Biomedical subjects

V G Macefield

Publications and source records attributed to V G Macefield.

At least 19 recordsLinked to original sources

PubMed2007

Vestibular inputs do not influence the fusimotor system in relaxed muscles of the human leg.

Descending vestibular pathways have been shown to influence recruitment thresholds of alpha motoneurones in both human and cat. However, whereas parallel connections to the fusimotor system have been shown in the cat, such connections have not yet been demonstrated in humans. In the present study we investigated whether vestibular inputs can influence the firing of spontaneously active muscle spindles in the leg via activation of gamma motoneurones. Unitary recordings were made from 30 muscle spindle afferents via tungsten microelectrodes inserted percutaneously into the common peroneal nerve of seated awake human subjects. Sinusoidal bipolar binaural galvanic vestibular stimulation (GVS; frequency 0.2, 0.5, 0.8 Hz, amplitude +/-2 mA, 100 cycles) was applied to the mastoid processes. This continuous stimulation produced a sustained frequency-dependent illusion of "rocking in a boat" or "swinging in a hammock". Despite these robust illusions none of the spontaneously active muscle spindles exhibited phase-locked modulation of firing during sinusoidal GVS. We conclude that this dynamic vestibular input was not sufficient to recruit gamma motoneurones, which are known to have little spontaneous activity in relaxed human muscles.

Adult↗

PubMed2006

Somatotopic organization of the processing of muscle and cutaneous pain in the left and right insula cortex: a single-trial fMRI study.

The insula is involved in processing noxious information. It is consistently activated by acute noxious stimuli, can elicit pain on stimulation, and lesions encompassing the insula can alter pain perception. Anatomical tracing, electrophysiological and functional brain imaging investigations have suggested that the insula is somatotopically organized with respect to noxious cutaneous inputs. It has also recently been revealed that the anterior insula displays differential activation during cutaneous compared with muscle pain. Given this difference, it is important to determine if an insula somatotopy also exists for muscle pain. Using high-resolution functional magnetic resonance imaging (fMRI) we compared insula activation patterns in 23 subjects during muscle and cutaneous pain induced in the right leg and forearm. Group and frequency analyses revealed somatotopically organized signal increases in the posterior contralateral (left) and ipsilateral (right) anterior insula. Within the posterior contralateral insula, signal increases during both cutaneous and muscle forearm pain were located lateral and anterior to those evoked by leg pain, whereas in the ipsilateral anterior insula the pattern was reversed. Furthermore, within the ipsilateral anterior insula, muscle pain activated a region anterior to that activated by cutaneous pain. This somatotopic organization may be crucial for pain localization or other aspects of the pain experience that differ depending on both stimulation site and type of tissue activated. This study reveals that the insula is organized somatopically with respect to muscle and cutaneous pain and that this organization is further separated according to the tissue in which the pain originates.

Adult↗

PubMed2006

Distinct forebrain activity patterns during deep versus superficial pain.

All pain is unpleasant, but different perceptual and emotional qualities are characteristic of pain originating in different structures. Pain of superficial (cutaneous) origin usually is sharp and restricted, whereas pain of deep origin (muscle/viscera) generally is dull and diffuse. Despite the differences it has been suggested previously that all pain is mediated by an invariant set ("neuromatrix") of brain structures. However, we report here, using functional magnetic resonance imaging (fMRI), that striking regional differences in brain activation patterns were the rule. Signal differences were found in regions implicated in emotion (perigenual cingulate cortex), stimulus localization and intensity (somatosensory cortex) and motor control (motor cortex, cingulate motor area). Further, most fMRI signal changes matched perceived changes in pain intensity. These findings clearly indicate that distinct neural activity patterns in distinct sets of brain structures are evoked by pain originating from different tissues of the body. Further, we suggest that these differences underlie the different perceptual and emotional reactions evoked by deep versus superficial pain.

Adult↗

PubMed2005

Neural sites involved in the sustained increase in muscle sympathetic nerve activity induced by inspiratory capacity apnea: a fMRI study.

