Biomedical subjects

V G Macefield

Publications and source records attributed to V G Macefield.

32 records · Page 2Linked to original sources

PubMed1998

Muscle sympathetic vasoconstrictor activity in hydrocortisone-induced hypertension in humans.

AIM: This study was undertaken to test the hypothesis that increased sympathetic vasomotor drive is responsible for cortisol-induced hypertension. METHODS: Ten healthy male subjects on a fixed sodium diet (150 mmol/day) were randomized to five days of treatment with cortisol (200 mg/day) or placebo in a double-blind crossover study. On day 5 of each treatment, multi-unit muscle sympathetic activity was recorded from the common peroneal nerve. Resting muscle sympathetic activity (MSA) was measured in the recumbent position and stimulated MSA was measured in the final 20 sec of end-inspiratory capacity apnoea and end-expiratory apnoea and in the second minute of a cold pressor stimulus. A subgroup of six subjects also underwent identical MSA measurements following 5 days treatment with dexamethasone (3 mg/day). MAJOR FINDINGS: Cortisol, but not placebo, significantly increased systolic (115+/-2 vs 129+/-3 mmHg precortisol vs cortisol day 5, p < 0.001) and diastolic blood pressure (53+/-3 vs 61+/-3, p < 0.05). Resting MSA was significantly reduced by cortisol (23.9+/-2.3 to 5.0+/-2.0 bursts/min, placebo vs cortisol, p < 0.01). Cortisol significantly attenuated the increase in MSA observed at end-inspiratory apnoea (56.3+/-3.9 vs 35.4+/-6.6, p < 0.05) and end-expiratory apnoea (50.5+/-3.5 vs 26.3+/-6.2 bursts/min, n = 8, p < 0.05), and during the cold pressor response (55.0+/-12.7 vs 21.4+/-7.6, n = 5, p < 0.05). Dexamethasone significantly increased systolic blood pressure and suppressed resting and stimulated MSA. No changes in body weight, haematocrit or angiotensin II concentrations occurred during dexamethasone treatment. CONCLUSION: MSA is significantly suppressed by cortisol treatment. As suppression of MSA is also observed during treatment with the pure glucocorticoid dexamethasone, suppressed MSA cannot be attributed to increased plasma volume or to changes in angiotensin II concentration. We conclude that cortisol-induced hypertension is not due to increased muscle sympathetic vasomotor drive.

Adult↗

PubMed1997

Encoding of object curvature by tactile afferents from human fingers.

Isolated responses were recorded from fibers in the median nerves of human subjects by using microneurography. Mechanoreceptive afferent fibers with receptive fields on the fingerpads were selected. The fingers were immobilized and spherical stimuli were applied passively to the receptive field with a contact force of 40-, 60-, or 80-g weight. The radii of the spheres were 1.92, 2.94, 5.81, or 12.4 mm or infinity (flat); the corresponding curvatures, given by the reciprocal of the radii, were 694, 340, 172, 80.6, or 0 m-1, respectively. When the spheres were applied to the receptive field center of slowly adapting type I afferents (SAIs), the response increased as the curvature of the sphere increased and also increased as the contact force increased. All SAIs behaved in the same way except for a scaling factor proportional to the sensitivity of the afferent. When a sphere was located at different positions in the receptive field, the shape of the resulting response profile reflected the shape of the sphere; for more curved spheres the profile was higher and narrower (increased peak and decreased width). Slowly adapting type II afferents (SAIIs) showed different response characteristics from the SAIs when spheres were applied to their receptive field centers. As the curvature of the stimulus increased from 80.6 to 172 m-1, the response increased. However, further increases in curvature did not result in further increases in response. An increase in contact force resulted in an increase in the response of SAIIs; this increase was proportionately greater than it was for SAIs. For SAIIs, the shape of the receptive field profile did not change when the curvature of the stimulus changed. For fast-adapting type I afferents (FAIs), the responses were small and did not change systematically with changes in curvature or contact force. Fast-adapting type II afferents (FAIIs) did not respond to our stimuli. Human SAIs, FAIs, and FAIIs behaved like monkey SAIs, FAIs, and FAIIs, respectively. The response of the SAI population contains accurate information about the shape of the sphere and its position of contact on the finger and also indicates contact force. Conversely, whereas SAIIs possess a greater capacity to encode changes in contact force, they provide only coarse information on local shape.

