[show abstract][hide abstract] 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 metabolites 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.
The Journal of Physiology 12/1990; 430:105-17. · 4.38 Impact Factor
[show abstract][hide abstract] ABSTRACT: In anesthetized cats reducing local arterial pressure from 125 to 75 Torr decreased blood flow (53 +/- 5%) and force production (57 +/- 7%) in soleus and medial gastrocnemius. Force was produced in these muscles by aerobic, slowly fatiguing fibers. Similar reductions in arterial pressure did not affect force production in caudofemoralis, which contains mainly fast-fatiguing fibers. In human subjects the electromyogram produced by the ankle extensors during rhythmic constant-force contractions increased as the contracting muscles were raised above the heart during legs-up tilt. This suggests that force production of active muscle fibers at a given level of activation fell with muscle perfusion pressure, thus requiring augmentation of muscle activity to sustain the standard contractions. Because aerobic fibers contributed to these contractions, it appears that force production of human muscle fibers is sensitive to small changes in perfusion pressure and, presumably, blood flow. The critical dependence of developed muscular force on blood pressure is of importance to motor control and may also play a significant role in cardiovascular control during exercise.
Journal of Applied Physiology 09/1987; 63(2):834-9. · 3.48 Impact Factor
[show abstract][hide abstract] ABSTRACT: Exercise has been shown to reduce the ability of the baroreflex to slow the heart, and signals arising from cerebral cortex may cause this reduction. To test whether signals arising from the cerebral cortex are required to cause this inhibition, reflex slowing of the heart was assessed in decerebrate cats during rest and spontaneous walking. This reflex was quantified by the relation between systolic blood pressure and the subsequent heart beat interval or its inverse, beat to beat heart rate, during transient rises in pressure caused by injections of phenylephrine. Reflex slowing of the heart was reduced during spontaneous exercise compared to rest. Exercise may inhibit reflex cardiac slowing by activating beta-adrenoceptors that inhibit vagal effects on the heart. To test whether activation of beta-adrenoceptors caused the inhibition of reflex cardiac slowing produced by spontaneous walking in these decerebrate cats, the ability of the baroreflex to slow the heart during blockade of beta-receptors by propranolol was tested in 3 cats. Propranolol did not abolish the inhibitory effect of spontaneous walking on this reflex. These data indicate that the cerebral cortex and beta-adrenoceptors are not required for exercise to inhibit reflex cardiac slowing.
Journal of the Autonomic Nervous System 01/1987; 17(4):303-12.
[show abstract][hide abstract] ABSTRACT: To determine whether spinal transection affects the cardiovascular response and the sense of effort which accompany attempts to contract paralysed muscles in normal subjects, paraplegic patients tried to contract paralysed leg muscles. During attempted contractions, paraplegic subjects reported a sense of effort but did not change heart rate or blood pressure. However, these subjects had a normal cardiovascular response to handgrip contractions. These data suggest that pathways descending to and arising from the spinal cord below the lesion are required to generate a cardiovascular response but are not necessary for the sense of effort.
[show abstract][hide abstract] ABSTRACT: Differential nerve block from peridural anesthesia was used to determine a) if the pressor response to muscle ischemia in man is caused by stimulation of small sensory nerve fibers and b) if these fibers contribute to cardiovascular-respiratory responses during dynamic exercise. Four men exercised at 50-100 W for 5 min. Muscle ischemia and a sustained pressor response were produced by total circulatory occlusion of both legs beginning 30 s before the end of exercise and continuing for 3 min postexercise. During regression of full motor and sensory block, motor strength recovered while sensory block continued; the pressor response was blocked as long as sensory anesthesia persisted (two subjects). During blockade of the pressor response, cardiovascular-respiratory responses to exercise gradually returned from augmented to normal (preblock) levels. Sensory blockade was incomplete in two subjects and the pressor response was not fully blocked. We conclude that stimulation of small sensory fibers during ischemia elicits the pressor response, but that these fibers appear not to contribute to cardiovascular-respiratory responses during mild dynamic exercise with adequate blood flow.
The American journal of physiology 11/1979; 237(4):H433-9.
[show abstract][hide abstract] ABSTRACT: We sought to determine whether the pressor response to exercise-induced muscle ischemia is related to the mass of tissue rendered ischemic. Six men repeatedly exercised for 5 min at a fixed load between 75 and 150 W (bicycle ergometer). Thirty seconds before the end of exercise, circulation to one calf, two calves, one leg, and two legs was arrested with pneumatic cuffs in successive tests with 15-min recovery periods interspersed. Each occlusion was maintained until the 3rd min of exercise recovery. During postexercise occlusion we observed 1) mean arterial pressure (MAP) was elevated in proportion to the mass of ischemic muscle, 2) forearm blood flow (FBF) was elevated during the overlap of occlusion with exercise but did not show a uniform response during the following 3 min of occlusion--either vasoconstriction or vasodilation occurred, 3) heart rate (HR) was elevated only when two legs were occluded, and 4) occlusion did not affect ventilation or endtidal CO2. We conclude that the ischemic pressor response is muscle mass-dependent. Our findings suggest that the baroreflex alters peripheral vascular resistance so as to aid in the maintenance of elevated MAP.
Journal of applied physiology: respiratory, environmental and exercise physiology 12/1978; 45(5):762-7. · 3.73 Impact Factor