A maximal inspiratory breath hold (inspiratory capacity apnea) against a closed glottis evokes a large and sustained increase in muscle sympathetic nerve activity (MSNA). Because of its dependence on a high intrathoracic pressure, it has been suggested that this maneuver causes unloading of the low-pressure baroreceptors, known to increase MSNA. To determine the central origins of this sympathoexcitation, we used functional magnetic resonance imaging to define the loci and time course of activation of different brain areas. We hypothesized that, as previously shown for the Valsalvsa maneuver, discrete but widespread regions of the brain would be involved. In 15 healthy human subjects, a series of 90 gradient echo echo-planar image sets was collected during three consecutive 40-s inspiratory capacity apneas using a 3-T scanner. Global signal intensity changes were calculated and subsequently removed by using a detrending technique, which eliminates the global signal component from each voxel's signal intensity change. Whole brain correlations between changes in signal intensity and the known pattern of MSNA during the maneuver were performed on a voxel-by-voxel basis, and significant changes were determined by using a random-effects analysis procedure (P < 0.01, uncorrected). Significant signal increases emerged in multiple areas, including the rostral lateral medulla, cerebellar nuclei, anterior insula, dorsomedial hypothalamus, anterior cingulate, and lateral prefrontal cortexes. Decreases in signal intensity occurred in the dorsomedial and caudal lateral medulla, cerebellar cortex, hippocampus, and posterior cingulate cortex. Given that many of these sites have roles in cardiovascular control, the sustained increase in MSNA during an inspiratory capacity apnea is likely to originate from a distributed set of discrete areas.

Adult↗

PubMed2003

Why do human postganglionic neurones primarily only fire once during a sympathetic burst?

AIM: Single-unit recordings from muscle vasoconstrictor, cutaneous vasoconstrictor and sudomotor neurones in awake human subjects have shown that they tend to fire only once per sympathetic burst. We review the firing properties of human sympathetic neurones and examine the idea that the short duration of a sympathetic burst may limit the number of times a neurone can fire, using the human skeletomotor system as a model for the sympathetic nervous system. RESULTS: It is known that human alpha motor neurones usually fire in long trains during voluntary contractions, but what of their pattern when constrained by a brief burst? We recorded from single motor units in the tibialis anterior muscle while subjects generated brief electromyogram bursts in the intervals between heart beats, with a duration similar to that of muscle sympathetic bursts. Eight motor units fired mostly one spike per burst, with a pattern identical to that of sympathetic neurones. CONCLUSION: These results suggests that were it not for the constraint of the bursting pattern, individual sympathetic neurones would--like alpha motor neurones--tend to fire in long trains.

Action Potentials↗

PubMed2003

Pathological sympathoexcitation: how is it achieved?

AIM: Congestive heart failure (CHF) and obstructive sleep apnoea syndrome (OSAS) are both associated with an intense sympathoexcitation, including an increased muscle sympathetic nerve activity (MSNA). We have studied the firing characteristics of single vasoconstrictor fibres to the muscle vascular bed in CHF and OSAS patients, at rest and during transient sympathoexcitatory stimuli, to elucidate the mechanisms by which vasoconstrictor output is augmented in these conditions. RESULTS: The main alternatives for augmenting sympathetic output are an increased firing frequency of individual nerve fibres and an increased recruitment of nerve fibres. Starting with the frequency alternative, the inherent bursting character of MSNA provides two possibilities to increase the firing of individual fibres: (1) by increasing the proportion of neural bursts in which the fibre is active (increased firing probability) and (2) by increasing the number of spikes a fibre generates per burst (increased multiple within-burst firing). At rest and in cardiac sinus rhythm, an increased firing probability is seen in both CHF and OSAS patients, whereas increased multiple within-burst firing is found in OSAS but not in CHF. In response to transient sympathoexcitatory stimuli (such as pre-mature heart beats), both patient groups show marked shifts towards multiple within-burst firing. Thus, both mechanisms for augmenting discharge frequency are operating in these two pathological conditions, but the firing characteristics at rest differ significantly. During recording sessions in sympathoexcited patients, we have encountered vasoconstrictor fibres that are active almost exclusively during periods of transient sympathoexcitation, while being virtually silent at rest. This suggests that recruitment of previously inactive vasoconstrictor fibres, the second main alternative for increasing vasoconstrictor output, contributes to transient sympathoexcitatory responses in these patients. Although it seems reasonable to assume that recruitment may also contribute to the resting level of MSNA in CHF and OSAS, this issue is difficult to resolve in microneurographic studies. CONCLUSION: In conclusion, pathological sympathoexcitation appears to depend on both recruitment and increased firing frequency. A shift towards multiple within-burst firing, at rest or in response to transient stimuli, may constitute a risk factor per se as it entails neural volleys with high instantaneous firing frequencies and consequently higher release of neurotransmitters.

