Cardiovascular responses to static exercise in man: central and reflex contributions.

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Abstract
1. To assess the contributions of muscle chemoreflexes and central signals of motor command to cardiovascular to static exercise, blood pressure and heart rate were measured during three separate conditions: (i) isometric handgrip contractions, (ii) entrapment of metabolities produced by these contractions within the contracting muscles (chemoreflex effect), and (iii) attempted contractions of acutely paralysed muscles at three levels of effort (command effect). 2. The chemoreflex was assessed during circulatory occlusion applied as the contraction ceased. Paralysis was produced by local infusion of lignocaine distal to a sphygmomanometer cuff inflated above systolic pressure. 3. Blood pressure and heart rate increased progressively during isometric contraction of 33 and 50% maximal voluntary strength (for 120 and 75 s respectively). Muscle chemoreflexes during occlusion also increased blood pressure in proportion to the duration of contraction but did not increase heart rate. During attempted contraction of paralysed muscles at three measured levels of motor command, blood pressure and heart rate increased, but only heart rate was graded with the level of command. 4. The pattern of cardiovascular response for the muscle chemoreflex (as indicated by the ratio of the changes in heart rate and blood pressure) differed from that for isometric contractions and for motor commands in isolation. The pattern for contractions and for moderate but not high intensities of motor command was similar. 5. These data suggest that cardiovascular responses to moderate intensities of static contraction can be produced primarily by motor command, but that both motor command and muscle chemoreflexes contribute to cardiovascular responses at higher intensities of static exercise. When studied in isolation, central motor command and muscle chemoreflexes do not produce the same pattern of circulatory responses.