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Amplitude of the human soleus H reflex during walking and running.

1. The objective of the study was to investigate the amplitude and modulation of the human soleus Hoffmann (H) reflex during walking and during running at different speeds. 2. EMGs were recorded with surface electrodes from the soleus, the medial and lateral head of the gastrocnemius, the vastus lateralis and the anterior tibial muscles. The EMGs and the soleus H reflex were recorded while walking on a treadmill at 4.5 km h-1 and during running at 8, 12 and 15 km h-1. 3. The amplitudes of the M wave and the H reflex were normalized to the amplitude of a maximal M wave elicited by a supramaximal stimulus just after the H reflex to compensate for movements of the recording and stimulus electrodes relative to the nerve and muscle fibres. The stimulus intensity was set to produce M waves that had an amplitude near to 25 % of the maximal M wave measured during the movements. As an alternative, the method of averaging of sweeps in sixteen intervals of the gait cycle was applied to the data. In this case the amplitude of the H reflex was expressed relative to the maximal M wave measured whilst in the standing position. 4. The amplitude of the H reflex was modulated during the gait cycle at all speeds. During the stance phase the reflex was facilitated and during the swing and flight phases it was suppressed. The size of the maximal M wave varied during the gait cycle and this variation was consistent for each subject although different among subjects. 5. The peak amplitude of the H reflex increased significantly (P = 0.04) from walking at 4.5 km h-1 to running at 12 and 15 km h-1 when using the method of correcting for variations of the maximal M wave during the gait cycle. The sweep averaging method showed a small but non-significant decrease (P = 0. 3) from walking to running at 8 km h-1 and a small decrease with running speed (P = 0.3). The amplitude of the EMG increased from walking to running and with running speed. 6. The relatively large H reflex recorded during the stance phase in running indicates that the stretch reflex may influence the muscle mechanics during the stance phase by contributing to the motor output and enhancing muscle stiffness.

Adult↗

The mammalian exercise pressor reflex in health and disease.

The exercise pressor reflex (a peripheral neural reflex originating in skeletal muscle) contributes significantly to the regulation of the cardiovascular system during exercise. Exercise-induced signals that comprise the afferent arm of the reflex are generated by activation of mechanically (muscle mechanoreflex) and chemically sensitive (muscle metaboreflex) skeletal muscle receptors. Activation of these receptors and their associated afferent fibres reflexively adjusts sympathetic and parasympathetic nerve activity during exercise. In heart failure, the cardiovascular response to exercise is augmented. Owing to the peripheral skeletal myopathy that develops in heart failure (e.g. muscle atrophy, decreased peripheral blood flow, fibre-type transformation and reduced oxidative capacity), the exercise pressor reflex has been implicated as a possible mechanism by which the cardiovascular response to physical activity is exaggerated in this disease. Accumulating evidence supports this conclusion. This review therefore focuses on the role of the exercise pressor reflex in regulating the cardiovascular system during exercise in both health and disease. Updates on our current understanding of the exercise pressor reflex neural pathway as well as experimental models used to study this reflex are presented. In addition, special emphasis is placed on the changes in exercise pressor reflex activity that develop in heart failure, including the contributions of the muscle mechanoreflex and metaboreflex to this pressor reflex dysfunction.

Afferent Pathways↗

Neurones in commissural nucleus tractus solitarii required for full expression of the pulmonary C fibre reflex in rat.