Action Potentials↗

PubMed2002

Cortically evoked neural volleys to the human hand are increased during ischaemic block of the forearm.

Reorganisation of the motor cortex may occur after limb amputation or spinal cord injury. In humans, transcranial magnetic stimulation (TMS) shows expansion of motor cortical representations of muscles proximal to the injury. Similarly, ischaemic block of the hand can increase acutely the representation of the biceps muscle, measured by increased biceps motor potentials evoked by TMS. It is thought that this increase occurs at the expense of the cortical representation of the paralysed and deafferented hand muscles but this has never been investigated. To study what changes occur in the cortical representation of the hand muscles during ischaemic block, a tungsten microelectrode was inserted into the ulnar or median nerve above the elbow and the size of the neural potential elicited by TMS in fascicles supplying the hand was measured in seven subjects. Prior to ischaemia, TMS evoked EMG responses in the intrinsic hand muscles. In the nerve, a brief motor potential preceded the response in the muscle and was followed by a contraction-induced sensory potential. During 40 min of ischaemia produced by a blood pressure cuff inflated around the forearm to 210 mmHg, the EMG response to TMS and the sensory potential from the hand were progressively blocked. However, the motor neural evoked potential showed a significant increase in amplitude during the ischaemic period (30.5 %, P = 0.005). The increase in the neural potential suggests that output to the hand evoked from the cortex by TMS was not decreased by ischaemic block. Thus, we conclude that the increased response of biceps to TMS during distal ischaemia is not accompanied by a corresponding decrease in the motor cortical representation of the hand.

Adult↗

PubMed2001

Modulation of ongoing EMG by different classes of low-threshold mechanoreceptors in the human hand.

1. We have previously demonstrated that the input from single FA I and SA II cutaneous mechanoreceptors in the glabrous skin of the human hand is sufficiently strong to modulate ongoing EMG of muscles acting on the digits. Some unresolved issues have now been addressed. 2. Single cutaneous (n = 60), joint (n = 2) and muscle spindle (n = 34) afferents were recorded via tungsten microelectrodes inserted into the median and ulnar nerves at the wrist. Spike-triggered averaging was used to investigate synaptic coupling between these afferents and muscles acting on the digits. The activity of 37 % of FA I (7/19), 20 % of FA II (1/5) and 52 % of SA II afferents (11/21) evoked a reflex response. The discharge from muscle spindles, 15 SA I and two joint afferents did not modulate EMG activity. 3. Two types of reflex responses were encountered: a single excitatory response produced by irregularly firing afferents, or a cyclic modulation evoked by regularly discharging afferents. Rhythmic stimulation of one FA I afferent generated regularly occurring bursts which corresponded to the associated cyclic EMG response. 4. Selectively triggering from the first or last spike of each burst of one FA I afferent altered the averaged EMG profile, suggesting that afferent input modulates the associated EMG and not vice versa. 5. The discharge from single FA I, FA II and SA II afferents can modify ongoing voluntary EMG in muscles of the human hand, presumably via a spinally mediated oligosynaptic pathway. Conversely, we saw no evidence of such modulation by SA I, muscle spindle or joint afferents.

Action Potentials↗

PubMed2000

Discharge behaviour of single motor units during maximal voluntary contractions of a human toe extensor.