Adolescent↗

PubMed1996

The discharge behaviour of single sympathetic neurones supplying human sweat glands.

Firing properties of single sudomotor axons were studied via tungsten microelectrodes inserted percutaneously into cutaneous fascicles of the peroneal nerve in awake subjects. Sweating was induced by radiant heat and measured by changes in skin electrical resistance within the innervation territory on the dorsum of the foot. Eight units were classified as sudomotor neurones because spike-triggered averaging revealed a time-locked relationship between the unitary discharge and the subsequent decrease in skin resistance (1.12 +/- 0.05 s), but no relationship to skin blood flow (measured by a laser-doppler probe). Sudomotor units usually fired only one (maximum six) spike(s) in a sympathetic burst. The mean firing rate was 0.62 Hz, but instantaneous frequencies above 50 Hz could be generated. R-wave triggered histograms and coherence analysis revealed significant coupling between the firing of three sudomotor neurones and the ECG. Moreover, the firing of four sudomotor neurones showed a weak but significant correlation with the spontaneous fluctuations in cardiac interval, diastolic pressure, or the rate of fall in arterial pressure. We conclude that the discharge of human sudomotor neurones is modulated by baroreceptor input.

Adult↗

PubMed1996

The contribution of transcortical pathways to long-latency stretch and tactile reflexes in human hand muscles.

Long-latency electromyographic (EMG) responses can be evoked in the first dorsal interosseous muscle (FDI) by unexpected slips of an object (skin stretch) held between the index and thumb, or by forcible adduction of the metacarpophalangeal joint (muscle stretch). The former type of response is due to stimulation of tactile afferents in the skin of the digits, whereas the latter also activates muscle receptors. Previous studies have provided good evidence that long-latency reflex responses to stretch of distal muscles involve activity in a transcortical reflex pathway. The present experiments examined whether cutaneous reflexes also utilise a transcortical route. Transcranial magnetic or electrical stimuli were given over the motor cortex to evoke EMG activity during the period of the long-latency reflex response. When evoked by muscle stretch the responses to magnetic stimulation were facilitated more than those to electric stimulation. In contrast, facilitation was equal during the long-latency reflex elicited by cutaneous stimulation. Because of the different ways in which electrical and magnetic stimuli are believed to activate the motor cortex, we interpret these results to mean that the long-latency response to skin stretch is not mediated by a transcortical mechanism in the majority of subjects, whereas that following muscle stretch is. However, these are average data. In a few individual subjects, the opposite results were obtained. We suggest that there may be differences between subjects in the transcortical contribution to long-latency reflex responses. The implication is that, under normal circumstances, several pathways may contribute to these responses. If so, the relative roles of the pathways may change during different tasks, and in pathological states lesions in one system may well be accompanied by compensatory changes in other systems.

Adult↗

PubMed1996

Control of grip force during restraint of an object held between finger and thumb: responses of cutaneous afferents from the digits.

Unexpected pulling and pushing loads exerted by an object held with a precision grip evoke automatic and graded increases in the grip force (normal to the grip surfaces) that prevent escape of the object; unloading elicits a decrease in grip force. Anesthesia of the digital nerves has shown that these grip reactions depend on sensory signals from the digits. In the present study we assessed the capacity of tactile afferents from the digits to trigger and scale the evoked grip responses. Using tungsten microelectrodes inserted percutaneously into the median nerve of awake human subjects, unitary recordings were made from ten FA I and 13 FA II rapidly adapting afferents, and 12 SA I and 18 SA II slowly adapting afferents. While the subject held a manipulandum between a finger and the thumb, tangential load forces were applied to the receptor-bearing digit (index, middle, or ring finger or thumb) as trapezoidal load-force profiles with a plateau amplitude of 0.5-2.0 N and rates of loading and unloading at 2-8 N/s, or as "step-loads" of 0.5 N delivered at 32 N/s. Such load trials were delivered in both the distal (pulling) and proximal (pushing) direction. FA I afferents responded consistently to the load forces, being recruited during the loading and unloading phases. During the loading ramp the ensemble discharge of the FA I afferents reflected the first time-derivative of the load force (i.e., the load-force rate). These afferents were relatively insensitive to the subject's grip force responses. However, high static finger forces appeared to suppress excitation of these afferents during the unloading phase. The FA II afferents were largely insensitive to the load trials: only with the step-loads did some afferents respond. Both classes of SA afferents were sensitive to load force and grip force, and discharge rates were graded by the rate of loading. The firing of the SA I afferents appeared to be relatively more influenced by the subject's grip-force response than the discharge of the SA II afferents, which were more influenced by the load-force stimulus. The direction in which the tangential load force was applied to the skin influenced the firing of most afferents and in particular the SA II afferents. Individual afferents within each class (except for the FA IIs) responded to the loading ramp before the onset of the subject's grip response and may thus be responsible for initiating the automatic increase in grip force. However, nearly half of the FA I afferents recruited by the load trials responded to the loading phase early enough to trigger the subject's grip-force response, whereas only ca. one-fifth of the SA Is and SA IIs did so. These observations, together with the high density of FA I receptors in the digits, might place the FA I afferents in a unique position to convey the information required to initiate and scale the reactive grip-force responses to the imposed load forces.