1. The pulmonary C fibre reflex, triggered by activating pulmonary C fibre endings in the lung, consists of rapid shallow breathing (which may be preceded by apnoea), bradycardia, and hypotension. The purpose of this work was to identify proximal synapses in this reflex. From pilot data, we hypothesized that neurones in a discrete region of the commissural nucleus in the nucleus tractus solitarii (NTS) are required for full expression of the pulmonary C fibre reflex. Studies were carried out in urethane-anaesthetized, unilaterally vagotomized, spontaneously breathing rats, in which diaphragm electromyogram, arterial pressure, and blood gases were measured. Phenyldiguanide (PDG) was injected in the right atrium to elicit the pulmonary C fibre reflex. Unilateral NTS injections were made through multibarrelled pipettes containing DL-homocysteic acid (DLH) to mimic the reflex, cobalt chloride to reversibly impair the reflex, and/or dye to mark the injection sites. 2. PDG (5-16 micrograms kg-1) injected in the right atrium of twenty-six rats produced the classic pulmonary C fibre reflex: a vagally mediated, rapid onset of rapid shallow breathing, bradycardia and hypotension. 3. Injection of DLH (3-12 nl of 20 mM for a total of 60-240 pmol) in the dorsomedial aspect of the commissural nucleus of the NTS in thirty rats mimicked the pulmonary C fibre reflex, producing rapid shallow breathing, hypotension, and a slight bradycardia. 4. Interruption of neuronal transmission by injecting cobalt chloride (15-30 nl of 100 mM) in the site where DLH produced rapid shallow breathing, reversibly impaired the rapid shallow breathing and bradycardia produced by right atrial injections of PDG in fifteen rats. The commissural region where DLH produced rapid shallow breathing and cobalt impaired the pulmonary C fibre reflex extended from 720-1100 microns caudal to the obex, 30-200 microns lateral to mid-line, and 200-600 microns ventral to the dorsal surface of the brain stem within the NTS. 5. Taken together, the results suggest that neurones within a discrete region in the dorsomedial commissural nucleus in caudal NTS are required for full expression of the pulmonary C fibre reflex.

Animals↗

Interaction between short- and long-latency components of the human stretch reflex during sinusoidal stretching.

1. Using wrist muscles, the subdivision of the human stretch reflex into separate components was examined with small amplitude sinusoidal stretching of relatively high frequency (10-40 Hz). The reflex was evoked by angular rotation of the wrist (below 1 deg amplitude), applied via the hand during maintained voluntary contraction of the muscle studied; both flexors and extensors were tested. 2. The reflex response was recorded electromyographically rather than mechanically. For each condition, the surface EMG was rectified and averaged to give a cycle average showing the mean response evoked by a cycle of stretching. The cycle average was fitted with a sinusoid, the amplitude and phase of which were used to assess the reflex; their value reflects the combined action of its various sub-components. Fourier analysis gave similar results (the EMG was then rectified but not averaged). 3. The amplitude of the reflex response typically fell to a minimum in the region of 20-25 Hz. The phase lag of the response in relation to the stimulus increased approximately linearly with frequency, except in the region of the amplitude minimum. Here the lag tended to remain constant, or to decrease slightly; this created a discontinuity between the upper and lower limbs of the phase plot. 4. Such effects are attributed to an interaction between two components of the reflex that differ in latency by 20-25 ms. These would progressively change their relative phase as the frequency increased. At first they would come to interfere with each other, but then the more delayed reflex produced by a given cycle of stretching would begin to sum with the shorter latency reflex evoked by the next stretch. 5. At high and low frequencies the cycle averages were normally well fitted by a single sinusoid. Around 20-25 Hz, however, they typically showed appreciable harmonic distortion, with the second harmonic larger than the fundamental. The cycle average then showed two separate responses per cycle of stretching. These were considered to represent the uncancelled non-linear residua of separate components of the reflex response. Their relative timing shifted appropriately with change of frequency. 6. These 'double responses' are unlikely to be due to mechanical resonance. First, the relative sizes of the two components could be altered by the reflex action of cutaneous afferents. Second, the same pattern of behaviour was found when the mechanical stimuli were applied directly to the tendon of flexor carpi radialis while the hand remained fixed.(ABSTRACT TRUNCATED AT 400 WORDS)

Electromyography↗

Cutaneous reflexes evoked during human walking are reduced when self-induced.

