REFLEX REGULATION OF MUSCLE PERFUSION DURING EXERCISE

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The enormous levels of blood flow demanded by skeletal muscle during dynamic exercise probably creates the most severe, routinely imposed challenge to the neural control of the circulation. If blood flow to muscle is too low for its metabolism, metabolites accumulate and activate sensory nerves in the muscle. Activation of these nerves elicits a reflex rise in arterial pressure--called a muscle chemoreflex. Muscle chemoreflexes are potentially a powerful regulator of the circulation and probably account for the exaggerated rise in arterial pressure during exercise when patients with peripheral vascular disease experience claudication. When and how do muscle chemoreflexes regulate muscle blood flow? Studies are to be carried out in exercising dogs (treadmill) thereby ensuring normal patterns of motor unit recruitment while avoiding detrimental effects of anesthesia and acute surgical trauma. The first aim is to determine when, if ever, muscle chemoreflexes are tonically active during dynamic exercise. The approach is to produce a supranormal blood flow in a freely perfused limb to see if a reduction in muscle metabolites reduces the chemoreflex drive from this limb (shuts the reflex off). The second aim is to determine how muscle chemoreflexes regulate muscle blood flow when chemoreflexes from all active muscles are activated simultaneously during heavy dynamic exercise. The approach here is to reduce cardiac output (blood flow to all muscles) by reducing the rate of ventricular pacing in dogs with surgically induced atrioventricular (AV) block. The key question is: do muscle chemoreflexes vasoconstrict active muscle? The third aim is to determine if tachycardia alone, generated by descending neural command signals produces a normal rise in cardiac output and arterial pressure at the onset of mild dynamic exercise. The approach here is to mimic the command signals by increasing ventricular pacing at the onset of exercise in dogs with AV-block made are flexic by ganglionic blockade. The fourth aim is to determine whether muscle chemoreflexes directly influence arterial baroreflexes. The approach here is to compare baroreflex curves (atrial rate vs. arterial pressure) in AV-blocked dogs when 1) there is no chemoreflex activation (mild exercise) and 2) there is a constant level of muscle chemoreflex activation (constant low muscle blood flow by iliac artery compression). The fifth aim is to determine whether sympathetic vasoconstrictor nerve activity is normally directed to active muscle. The approach here is to compare muscle vascular conductance at the same blood flow and work rate before and after blockade of sympathetic nerves. The final aim is to quantify the contribution to muscle perfusion of a non-reflex mechanism, the muscle pump. The approach here is to see if hypermetabolism induced by dinitrophenol infusion (low blood flow and no muscle pump) combined with the muscle-pumping action of mild dynamic exercise raises muscle blood flow to the level achieved during moderate exercise at a similar oxygen consumption.