Adolescent↗

PubMed1996

Control of grip force during restraint of an object held between finger and thumb: responses of muscle and joint afferents from the digits.

Pulling or pushing forces applied to an object gripped between finger and thumb excite tactile afferents in the digits in a manner awarding these afferents probable roles in triggering the reactive increases in grip force and in scaling the changes in grip force to the changes in applied load-force. In the present study we assessed the possible contributions from slowly adapting afferents supplying muscles involved in the generation of grip forces and from digital joint afferents. Impulses were recorded from single afferents via tungsten microelectrodes inserted percutaneously into the median or ulnar nerves of awake human subjects. The subject held a manipulandum with a precision grip between the receptor-related digit (index finger, middle finger, ring finger or thumb) and an opposing digit (thumb or index finger). Ramp-and-hold load forces of various amplitudes (0.5-2.0 N) and ramp rates (2-32 N/s) were delivered tangential to the parallel grip surfaces in both the distal (pulling) and the proximal (pushing) directions. Afferents from the long flexors of the digits (n = 19), regardless of their muscle-spindle or tendon-organ origin, did not respond to the load forces before the onset of the automatic grip response, even with the fastest ramp rates. Their peak discharge closely followed the peak rate of increase in grip force. During the hold phase of the load stimulus, the afferents sustained a tonic discharge. The discharge rates were significantly lower with proximally directed loads despite the mean grip-force being similar in the two directions. This disparity could be explained by the differing contributions of these muscles to the finger-tip forces necessary to restrain the manipulandum in the two directions. Most afferents from the short flexors of the digits (n = 17), including the lumbricals, dorsal interossei, opponens pollicis, and flexor pollicis brevis, did not respond at all, even with the fastest ramps. Furthermore, the ensemble pattern from the joint afferents (n = 6) revealed no significant encoding of changes in finger-tip forces before the onset of the increase in grip force. We conclude that mechanoreceptors in the flexors of the digits and in the interphalangeal joints cannot be awarded a significant role in triggering the automatic changes in grip force. Rather, their responses appeared to reflect the reactive forces generated by the muscles to restrain the object. Hence, it appears that tactile afferents of the skin in contact with the object are the only species of receptor in the hand capable of triggering and initially scaling an appropriate change in grip force in response to an imposed change in load force, but that muscle and joint afferents may provide information related to the reactive forces produced by the subject.

Adolescent↗

PubMed1996

Contractile properties of single motor units in human toe extensors assessed by intraneural motor axon stimulation.