Reflex responses are often less pronounced when they are self-induced, but this question has barely been investigated quantitatively. The issue is particularly relevant for locomotion since it has been shown that reflexes elicited during normal gait are important for the regulation of locomotion. The cortex is thought to be involved in the control of reflexes during gait, but it is unclear whether it plays a role in the modulation of these reflexes during the step cycle. During gait, weak electrical stimulation of the sural nerve elicits reflexes in various leg muscles. Are these reflexes different when subjects themselves trigger the stimuli instead of being randomly released by the computer? Cutaneous reflexes were elicited by sural nerve stimulation in 16 phases of the gait cycle in healthy subjects. The stimuli were triggered either by computer or by the subjects themselves. In 6 out of 7 subjects it was observed that the facilitatory responses in leg muscles were smaller and the suppressive responses were more suppressive following self-generated stimuli. In some muscles such as tibialis anterior (TA) both effects were seen (reduced facilitation at end stance and exaggerated suppression at end swing). In all subjects the modulation of anticipatory influences was muscle specific. In the main group of six subjects, the mean reduction in reflex responses was strongest in the TA (max. 30.7%; mean over 16 phases was 12.5%) and weakest in peroneus longus (PL, max. 10.1%; mean over 16 phases was 2.6%). The observation that facilitation is reduced and suppression enhanced in several muscles is taken as evidence that anticipation of self-induced reflex responses reduces the excitatory drive to motoneurones, for example through presynaptic inhibition of facilitatory reflex pathways.

Adult↗

Identification of static and dynamic components of reflex sensitivity in spastic elbow flexors using a muscle activation model.

Static and dynamic components of the stretch reflex were studied in elbow flexors of 13 hemiparetic brain-injured individuals. Constant-velocity joint rotations were applied to the elbow, and the resulting stretch reflex torque and electromyographic responses were recorded in the biceps brachii and brachioradialis muscles. Ten elbow extension velocities between 6 and 150 deg s(-1) were applied in random order. The resulting reflex torque response was plotted as a function of elbow angle and fitted with a mathematical model designed to depict elbow flexor activation. We found that four of the six model parameters were essentially independent of test velocity. Conversely, 73% (19/26) of cases involving the other two model parameters were dependent on velocity of joint extension (p<0.05). We conclude from these results that four of the model parameters reflect the static reflex response while the two remaining velocity-dependent parameters reflect the dynamic reflex response. To describe overall velocity dependence of stretch reflexes in spastic elbow muscles, the two dynamic reflex parameters were fitted to a fractional exponential function of velocity, similar to a model previously used to describe spindle firing rate in the cat hindlimb. We found that the mean velocity exponent of the dynamic reflex parameters was 0.24 + 0.17 (s.d.) (N = 13), a value similar to that for muscle spindle velocity sensitivity in reduced animal preparations. We conclude that both static and dynamic reflex sensitivities can be measured by examining different aspects of the torque/angle relation associated with the reflex response to a large-amplitude ramp stretch of the elbow.

Adult↗

The behaviour of the long-latency stretch reflex in patients with Parkinson's disease.

The size of the long-latency stretch reflex was measured in a proximal (triceps) and distal (flexor pollicis longus) muscle in 47 patients with Parkinson's disease, and was compared with that seen in a group of 12 age-matched normal control subjects. The patients were classified clinically into four groups according to the degree of rigidity at the elbow or tremor. Stretch reflexes were evaluated while the subject was exerting a small force against a constant preload supplied by a torque motor, and the size of the reflex response was measured as fractional increase over basal levels of activity. When stretches were given at random intervals by increasing the force exerted by the motor by a factor of 2 or 3, there was a clear trend for the more severely affected patients to have larger long latency responses in the triceps muscle, although there was no change in the size of the short-latency, spinal component of the response. In contrast, there was no change in the size of the long-latency response of the flexor pollicis longus in any group of patients with Parkinson's disease. Despite any differences in reflex size, the inherent muscle stiffness of both muscles appeared to be normal in all groups of patients with Parkinson's disease, since the displacement trajectory of the limb following the force increase was the same as control values in the short (25 ms) period before reflex compensation could intervene. In 20 of the patients and in seven of the control subjects, servo-controlled, ramp positional disturbances were given to the thumb. Up to a velocity of 300°/s, the size of the long-latency stretch reflex was proportional to the log velocity of stretch. This technique revealed, in both moderately and severely rigid patients, increases in the reflex sensitivity of the flexor pollicis longus, which had not been clear using step torque stretches alone. However, whether using ramp or step displacements, long latency stretch reflex gain was not closely related to rigidity; reflex size was within the normal range in many patients with severe rigidity. Enhanced long latency stretch reflexes thus contribute to, but may not be solely responsible for, rigidity in Parkinson's disease.

