to be stimulated by the mechanical effects of muscular contraction, whereas at least some group IV fibers were likely to be stimulated by the metabolic products of muscular contraction.

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Static muscular contraction has been firmly established to reflexly increase cardiovascular and ventilatory function. Although group III and IV fibers with endings in muscle have been shown to comprise the afferent arm of this reflex arc, little is known about the nature of the contraction-induced stimulus causing the activation of these fibers. This stimulus has often been suggested to be a metabolic product of muscular contraction. We have therefore recorded the impulse activity of group III and IV afferents with endings in the triceps surae muscles of barbiturate-anesthetized cats while we injected into the femoral artery substances believed to be metabolic products of muscular contraction. We found that lithium and sodium lactate (400 mM; 1 ml) had little or no effect on the discharge of group III and IV afferents. Likewise, monobasic sodium phosphate (20 and 400 mM; 1 ml) and 2-chloroadenosine (50-100 micrograms) had only trivial effects on the discharge of these afferents. By contrast, lactic acid (25 and 400 mM; 1 ml) and arachidonic acid (0.5-2.0 mg) caused significant increases in the activity of group III and IV afferents. Most of the excitatory effect of arachidonic acid on the discharge of the afferents was prevented by indomethacin, a cyclooxygenase inhibitor. We conclude that of the substances tested in our experiments, lactic acid and some cyclooxygenase products, such as prostaglandins and thromboxanes, are the most likely to be responsible for any metabolic stimulation of group III and IV afferents during muscular contraction.

The sections in this article are: Reflex Cardiovascular Responses to Muscular Contraction in Anesthetized and Decerebrate Animals Sensory Innervation of Skeletal Muscle Reflex Autonomic Responses to Stimulation of Muscle Afferents in Anesthetized Animals Discharge Properties of Group III and IV Muscle Afferents The Site of the First Synapse—The Dorsal Horn Role of Spinal Neurotransmitters and Neuromodulators in the Exercise Pressor Reflex Pathways Ascending from the Dorsal Horn The Ventrolateral Medulla Other Central Neural Structures Final Common Pathways Interaction Between the Arterial Baroreflex and the Exercise Pressor Reflex in Anesthetized and Decerebrate Animals Evidence for the Exercise Pressor Reflex in Humans and Conscious Animals Feedback from Contracting Limb Skeletal Muscle in Humans and Conscious Animals The Nature of the Stimulus Evoking the Exercise Pressor Reflex Contribution of Peripheral Afferents to the Exercise Hyperpnea Afferents from the Exercising limbs The Carotid Chemoreceptor Afferents Role in Hyperventilation During Heavy Exercise The Pulmonary Afferents Cardiac Afferents Respiratory Muscle Afferents Mediation of the Exercise Hyperpnea by Multiple Mechanisms Summary and Conclusions Peripheral Afferent Contribution to Circulatory Responses to Exercise Peripheral Afferent Contribution to Ventilatory Responses to Exercise

The exercise pressor reflex is believed to play a role in causing the cardiovascular and ventilatory responses to exercise. This review will discuss the evidence that the reflex is active in both humans and animals. In addition, this review will discuss the nature of the mechanical and metabolic stimuli that evoke the exercise pressor reflex. Particular attention will be paid to the discharge properties of the thin fiber sensory nerves (i. e., group III and IV muscle afferents) whose activation by these mechanical and metabolic stimuli is responsible for evoking the reflex. Finally, some current findings and controversies will be discussed.