1. Single motor axons innervating human toe extensor muscles were selectively stimulated through a tungsten microelectrode inserted percutaneously into the peroneal nerve. Twitch and tetanic forces were measured from a strain gauge over the proximal phalanx of the toe generating the greatest force. Twitch data were obtained from 19 single motor units in nine subjects: 8 motor units supplied extensor hallucis longus (EHL), 5 motor units supplied extensor digitorum longus (EDL), and 6 motor units supplied extensor digitorum brevis (EDB). Unpotentiated twitch forces ranged from 6.3 to 78.1 mN (20.0 +/- 4.0 mN, mean +/- SE), with the distribution highly skewed toward small forces. Twitch contraction and half-relaxation times were 74.8 +/- 3.9 and 78.6 +/- 6.0 ms, respectively. Compared with motor units in human thenar muscles, those in human toe extensor muscles were stronger but slower. However, as in thenar motor units, twitch force and contraction time were not related. 2. Force-frequency relationships were determined for 13 units (5 EDL, 5 EHL, 3 EDB) by stimulating each unit with short trains (1.0-5.0 s) of constant frequency (2-100 Hz). Peak force was related to stimulus frequency in a sigmoid fashion. The steep region of the curve extended from 5.5 +/- 0.7 (SE) Hz to 16.3 +/- 1.1 Hz for all units, and the stimulus frequency required to generate half-maximal force (9.6 +/- 0.6 Hz) was close to the center of the steep range. This frequency, which was inversely related to twitch contraction time, was lower than the frequency required to develop half-maximal force of human thenar motor units (12 +/- 4 Hz, mean +/- SD). The slopes of the regression lines relating force to frequency, computed over the steep range for each unit, were also lower for the toe extensors (3.7 +/- 0.7 mN/Hz) than for the thenar muscles (6 +/- 1 mN/Hz). 3. Maximal tetanic forces ranged from 29.9 to 188.1 mN (89.0 +/- 16.5 mN, mean +/- SE), and were generated at stimulus frequencies from 15 to 100 Hz (median 50 Hz). The stimulation frequency required for fused tetani (absence of noticeable force fluctuation) was generally less than that required for maximum tetanic force. The mean twitch-tetanus ratio, calculated for unpotentiated twitches, was 0.22 +/- 0.02 (range 0.15-0.41). This ratio was higher than for human thenar motor units (0.14 +/- 0.06, mean +/- SE). After twitch potentiation of 10 units, the mean twitch-tetanus ratio increased to 0.28 +/- 0.04. 4. The effects of preceding each stimulus train with a short interstimulus interval (10 ms) on force production at each frequency were examined in nine motor units. Peak forces at the onset of each contraction were higher when such an "initial doublet" preceded stimulus trains of < or = 20 Hz, but the mean force at the end of each stimulus train was not significantly affected at any frequency. 5. Eight units were stimulated with a train that increased in frequency continuously from 2 to 80 Hz, and then decreased symmetrically. This pattern resulted in peak forces that were higher on the descending limb of the stimulus train, the force-frequency relationship tracing a hysteresis loop. Hysteresis was exhibited because damping in the neuromuscular system causes the mechanical output of muscle to lag behind neural input. Thus, in non-steady-state conditions (as in most forms of natural activity), somewhat higher firing rates may be required to attain a particular level of force; once attained, force output will be transiently unresponsive to diminution of firing rate. 6. We conclude that there are differences in the contractile properties of single motor units in human toe extensor muscles (involved in posture and locomotion) and thenar muscles (involved in prehension and manipulation). Twitch-tetanus ratios were greater for motor units in the toe extensors, and this property accounted for the lower force sensitivity of these units to increases in frequency. (ABSTRACT TRUNCATED)

Adult↗

PubMed1995

Modulation of muscle sympathetic activity during spontaneous and artificial ventilation and apnoea in humans.

Respiratory modulation of muscle sympathetic activity was compared in relaxed subjects breathing spontaneously and in anaesthetized and non-anaesthetized subjects ventilated artificially with intermittent positive pressure. Muscle sympathetic activity was recorded directly from the peroneal nerve using the microneurographic technique. Arterial pressure was monitored continuously either by finger-pulse photoplethysmography (Finapres) or intraarterially. Respiratory modulation of sympathetic activity, heart rate and arterial pressure was measured by averaging consecutive breaths to the ECG R-wave closest to the onset of inspiration. In relaxed subjects (n = 15) breathing quietly the averaged sympathetic activity was greatest during late expiration and the first half of inspiration and minimal after the peak of inspiration, after correcting for delays within the baroreflex loop. Systolic and diastolic pressures fell during inspiration. In anaesthetized or awake subjects ventilated artificially at normal tidal volumes the pattern of respiratory modulation of sympathetic activity was preserved but the changes in arterial pressure were reversed and respiratory sinus arrhythmia abolished. Ventilation with positive end-expiratory pressure (20 cmH2O) increased the overall level of sympathetic activity and enhanced the breath-to-breath modulation. We conclude that, although baroreceptors provide potent modulation of muscle sympathetic activity in humans, the inspiratory inhibition of sympathetic activity does not depend on an increase in arterial pressure and hence an increase in baroreceptor input.

Adult↗

PubMed1995

Effects of static lung inflation on sympathetic activity in human muscle nerves at rest and during asphyxia.