1. While it is known that the average firing rate of a population of motoneurones declines with time during a maximal voluntary contraction, at least for many muscles, it is not known how the firing patterns of individual motoneurones adapt with fatigue. To address this issue we used tungsten microelectrodes to record spike trains (mean +/- s.e.m., 183 +/- 27 spikes per train; range, 100-782 spikes) from 26 single motor units in extensor hallucis longus during sustained (60-180 s) maximal dorsiflexions of the big toe in seven human subjects. 2. Long spike trains were recorded from 13 units during the first 30 s of a maximal voluntary contraction (mean train duration, 9.6 +/- 1.2 s; range, 3.6-21.9 s) and from 13 units after 30 s (mean train duration, 16.6 +/- 3.7 s; range, 7.1-58.1 s). Maximal isometric force generated by the big toe declined to 78.3 +/- 6.3 % of its control level by 60-90 s and to 39.5 +/- 1.4 % of control by 120-150 s. Despite this substantial fatigue, mean firing rates did not change significantly over time, declining only slightly from 15.8 +/- 0.7 Hz in the first 30 s to 14.0 +/- 0.5 Hz by 60-90 s and 13.6 +/- 0.3 Hz by 120-150 s. 3. To assess fatigue-related adaptation in discharge frequency and variability of individual motor units, each spike train was divided into 2-15 equal segments containing at least 50 interspike intervals. Discharge variability was measured from the coefficient of variation (s.d. /mean) in the interspike intervals, with the s.d. being calculated using a floating mean of 19 consecutive intervals. Adaptation was computed as the average change in firing rate or variability that would occur for each 1 s of activity. There were no systematic changes in either firing rate or variability with time. 4. We conclude that single motoneurones supplying the extensor hallucis longus, a muscle comprised primarily of slow twitch muscle units, show little adaptation in firing with fatigue, suggesting that a progressive reduction in firing rate is not an invariable consequence of the fatigue associated with sustained maximal voluntary contractions.

Action Potentials↗

PubMed2000

Comparison of contractile properties of single motor units in human intrinsic and extrinsic finger muscles.

1. The purpose of the present study was to compare the contractile properties of single motor units in the intrinsic (short) and extrinsic (long) finger muscles in awake human subjects using intraneural motor axon stimulation. 2. Twitch properties were measured for 17 intrinsic and 11 extrinsic motor units by selective stimulation of a single motor axon in the ulnar or the median nerve. Force was measured from the appropriate digit, just distal to the muscle's point of insertion and single unit EMG was recorded with surface electrodes. Force-frequency relationships (2-100 Hz) were established for 16 of these units (7 intrinsic, 9 extrinsic). Across the 16 motor units for which force-frequency data were obtained, twitch contraction time (63.7 +/- 6.0 ms, mean +/- s.e.m.) was inversely correlated with the frequency required to generate half-maximum tetanic force (12.0 +/- 1.1 Hz). 3. We found no systematic differences between the contractile properties of intrinsic and extrinsic motor units. There was no evidence of a bimodal distribution into large/small or fast/slow units based on maximum force or contraction times, although both fast and slow motor units were encountered. 4. The peak slope of the sigmoidal force-frequency relationship for intrinsic motor units (9.1 and 4.4-12.9 mN Hz-1, median and interquartile range) was significantly higher than that for extrinsic motor units (2.9 and 2.3-3.1 mN Hz-1; P = 0.028), i.e. greater force steps were produced by the intrinsic motor units for a given change in stimulation frequency. This difference suggests that motor units in the intrinsic muscles of the hand are more sensitive to modulating force output by changes in motoneurone firing rates than are those in the extrinsic muscles. This reflects the important role of the intrinsic hand muscles in the fine manipulation of objects.

Adolescent↗

PubMed1999

Firing properties of single muscle vasoconstrictor neurons in the sympathoexcitation associated with congestive heart failure.

