SUMMARY. The purpose of this study was to determine the contribution of muscle afferents and central command in regulating sympathetic nerve activity during static exercise in humans. In 20 healthy subjects, we recorded heart rate, arterial pressure, and efferent sympathetic nerve activity in the leg during arm exercise. Microelectrodes were inserted percutaneously into a fascicle of the peroneal nerve to measure sympathetic discharge to muscle. Measurements were obtained in nine subjects during sustained handgrip (30% maximal voluntary contraction) followed by relaxation or by arrested circulation of the forearm. Heart rate and arterial pressure increased during the first and second minutes of handgrip. Muscle sympathetic nerve activity increased from 261 ± 46 to 504 ± 97 units (mean ± SE; units = burst frequency x amplitude; P < 0.05) during the second minute of handgrip. During forearm ischemia following handgrip, heart rate returned promptly to control, whereas arterial pressure and muscle sympathetic nerve activity (631 ±115 units) remained elevated. In contrast, muscle sympathetic nerve activity returned toward control during relaxation without arrested circulation. These data indicate that muscle sympathetic nerve activity is increased by stimulation of chemically sensitive muscle afferents. To determine the influence of central command on muscle sympathetic nerve activity, we compared responses during ar. involuntary and a voluntary biceps contraction, each at 20% maximal voluntary contraction. Both maneuvers raised arterial pressure, but heart rate increased only during voluntary contraction. More importantly, muscle sympathetic nerve activity rose during involuntary contraction, but fell during voluntary effort. These studies demonstrate that during sustained handgrip in humans, stimulation of chemically sensitive muscle afferents increases muscle sympathetic nerve activity in the leg, and central command causes tachycardia, but inhibits muscle sympathetic outflow in the leg. (Circ Res 57: 461-469, 1985)

SUMMARY1. We studied the influence of respiration on muscle sympathetic and cardiac vagal activities in twenty conscious, healthy young adult subjects. Efferent post-ganglionic muscle sympathetic activity was measured directly with electrodes inserted percutaneously into a peroneal nerve, and vagal cardiac activity was measured indirectly from electrocardiographic changes of heart period.2. Muscle sympathetic activity waxed and waned with respiration; maximum activity occurred at end-expiration and minimum activity occurred at end-inspiration. Voluntary control of breathing did not alter the time course or magnitude of muscle sympathetic outflow.3. Spectral analyses showed that respiratory periodicities were present in sympathetic and vagal records. Average power at frequencies below respiratory frequencies exceeded or equalled that at respiratory frequencies in both muscle sympathetic and vagal cardiac records. A cardiac periodicity was present and conspicuous in muscle sympathetic recordings in all but one subject.4. Diastolic arterial pressure increased during inspiration and decreased during expiration. Heart period and muscle sympathetic activity paralleled each other and were related reciprocally to changes of diastolic pressure.5. Brief reductions of carotid baroreceptor afferent traffic provoked by neck pressure were more effective in increasing sympathetic activity in expiration than inspiration.6. We conclude that quiet respiration is associated with parallel phasic changes in activity of medullary vagal cardiac and spinal muscle sympathetic motonuclei in man; spontaneous activity and susceptibility to excitation or inhibition by autonomic inputs are greater in expiration than inspiration. Substantial power is present in both muscle sympathetic and cardiac vagal recordings at frequencies below respiratory frequencies.

Bilateral lidocaine blocks of glossopharyngeal and vagus nerves in the neck were made in two healthy subjects to achieve deafferentation of arterial and cardiopulmonary baroreceptors. Microelectrode recordings of muscle nerve sympathetic activity (MSA) were made in one peroneal nerve; in one subject skin sympathetic activity (SSA) was recorded simultaneously in the other peroneal nerve. Following the nerve block in the neck there was a strong increase of MSA accompanied by temporary hypertension and tachycardia. The normal cardiac rhythmicity of MSA disappeared and the outflow appeared as bursts of impulses of variable duration occurring in a slow, irregular rhythm. Thus MSA became similar to SSA, but the activities never became synchronous. During the nerve block arousal stimuli evoked single bursts of MSA, a reflex response which normally occurs in SSA but not in MSA. It is concluded that (1) cardiac rhythmicity of MSA is due to baroreceptor influence; (2) a low level of MSA at rest depends on strong baroreceptor inhibition and not on a weak central drive; (3) central sympathetic outflows to skin and muscle are similar though not identical and the different characteristics normally observed are due to a large extent to different modulatory influences from afferent activity (presumably of baroreceptor origin) in glossopharyngeal and vagus nerves; and (4) baroreceptor deafferentation resulting in resting tachycardia and hypertension may explain sympathetic hyperactivity in the Guillain-Barré syndrome.

Recordings of multiunit sympathetic activity were made from muscle branches of the peroneal nerve in eight previously untreated subjects with essential hypertension during intravenous administration of the cardioselective beta-adrenoceptor antagonist, metoprolol. Intraarterial blood pressure and central venous pressure were monitored simultaneously. After metoprolol, heart rate fell and central venous pressure increased in all subjects. Blood pressure increased in some subjects and decreased in others whereas the rate of rise of the systolic pulse wave regularly decreased. Sympathetic activity, discharged in pulse synchronous bursts of action potentials, was quantitated by counting the number of bursts and their amplitudes in the mean voltage neurogram. In all subjects, the average diastole was associated with outflow of more sympathetic impulses after metoprolol than before. Total sympathetic activity (expressed as bursts/min multiplied by mean burst strength) also increased after the drug. The mechanism behind the increase of sympathetic activity may be either a direct central nervous effect or a reflex effect elicited from arterial baroreceptors or cardiac receptors.

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