Muscle sympathetic activity is inhibited during the second half of phasic lung inflation associated with normal (negative pressure) breathing or artificial ventilation with intermittent positive-pressure, and this inspiratory inhibition appears unrelated to the associated changes in arterial pressure. In this present study we tested the hypothesis that a static inflation of the lungs would cause a sustained inhibition of muscle sympathetic activity. Microneurographic techniques were used to record muscle sympathetic activity from the peroneal nerve, and arterial pressure was monitored continuously by finger-pulse photoplethysmography (Finapres). In nine subjects static lung inflation, brought about either actively or passively, caused a pronounced and sustained increase in sympathetic activity (not the predicted decrease) that could not be explained by changes in arterial pressure. When delivered at the end of a voluntary end-expiratory apnoea, static lung inflation caused an initial inhibition of the large chemoreceptor-induced sympathetic bursts and a subsequent excitation that was sustained for the duration of the lung inflation. These observations indicate that respiration can affect muscle sympathetic activity in humans in two opposing ways: inhibition during phasic increases in lung volume, and excitation during large static increases in lung volume. Neither phenomenon depends on changes in arterial pressure, and hence influences of carotid arterial and aortic (high-pressure) baroreceptors can be excluded. We suggest that the initial inhibition is evoked from lung or chest-wall receptors and the static exitation from unloading of cardiopulmonary (low pressure) baroreceptors.

Adult↗

PubMed1995

The fusimotor system. Its role in fatigue.

Several lines of evidence point to an important role of the fusimotor system in the "muscle-wisdom" phenomenon during peripheral fatigue of some human voluntary contractions: 1) muscle afferents provide a net amplification of skeletomotor output, with the only known afferent species capable of this being the muscle spindle; 2) muscle spindle firing rates decline during constant-force voluntary contractions, so fusimotor support to skeletomotor output decreases; 3) this waning support can be offset by application of high-frequency vibration to the fatiguing muscle, which excites spindle endings; and 4) the progressive decline in motor unit firing rates during maximal voluntary contractions is abolished by blocking muscle afferent inputs, and it is argued that, at least in the initial stages of a contraction, this must be due to a progressive withdrawal of spindle support.

Efferent Pathways↗

PubMed1994

The discharge behaviour of single vasoconstrictor motoneurones in human muscle nerves.

1. The discharge behaviour of fourteen single sympathetic vasoconstrictor efferents was studied using a tungsten microelectrode inserted percutaneously into a motor fascicle of the radial or peroneal nerve in eight awake supine subjects. Units were classified as vasoconstrictor because their firing properties correlated appropriately to changes in cardiac interval and arterial pressure. 2. On average, individual vasoconstrictor units discharged in only 21% of heart beats, with an overall mean frequency of 0.47 Hz. Usually only one spike was generated per cardiac cycle. Calculated from cardiac cycles in which a unit fired from two to seven spikes, the mean within-burst firing rate was 18.8 +/- 2.5 Hz (mean +/- S.E.M.); but instantaneous frequencies above 50 Hz were occasionally observed. 3. Measured from a defined R-wave of the ECG, the spike onset latency varied over 358 +/- 33 ms, suggesting considerable variation of synaptic delays in the baroreflex arc. This latency had a relatively uniform temporal relationship with the burst onset or peak latency, compatible with a fixed recruitment order of individual sympathetic neurones. 4. In view of the low average firing rate of individual units we suggest that the variable instantaneous firing rates may optimize the contractile responses of vascular smooth muscle.

Adult↗

PubMed1994

Electrical signs of cortical involvement in the automatic control of grip force.

Evoked potentials were recorded in 10 subjects to assess cortical involvement in automatic control of grip force during restraint of a manipulandum held between finger and thumb. Brisk pulling loads elicited an increase in first dorsal interosseous EMG after 60.6 +/- 2.4 ms. Preceding this response were several time-locked scalp potentials, the most significant being a widespread negativity that appeared first over the frontal cortex and peaked 19.5 +/- 1.8 ms before the EMG peak, and a positivity that followed the EMG by 24.3 +/- 5.4 ms. The slope of the negativity and the amplitude of the positivity were greater than during passive conditions, suggesting that these potentials reflect cortical processes associated with automatic regulation.

Adolescent↗

PubMed1993

Motoneuronal output and gradation of effort in attempts to contract acutely paralysed leg muscles in man.