Electromyography↗

Catching a ball: contributions of intrinsic muscle stiffness, reflexes, and higher order responses.

In three sets of experiments in nine normal subjects and a patient with a percutaneous wrist-stabilizing splint, we quantified the open-loop gain (OLG) of the stretch reflex acting about the elbow. The subjects exerted a steady mean flexing force and were instructed not to intervene (i.e., not to resist actively) when force or displacement perturbations were imposed on the forearm. The method was either to reconstruct transmission around the entire loop in a two-part experiment, or to use the attenuation of external perturbations in normal and electrically stimulated muscle to compute gain. Across all experiments, the mean magnitude of stretch reflex OLG was close to unity in the frequency range 1-2 Hz, and declined at higher frequencies, as required to ensure stability, given that the phase lag approached 180 degrees at 5 Hz. Inherent muscle stiffness was approximately equal to reflex stiffness. In functional terms, an OLG of 1 means that the yield caused by a force perturbation is approximately halved by reflex action (prevailing inherent muscle stiffness is doubled). Automatic scaling of reflex transmission at Ia/alpha-motoneuronal synapses ensures that the OLG remains close to unity as inherent stiffness increases. Trials in the patient with the wrist fixator gave similar results, indicating that the reflexes were proprioceptive ly mediated. In a fourth experiment in which the task was to catch a heavy ball, we compared the efficacy of inherent muscle stiffness and reflexes alone, with the subject's intentional reactions, which included predictive and voluntary components of response. The latter were far more effective in maintaining the position of the hand after the ball was caught than inherent and reflex stiffnesses alone. We conclude that stability requirements limit the extent to which stretch reflexes can augment inherent muscle stiffness. When inherent muscle stiffness is low, such as in our ball-catching task, the reflex stiffness is also low, and predictive and pre-programmed reactions predominate in load compensation, thus shifting the emphasis from automatic servo or equilibrium-point behaviour to higher order control.

Elbow Joint↗

Pressor reflex evoked by muscular contraction: contributions by neuraxis levels.

The pressor reflex evoked by muscular contraction (exercise pressor reflex) is one important model of cardiovascular adjustments during static exercise. The central nervous system (CNS) structures mediating this reflex have remained largely obscure. Therefore, we examined the contribution of selected levels of the neuraxis in mediating the pressor reflex evoked by muscular contraction from stimulation of ventral roots. Decerebrate cats exhibited larger pressor reflexes than those found in intact alpha-chloralose-anesthetized cats, a difference more apparent at low (5 Hz or repeated twitch) rather than at high (50 Hz or tetanic) stimulus frequencies. Although a depressor response to 5-Hz stimulation was observed in the intact anesthetized cats, it appeared to be primarily due to anesthetic level, since a depressor response was not observed in decerebrate animals (nonanesthetized). Cerebellectomy produced no changes in the reflexes of the decerebrate animal. Further transection of the neuraxis (caudal to the midcollicular level) attenuated the exercise pressor reflex. The spinal cat demonstrated slight evidence of exercise pressor reflex activity. These results provide clarification as to representation of this pressor reflex within the CNS and establish the reflex's characteristics at several levels of neuraxis integration.

