The proposed experiments have two goals. The first goal is to identify the stimulus to the group III and IV afferents whose activation by static muscular contraction signals the central nervous system that blood supply and demand in a working muscle are not properly matched. These afferents will be identified by showing that they respond more to and ischemic static contraction than to a freely perfused contraction, even though both types of contraction than to an ischemic static contraction than to a freely perfused contraction, even though both types of contraction develop the same tension. The hypothesis to be tested is that lactic acid infusion and hypoxemia stimulate group III and IV afferents sensing a mismatch between blood supply and demand in the working muscle, but have no effect on the discharge of afferents not sensing this mismatch. The second hypothesis to be tested that dichloracetate, which attenuates lactic acid production by skeletal muscle, decreases the responses to contraction of afferents not sensing this mismatch. These experiments will be performed in unanesthetized decerebrate cats. Afferent impulse activity arising from the triceps surae muscles will be recorded from the dorsal roots. The second goal is to demonstrate in decorticate unanesthetized cats that group III and IV hindlimb muscle afferents are stimulated by true "true dynamic exercise", induced by activation of the subthalamic locomotor region. Stimulation of this region is known to cause a discharge pattern in alpha motoneurons that is identical to that evoked by dynamic exercise. The effect of ischemia, induced by occlusion of the arterial blood supply to the working muscle, on the afferents' response to dynamic exercise will be examined. In addition, the effect of infusing lactic acid on the afferents' response to dynamic exercise will be examined. The hypothesis to be tested is that true dynamic exercise stimulates group III afferents by mechanical means and group IV afferents are stimulated by exercise, these experiments may shed new light on the puzzling question as to the nature of the metabolic stimulus causing these afferents to signal the central nervous system that blood supply and demand in a contracting muscle are mismatched