BACKGROUND: Congestive heart failure (CHF) in humans is associated with a marked sympathoexcitation, including an augmented muscle sympathetic nerve activity (MSNA) in intraneural multiunit recordings. In the present study, single-unit recording was used to evaluate whether the firing properties of individual muscle vasoconstrictor neurons can reveal underlying mechanisms for this increase in MSNA. METHODS AND RESULTS: Eight patients with CHF (NYHA class II to IV; left ventricular ejection fraction, 29+/-5%, mean+/-SEM) were studied. In standard multiunit recordings, MSNA burst incidence (bursts/100 heartbeats) ranged from 65% to 100% (88+/-5%). Using selective tungsten microelectrodes, we made recordings from 16 single muscle vasoconstrictor axons. Mean unit firing probability (ie, the percentage of cardiac intervals in which a single axon fired) was 54.5+/-5.2% (range, 21 to 89%), and mean firing frequency was 0.98+/-0.22 Hz (0.14 to 3.86 Hz), both of which were higher than seen previously in healthy subjects (P<0.001). Although single neurons occasionally generated multiple spikes per sympathetic burst, such multiple firing was rare and was not different from that seen in healthy subjects. CONCLUSIONS: An increased firing frequency of individual vasoconstrictor neurons is one mechanism for the increased number of multiunit MSNA bursts at rest in CHF. The neurons discharge in more diastoles than in healthy subjects (ie, firing probability is increased), but the likelihood of discharging >1 impulse per sympathetic burst is not increased. Despite the intense multiunit activity at rest, the firing characteristics of individual vasoconstrictor axons indicate a remaining capacity for transient increases of MSNA in CHF.

Adult↗

PubMed1999

Evidence for strong synaptic coupling between single tactile afferents and motoneurones supplying the human hand.

1. Electrical stimulation of digital nerves elicits short-latency excitatory and inhibitory spinal reflex responses in ongoing EMG in muscles acting on the fingers and thumb. Similar responses are elicited by stimulating a population of muscle spindles but not when a single muscle spindle is activated. The current study investigated whether short-latency EMG responses could be evoked from the discharge of a single cutaneous afferent. 2. Thirty-three tactile afferents were recorded via tungsten microelectrodes in the median nerve of awake humans. Spike-triggered averaging revealed EMG events time-locked to the afferent discharge. The afferents were activated by an external probe and the EMG was elicited by a weak voluntary contraction. 3. Eleven cutaneous afferents (33 %) showed a short-latency response in the ongoing EMG. Overt increases or decreases in EMG were observed for seven afferents (onset latency 20.0-41.1 ms). For four slowly adapting (SA) type II afferents, EMG showed a periodicity that was correlated to the afferent interspike interval (r = 0.99). 4. The EMG associated with two rapidly adapting (FA) type I afferents (29 %) showed a short-latency excitation while five showed neither excitation nor inhibition. Seven SA II afferents (39 %) showed excitation and 11 no response; and none of the six SA I afferents showed any response. 5. We conclude that, unlike muscle spindle afferents, the input from a single cutaneous afferent is strong enough to drive, via interneurones, motoneurones supplying muscles acting on the digits. The potent short-latency response we found supports the important role of cutaneous mechanoreceptors in fine motor control of the human hand.

Adolescent↗

PubMed1999

Firing properties of single vasoconstrictor neurones in human subjects with high levels of muscle sympathetic activity.

1. Single-unit recordings were made from 19 postganglionic muscle vasoconstrictor axons via tungsten microelectrodes in the peroneal nerve in seven healthy subjects with many multi-unit sympathetic discharges at rest ('high group', 75 +/- 5 multi-unit bursts per 100 heart beats, mean +/- s.e.m.). The results were compared with previous data from 14 units in subjects with 21 +/- 2 multi-unit bursts per 100 heart beats ('low group'). 2. In the 'high group' the units fired spontaneously in 35 +/- 4 % of all cardiac intervals. One unit only ever fired once per cardiac interval, 14 units (74 %) generated maximally two to three spikes, and four units (21 %) up to four to five spikes. Of those cardiac intervals in which a unit fired, a single spike occurred in 78 %, two spikes in 18 %, three spikes in 4 % and four spikes in less than 1 % of cardiac intervals. Measured as the inverse of all interspike intervals, the mean rate was 0.33 +/- 0.04 Hz and the mean intraburst frequency 22.2 +/- 1.6 Hz. Most results were similar to those in the 'low group', but in the 'low group' heart rate was higher (64.5 vs. 50.4 beats min-1) and mean firing frequency was higher (0.49 +/- 0.06 Hz). 3. During increases of multi-unit burst activity evoked by sustained inspiratory-capacity apnoea the firing probability of nine units in the 'high group' increased from 33 +/- 6 to 56 +/- 3 % of the cardiac intervals. Simultaneously, the incidence of single spikes decreased and the incidence of multiple spikes per cardiac interval increased, resulting in an increase of mean firing frequency from 0. 23 +/- 0.04 Hz at rest to 1.04 +/- 0.14 Hz during the apnoea. 4. We conclude that single muscle vasoconstrictor neurones usually fire only a solitary spike during sympathetic bursts both in subjects with a high and in subjects with a low number of bursts at rest. Presumably, differences in the numbers of bursts are due mainly to differences in firing probability and recruitment of sympathetic fibres. During acute increases of multi-unit activity, both increases in discharge frequency and recruitment of additional neurones contribute to the increased intensity of an individual sympathetic burst.