Anesthesia↗

Respiratory reflex responses to stimulation of tracheal mucosa in enflurane-anesthetized humans.

We investigated respiratory reflex responses to tracheal mucosa stimulation induced by injection of distilled water in 13 female patients under three different depths of enflurane anesthesia (0.7, 1.0, and 1.3 minimum alveolar concentration). Detailed analysis of the types of reflex responses revealed that there are at least six different responses: 1) the apneic reflex, 2) the expiration reflex, 3) spasmodic, panting breathing, 4) the cough reflex, 5) slowing of breathing, and 6) rapid, shallow breathing. Among these reflex responses, the cough reflex was the most sensitive and the apneic reflex followed by slowing of breathing was the most resistant to deepening anesthesia, whereas the sensitivity of other types of reflex responses was in between. Our results indicate that the types of respiratory reflex responses to tracheal mucosa stimulation are associated with depths of anesthesia and that the differences in sensitivity to anesthesia may be a valuable sign in clinical assessment of depth of anesthesia.

Adult↗

Influence of CPAP on reflex responses to tracheal irritation in anesthetized humans.

We investigated the effects of lung inflation during continuous positive airway pressure breathing (CPAP) on airway defensive reflexes in 10 enflurane-anesthetized spontaneously breathing humans. The airway defensive reflexes were induced by instillation into the trachea of 0.5 ml of distilled water at two different levels of end-expiratory pressure (0 and 10 cmH2O CPAP). The tracheal irritation at an end-expiratory pressure of 0 cmH2O caused a variety of reflex responses including apnea, spasmodic panting, expiration reflex, cough reflex, an increase in heart rate, and an increase in blood pressure. Lung inflation during CPAP of 10 cmH2O did not exert any influence on these reflex responses in terms of the types, latencies, and durations of reflex responses although the intensity of the expiration reflex and cough reflex was augmented by lung inflation. Our results suggest that the pulmonary stretch receptors do not play an important role in the mechanisms of airway defensive reflexes in humans.

Adult↗

Hering-Breuer reflex in conscious newborn rats: effects of changes in ambient temperature during hypoxia.

In a previous study in conscious normoxic newborn rats, we found that the strength of the Hering-Breuer reflex (HB reflex) was greater (188%) at high (36 degrees C) than at low (24 degrees C) ambient temperature (T(a); D. Merazzi and J. P. Mortola. Pediatr. Res. 45: 370-376, 1999). We now asked what the effect would be of changes in T(a) during hypoxia. Rat pups at 3-4 days of age were studied in a double-chamber airflow plethysmograph. The HB reflex was induced by negative body surface pressures of 5 or 10 cmH(2)O and quantified from the inhibition of breathing during maintained lung inflation. Rats were first studied at T(a) = 32 degrees C in normoxia, followed by hypoxia (10% O(2) breathing). During hypoxia, oxygen consumption (VO(2)) averaged 47%, and HB reflex 115%, of the corresponding normoxic values, confirming that in the newborn, differently from the adult, hypoxia does not decrease the strength of the HB reflex. As hypoxia was maintained, lowering T(a) to 24 degrees C or increasing it to 36 degrees C, on average, had no significant effects on VO(2) and the HB reflex. However, with 5-cmH(2)O inflations, the HB reflex during the combined hypoxia and hyperthermia was significantly stronger than in normoxia. We conclude that in conscious newborn rats during normoxia the T(a) sensitivity of the HB reflex is largely mediated by the effects of T(a) on thermogenesis and VO(2); in hypoxia, because thermogenesis is depressed and VO(2) varies little with T(a), the HB reflex is T(a) independent. The observation that the reflex response to lung inflations during hypoxic hyperthermia can be greater than in normoxia may be of importance in the pathophysiology of apneas during the neonatal period.

Animals↗

Spastic long-lasting reflexes in the awake rat after sacral spinal cord injury.