1. The study was designed to determine the degree to which normal subjects can control motoneurones innervating a leg muscle when acutely deprived of muscle afferent feedback. Microneurographic recordings were made from eighteen motor fascicles in the common peroneal nerve, of which thirteen innervated tibialis anterior and five toe dorsiflexor muscles. The nerve was then blocked completely at a distal site near the fibular head with local anaesthetic. A sequence of tests was performed with each fascicle to determine the degree to which the subject could control the motoneuronal drive to the paralysed muscle. 2. During a complete distal block of the common peroneal nerve, motoneurones innervating tibialis anterior were frequently activated during weak attempted contraction of the synergist toe extensors and vice versa. 3. When subjects attempted contractions of the paralysed muscles at a constant effort, pressure applied to the dorsum of the foot caused relatively small changes in the level of neural output, producing a small increase in motoneuronal drive to tibialis anterior, but no consistent change in the drive to toe extensor fascicles. 4. Subjects were able to increase the motoneuronal drive to the paralysed tibialis anterior in five steps of effort each lasting 10 s. The level of motor output increased linearly with step number, but declined as the step was maintained, more so when auditory feedback was withdrawn. 5. There was hysteresis in the relationship between motoneuronal output and force (measured on the contralateral side) during attempts to make slowly increasing then decreasing ramps of effort on both sides over 20-120 s. Motor drive to the paralysed muscle increased disproportionately rapidly compared with contralateral force when subjects attempted bilaterally symmetrical increasing efforts. 6. Subjects attempted to activate the paralysed muscle group maximally for 20-30 s with auditory feedback of the neurogram and verbal encouragement. There was a small statistically significant reduction in the motoneuronal output 5-10 s into the 30 s effort but, with further encouragement, it recovered towards the end of the effort. 7. When compared directly in the same recording sequences, attempts to make rapid brief maximal efforts (2-3 s duration) produced the same motoneuronal output as attempts to make sustained efforts. 8. Similar results occurred when the motoneuronal output to tibialis anterior was recorded during a selective distal block of tibialis anterior sparing toe dorsiflexors.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1993

The firing rates of human motoneurones voluntarily activated in the absence of muscle afferent feedback.

1. To quantify the net influence of muscle afferent feedback on the firing rates of human motoneurones, the discharge frequencies of single motor axons in the common peroneal nerve were recorded during sustained voluntary efforts performed in the absence of feedback from the target muscle. These data were compared with the firing rates of single motor units in the intact tibialis anterior muscle. In five subjects, recordings were made from fifty-two motor axons innervating tibialis anterior during acute deafferentation and paralysis of the dorsiflexor muscles produced by anaesthetic block of the nerve distal to the recording site. 2. Maximal sustainable firing rates were determined for twenty-four motoneurons, twelve of which were classified as relatively low threshold (estimated recruitment level < or = 10% maximal) and six as high threshold. Mean firing rates of the low-threshold motoneurones (21.7 +/- 2.7 Hz; +/- S.E.M.) were significantly higher than those of the high-threshold motoneurones (14.0 +/- 4.4 Hz). The mean firing rate of the twenty-four deafferented motoneurones during maximal efforts to contract the paralysed muscle was 18.6 +/- 1.9 Hz, significantly lower than the maximal firing rates of single motor units recorded from the normally innervated tibialis anterior muscle (28.2 +/- 0.6 Hz). 3. During half-maximal efforts, the mean firing rate of eight deafferented motoneurones (10.8 +/- 1.1 Hz) was significantly lower than that of intact motor units (16.5 +/- 0.2 Hz). A similar finding was apparent during minimal efforts; the mean discharge frequency of seven deafferented motoneurones during weak voluntary efforts was 6.0 +/- 0.9 Hz, compared with 7.3 +/- 0.13 Hz for intact motor units. Overall, the range of motoneurone firing rates (from minimal to maximal levels of voluntary effort) was significantly affected by the acute deafferentation, but was shifted significantly to lower rates. 4. During sustained maximal voluntary efforts of at least 30 s duration the firing rate of deafferented motoneurones decreased over the first 5 s but was then maintained, i.e. there was no progressive decline as occurs with normally innervated motor units during fatiguing contractions. This observation supports a reflex origin for the normal decline in motoneurone discharge. 5. It is concluded that muscle afferents in the common peroneal nerve provide a net facilitation to the tibialis anterior motoneurone pool, reflexly increasing the motor output at all levels of voluntary drive by approximately one-third.

Action Potentials↗