Adult↗

PubMed1999

Respiratory and cardiac modulation of single sympathetic vasoconstrictor and sudomotor neurones to human skin.

1. The firing of single sympathetic neurones was recorded via tungsten microelectrodes in cutaneous fascicles of the peroneal nerve in awake humans. Studies were made of 17 vasoconstrictor neurones during cold-induced cutaneous vasoconstriction and eight sudomotor neurones during heat-induced sweating. Oligounitary recordings were obtained from 8 cutaneous vasconstrictor and 10 sudomotor sites. Skin blood flow was measured by laser Doppler flowmetry, and sweating by changes in skin electrical resistance within the innervation territory on the dorsum of the foot. 2. Perispike time histograms revealed respiratory modulation in 11 (65 %) vasoconstrictor and 4 (50 %) sudomotor neurones. After correcting for estimated conduction delays, the firing probability was higher in inspiration for both classes of neurone. Measured from the oligounitary recordings, the respiratory modulation indices were 67. 7 +/- 3.9 % for vasoconstrictor and 73.5 +/- 5.7 % for sudomotor neurones (means +/- s.e.m.). As previously found for sudomotor neurones, cardiac rhythmicity was expressed by 7 (41 %) vasoconstrictor neurones, 5 of which showed no significant coupling to respiration. Measured from the oligounitary records, the cardiac modulation of cutaneous vasoconstrictor activity was 58.6 +/- 4.9 %, compared with 74.4 +/- 6.4 % for sudomotor activity. 3. Both vasoconstrictor and sudomotor neurones displayed low average firing rates (0.53 and 0.62 Hz, respectively). The percentage of cardiac intervals in which units fired was 38 % and 35 %, respectively. Moreover, when considering only those cardiac intervals when a unit fired, vasoconstrictor and sudomotor neurones generated a single spike 66 % and 67 % of the time. Rarely were more than four spikes generated by a single neurone. 4. We conclude that human cutaneous vasoconstrictor and sudomotor neurones share several properties: both classes contain subpopulations that are modulated by respiration and/or the cardiac cycle. The data suggest that the intensity of a multi-unit burst of vasoconstrictor or sudomotor impulses is probably governed primarily by firing incidence and the recruitment of additional neurones, rather than by an increase in the number of spikes each unit contributes to a burst.

Adult↗

PubMed1999

Force-frequency and fatigue properties of motor units in muscles that control digits of the human hand.

Modulation of motor unit activation rate is a fundamental process by which the mammalian nervous system encodes muscle force. To identify how rate coding of force may change as a consequence of fatigue, intraneural microstimulation of motor axons was used to elicit twitch and force-frequency responses before and after 2 min of intermittent stimulation (40-Hz train for 330 ms, 1 train/s) in single motor units of human long finger flexor muscles and intrinsic hand muscles. Before fatigue, two groups of units could be distinguished based on the stimulus frequency needed to elicit half-maximal force; group 1 (n = 8) required 9.1 +/- 0.5 Hz (means +/- SD), and group 2 (n = 5) required 15.5 +/- 1.1 Hz. Twitch contraction times were significantly different between these two groups (group 1 = 66. 5 ms; group 2 = 45.9 ms). Overall 18% of the units were fatigue resistant [fatigue index (FI) > 0.75], 64% had intermediate fatigue sensitivity (0.25 </= FI </= 0.75), and 18% were fatigable (FI < 0. 25). However, fatigability and tetanic force were not significantly different among groups. Therefore unlike findings in some other mammals, fast-contracting motor units were neither stronger nor more susceptible to fatigue than slowly contracting units. Fatigue, however, was found to be greatest in those units that initially exerted the largest forces. Despite significant slowing of contractile responses, fatigue caused the force-frequency relation to become displaced toward higher frequencies (44 +/- 41% increase in frequency for half-maximal force). Moreover, the greatest shift in the force-frequency relation occurred among those units exhibiting the largest force loss. A selective deficit in force at low frequencies of stimulation persisted for several minutes after the fatigue task. Overall, these findings suggest that with fatigue higher activation rates must be delivered to motor units to maintain the same relative level of force. Questions regarding classification of motor units and possible mechanisms by which fatigue-related slowing might coexist with a shift in the force-frequency curve toward higher frequencies are discussed.