Following chronic sacral spinal cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of the present paper was to characterize the long-lasting reflex seen in tail muscles in response to electrical stimulation of the tail nerves in the awake spastic rat, including its development with time and relation to spasticity. Before and after sacral spinal transection, surface electrodes were placed on the tail for electrical stimulation of the caudal nerve trunk (mixed nerve) and for recording EMG from segmental tail muscles. In normal and acute spinal rats caudal nerve trunk stimulation evoked little or no EMG reflex. By 2 wk after injury, the same stimulation evoked long-lasting reflexes that were 1) very low threshold, 2) evoked from rest without prior EMG activity, 3) of polysynaptic latency with >6 ms central delay, 4) about 2 s long, and 5) enhanced by repeated stimulation (windup). These reflexes produced powerful whole tail contractions (spasms) and developed gradually over the weeks after the injury (< or =52 wk tested), in close parallel to the development of spasticity. Pure low-threshold cutaneous stimulation, from electrical stimulation of the tip of the tail, also evoked long-lasting spastic reflexes, not seen in acute spinal or normal rats. In acute spinal rats a strong C-fiber stimulation of the tip of the tail (20 x T) could evoke a weak EMG response lasting about 1 s. Interestingly, when this C-fiber stimulation was used as a conditioning stimulation to depolarize the motoneuron pool in acute spinal rats, a subsequent low-threshold stimulation of the caudal nerve trunk evoked a 300-500 ms long reflex, similar to the onset of the long-lasting reflex in chronic spinal rats. A similar conditioned reflex was not seen in normal rats. Thus there is an unusually long low-threshold polysynaptic input to the motoneurons (pEPSP) that is normally inhibited by descending control. This pEPSP is released from inhibition immediately after injury but does not produce a long-lasting reflex because of a lack of motoneuron excitability. With chronic injury the motoneuron excitability is increased markedly, and the pEPSP then triggers sustained motoneuron discharges associated with long-lasting reflexes and muscle spasms.

Anesthesia↗

Firing patterns of human flexor carpi radialis motor units during the stretch reflex.

Single motor unit and gross surface electromyographic responses to torque motor-produced wrist extensions were studied in human flexor carpi radialis muscle. Surface EMG typically showed two "periods" of reflex activity, at a short and long latency following stretch, but both periods occurring before a subject's voluntary reaction to the stretch. The amplitude of EMG activity in both reflex periods increased monotonically with an increase in the torque load. The amplitude of the short-latency reflex response was very dependent on the motoneuron pool excitability, or preload. The amplitude of the long-latency reflex response also varied with the preload, but could, in addition, be modulated by the subject's preparatory set for a voluntary response to the imposed displacement. When a single motor unit that was not tonically active began to fire during the stretch reflex, it did so primarily during the long-latency period. When caused to fire repetitively by voluntary facilitation of the motoneuron pool, that same unit now showed activity during both periods of the stretch reflex. Further increases in either motoneuron pool facilitation or in perturbation strength resulted in a monotonic increase in response probability of a single motor unit during the short-latency period. However, the response probability of a single unit during the long-latency reflex period did not always vary in a monotonic way with increases in either torque load or motoneuron pool facilitation. For an additional series of experiments, the subject was instructed on how to respond voluntarily to the upcoming wrist perturbation. The three instructions to the subject had no effect on the response probability of a single motor unit during either the background or short-latency periods of the stretch reflex. However, prior instruction clearly affected a unit's response probability during the long-latency reflex period. Changes in the firing rate of motor units, and in the recruitment or derecruitment of nontonic units, contributed to this modulation of reflex activity during the long-latency period.

Adult↗

Analysis of short-latency reflexes in human elbow flexor muscles.