Action Potentials↗

PubMed1998

Sustained activation of muscle sympathetic outflow during static lung inflation depends on a high intrathoracic pressure.

Muscle sympathetic nerve activity is strongly activated during a static inflation of the lungs in awake human subjects. The purpose of the present study was to test the hypothesis that this sustained activation is due to the associated increase in intrathoracic pressure. In ten subjects microneurographic techniques were used to record muscle sympathetic activity from the peroneal nerve and arterial pressure was monitored continuously by finger-pulse photoplethysmography. Holding the breath at inspiratory capacity with the glottis closed and inspiratory muscles relaxed caused a sustained activation of muscle sympathetic nerve activity but not of skin sympathetic activity. Conversely, when subjects held the lungs maximally inflated by a constant inspiratory effort and an open glottis there was no sympathetic activation despite a similar initial fall in mean arterial pressure. Because intrathoracic pressure was below or close to atmospheric in the latter condition, it is concluded that a high intrathoracic pressure is required for the sympathetic response. Furthermore, the present results provide further support for the idea that unloading of cardiopulmonary baroreceptors is responsible for the sustained activation of muscle sympathetic nerve activity during static lung inflations in human subjects.

Adult↗

PubMed1998

Inhibition of muscle sympathetic outflow following transcranial cortical stimulation.

The possible contribution of cerebral cortical activity to sympathetic outflow to the muscle vascular bed was assessed in normal human subjects. Muscle sympathetic activity was recorded from motor fascicles of the peroneal nerve in 8 subjects while transcranial magnetic stimulation was applied over the vertex, or unilaterally over the hand area of cortex. By triggering the cortical stimulus from the R-wave of the ECG and introducing delays of 0-600 ms between the trigger and the stimulus, we found that a single cortical stimulus delayed by 200-400 ms caused a pronounced inhibition of one pulse-synchronous sympathetic burst. Stimulation over the vertex was more effective than stimulation over the hand area of cortex. In addition to this inhibition of muscle sympathetic outflow, brain stimulation caused an increase in cutaneous sympathetic activity, both sudomotor (sweating) and vasoconstrictor (decrease in skin blood flow). We suggest that the cerebral cortex may normally suppress muscle sympathetic outflow and speculate that lesions that interrupt this source of inhibition (such as those caused by stroke) may result in an augmented muscle sympathetic outflow.

Adult↗

PubMed1998

Spontaneous and evoked ectopic discharges recorded from single human axons.

A quantitative assessment was made of the firing characteristics of repetitive axonal discharges encountered during microneurographic recordings from human peripheral nerves. Spontaneous activity was recorded from 16 single axons using tungsten microelectrodes inserted percutaneously into fascicles of the median or peroneal nerves in normal subjects. These discharges typically consisted of brief bursts of 2-5 spikes occurring at a frequency of 7-10 Hz. Peak instantaneous frequencies usually exceeded 300 Hz. Based on their similarity with spontaneous high-frequency discharges recorded from single axons following nerve damage, ischemia, prolonged electrical stimulation, or hyperventilation, it is concluded that they are generated ectopically at the site of a previous impalement of a nerve fiber. It is suggested that short-term damage to the nerve fiber caused by the microelectrode may allow accumulation of K+ underneath the myelin, triggering an inward flow of K+ and regenerative depolarizations. Alternatively, internodal channels may be exposed following damage to the myelin, resulting in the generation of spontaneous pacemaker potentials and repetitive discharges.

Action Potentials↗