1. A motor and digital controller have been developed to apply rapid stretches to the human elbow joint. The digital controller returns the forearm to the initial position before the reflex contraction. Thus short-latency reflex responses can be cleanly separated in time from the mechanical effects of the stretch under a wide variety of loading conditions. 2. The reflex force varies linearly with the velocity of stretch over nearly 2 orders of magnitude. The reflex force also varies linearly with the tonic level of force over the entire range of forces studied (0-100 N). This contrasts sharply with, for example, the human ankle joint, which shows a very limited linear range. 3. As the digital controller is made more compliant (less stiff), reflex shortening increases dramatically and becomes more prolonged, whereas the reflex force becomes somewhat smaller and shorter. With compliant loads and the brief stretches we applied, the reflex shortening is approximately equal to the stretch that generated it. 4. Simulations of the results confirm that the dependence of reflex shortening and force on the stiffness of the load is mainly determined by the mechanics of the limb and muscles. The simulations also indicate that 1) the gain of the reflex is as high as it can be without causing instability and 2) the presence of a rectification nonlinearity (e.g., lengthening the muscle produces a reflex, but shortening the muscle does not) is mainly responsible for preserving the stability of the elbow system.

Adult↗

Inhibition of canine H reflexes during locomotor-like rotation about the knee arises from muscle mechanoreceptors in quadriceps.

1. H reflexes were elicited in the small muscles of the foot in the canine and human during passive locomotor-like rotation of the shank about the ipsilateral knee. The movement-induced effect was similar in the two species. In the anesthetized dog, the reflex gain was reduced by 36 +/- 8.4% (mean +/- SE) on average, compared with appropriate stationary controls. Reflexes in the human were reduced during movement to 45 +/- 3.5% of their stationary control values. 2. H reflexes were elicited in the anesthetized dog during passive locomotor-like rotation about the knee and were compared with reflexes obtained with the limb stationary. Populations of mechanoreceptors were then systematically removed to ascertain which group or groups provided the sensory input that leads to the decrease in reflex gain during movement. We hypothesized that the majority of the reflex attenuation could be attributed to muscle mechanoreceptors. 3. Reflexes continued to be significantly reduced (P < 0.05) during passive movement about the knee until the muscle mechanoreceptors of the quadriceps muscle group were deactivated. The removal of input from joint receptors or cutaneous receptors did not eliminate the gain reduction induced by the passive movement. 4. It is concluded that muscle mechanoreceptors of the quadriceps muscle group provide an inhibitory input to the H reflex pathway of the dog plantar muscle when the knee is passively moved in a locomotor-like fashion. This source of inhibition likely also contributes to the soleus H reflex gain reduction in humans.

Animals↗

Effect of temperature on the normal and adapted vestibulo-ocular reflex in the goldfish.

1. The vestibulo-ocular reflex, a sensorimotor process, operates in a similar manner for homeothermic (mammals) and poikilothermic (fish) animals. However, individual physiological, biochemical, and/or pharmacological thermolabile processes that underlie the operation of this reflex could alter the operation of this reflex in a poikilotherm. The object of this study was to determine what aspects of the vestibulo-ocular reflex are affected by temperature changes naturally experienced by a poikilothermic animal, the goldfish. 2. Experiments were conducted on the visuovestibulo-(Vis-VOR) and vestibulo-ocular reflex (VOR) during normal operation as well as during the acquisition (learning) and retention (memory) phases of adaptive gain change. These studies were carried out at temperatures to which goldfish had been acclimated over several weeks and after rapid (< 5 min) shifts from this acclimation temperature. 3. Normal sinusoidal Vis-VOR and VOR gains before adaptation were found to be independent of the acclimation temperature over a wide range. Acute temperature changes of up to 10 degrees C either above or below a 20 degrees C acclimation temperature (Ac degree C = 20 degrees C) did not significantly modify normal visual and/or vestibular oculomotor reflex gains. 4. Surprisingly, slight reductions in temperature, as small as 2.5 degrees C, noticeably reduced Vis-VOR and VOR gain adaptations. Both short (3 h) and intermediate (up to 48 h) term reflex modifications were affected. Loss of adaptation was observed 10 degrees C below the acclimation temperature (Ac - 10 degrees C); however, return to the original temperature immediately restored most (60-100%) of the previously acquired Vis-VOR and VOR gain changes. In contrast, elevation of temperature up to 10 degrees C above the acclimation temperature (Ac + 10 degrees C) did not alter either increases or decreases in the adapted Vis-VOR or VOR gain. 5. A decrease in temperature reduced the magnitude of an adapted VOR gain increase and elevated the magnitude of an adapted gain decrease, thus returning the VOR gain back toward its normal control gain before adaptation. Because both increases and decreases in VOR gain were affected by the same temperature reduction, the cold effect was not a generalized reflex suppression, but inactivation of a process responsible for maintaining VOR adaptation. 6. During the acquisition phase, the time course and magnitude of adaptive VOR gain increases at temperatures acutely set 8-10 degrees C below the acclimation temperature were similar to those obtained at the acclimation temperature. Because the same temperature decrease inactivated retention of adapted VOR gain changes, the neuronal processes underlying the acquisition and the retention phases of Vis-VOR or VOR adaptation are suggested to differ qualitatively. 7. With the use of velocity step stimuli, both the adapted dynamic (< 100 ms) and sustained (> 100 ms) components of VOR adaptation were reduced by cooling. This effect on the dynamic component demonstrates an alteration in the shortest latency pathway through the vestibular nucleus and indicates that one thermosensitive site resides in the brain stem. 8. These results also show that, over a wide range of temperatures (20 +/- 10 degrees C), the neuronal processing that is responsible for the normal operation of the visuovestibulo- and/or vestibulo-ocular reflex and for the retention of reflex adaptation functions by separate physiological processes within the same brain stem and cerebellar circuitry. 9. We conclude that temperature exhibits a unique, and unexpected, state-dependent effect on sensorimotor regulation and adaptation for periods up to 48 h. Temperature does not alter normal VOR or the acquisition phase of an adapted gain change. (ABSTRACT TRUNCATED)

Adaptation, Physiological↗

Soleus stretch reflex modulation during gait in humans.

1. The modulation of the short-latency stretch reflex during walking at different walking speeds was investigated and compared with the stretch reflex during standing in healthy human subjects. 2. Ankle joint stretches were applied by a system able to rotate the human ankle joint during treadmill walking in any phase of the step cycle. The system consisted of a mechanical joint attached to the subject's ankle joint and connected to a motor placed beside the treadmill by means of bowden wires. The weight of the total system attached to the leg of the subject was 900 g. 3. The short-latency soleus stretch reflex was modulated during a step. In the stance phase, the amplitude equaled that found during standing at matched soleus background electromyogram (EMG). In the transition from stance to swing, the amplitude was 0 in all subjects. In late swing, the stretch reflex amplitude increased to 45 +/- 27% (mean +/- SD) of the maximal amplitude in the stance phase (stretch amplitude 8 degrees, stretch velocity 250 degrees/s). 4. The onset (42 +/- 3.2 ms) and peak latencies (59 +/- 2.5 ms) of the stretch reflex did not depend on the phase in the step cycle at which the reflex was elicited. 5. When the ankle joint is rotated, a change in torque can be measured. The torque measured over the first 35 ms after stretch onset (nonreflex torque) was at a maximum during late stance, when the leg supported a large part of the body's weight, and at a minimum during the swing phase. At heel contact the nonreflex torque was 50% of its maximal value. 6. During the stance phase the maximal EMG stretch reflex had a phase lead of approximately 120 ms with respect to the maximal background EMG and a phase lead of approximately 250 ms with respect to the maximal nonreflex torque. 7. The constant latency of the stretch reflex during a step implied that the ankle extensor muscle spindles are always taut during walking. 8. The relatively high amplitude of the stretch reflex in late swing and at heel contact made it likely that the stretch reflex contributed to the activation of the ankle extensor muscles in early stance phase.

Adult↗