The role of joint biomechanics in determining stretch reflex latency at the normal human ankle

Summary In order to study the influence of biomechanical factors on the timing of stretch reflex activity in the ankle extensor musculature, well defined, small amplitude and relatively rapid dorsiflexing stretch was applied to the ankle of seated normal human subjects at a series of angles within the range of physiological movement. If the ankle musculature was relaxed, a single reflex component appeared in the Triceps surae (TS) EMG with a latency compatible with a predominantly monosynaptic pathway. The latency of this response could be prolonged by applying stretch from an initially plantarflexed position and, similarly, decreased by applying stretch from a dorsiflexed position. A decrease in latency of 5–30 ms could be achieved by altering the pre-displacement ankle angle from 105 to 75 degrees. Intermediate changes in the start angle led to intermediate changes in latency. This trend was highly linear. If stretch was applied while the subject maintained a low level contraction in the TS, however, this shift in latency was abolished, with the earliest reflex components appearing with a latency obtained in the relaxed state at or close to maximum dorsiflexion. It is suggested that this shift in latency results from the properties of the long, compliant tendon through which joint movements are transmitted to the TS muscle. This shift in latency caused by passive alteration in the ankle angle at which a reflex was evoked should be taken into account when classifying reflexes arising from a mechanical input, or when using latency determinations as evidence for the involvement of particular pathways in their genesis.     

Enhanced stretch reflex excitability of the soleus muscle in experienced swimmers

The purpose of this study was to investigate effects of long-term participation to swimming on adaptations of spinal reflex excitability. To this end, mechanically induced stretch reflex (SR) and electrically induced Hoffmann (H-) reflex of the soleus muscle were investigated between swimmers with experience of more than 10 years and non-trained individuals while sitting at rest. The amplitude and the gain (stretch velocity vs. amplitude of the reflex response) of the SR were significantly greater in the swimming group than in the non-trained control group. Similarly, the responses of the H-reflex were also significantly greater in the swimming group than in the non-trained control group. Results of this study demonstrated that the spinal reflex excitability in experienced swimmers was far more enhanced than in non-trained individuals.     

Relationship between stretch reflex thresholds and voluntary arm muscle activation in patients with spasticity

Previous studies have shown that deficits in agonist–antagonist muscle activation in the single-joint elbow system in patients with spastic hemiparesis are directly related to limitations in the range of regulation of the thresholds of muscle activation. We extended these findings to the double-joint, shoulder-elbow system in these patients. Ten non-disabled individuals and 11 stroke survivors with spasticity in upper limb muscles participated. Stroke survivors had sustained a single unilateral stroke 6–36 months previously, had full pain-free passive range of motion of the affected shoulder and elbow and had some voluntary control of the arm. EMG activity from four elbow and two shoulder muscles was recorded during quasi-static (<5°/s) stretching of elbow flexors/extensors and during slow voluntary elbow flexion/extension movement through full range. Stretches and active movements were initiated from full elbow flexion or extension with the shoulder in three different initial positions (60°, 90°, 145° horizontal abduction). SRTs were defined as the elbow angle at which EMG signals began to exceed 2SD of background noise. SRT angles obtained by passive muscle stretch were compared with the angles at which the respective muscles became activated during voluntary elbow movements. SRTs in elbow flexors were correlated with clinical spasticity scores. SRTs of elbow flexors and extensors were within the biomechanical range of the joint and varied with changes in the shoulder angle in all subjects with hemiparesis but could not be reached in this range in all healthy subjects when muscles were initially relaxed. In patients, limitations in the regulation of SRTs resulted in a subdivision of all-possible shoulder-elbow arm configurations into two areas, one in which spasticity was present (“spatial spasticity zone”) and another in which it was absent. Spatial spasticity zones were different for different muscles in different patients but, taken together, for all elbow muscles, the zones occupied a large part of elbow-shoulder joint space in each patient. The shape of the boundary between the spasticity and no-spasticity zones depended on the state of reflex inter-joint interaction. SRTs in single- and double-joint flexor muscles correlated with the positions at which muscles were activated during voluntary movements, for all shoulder angles, and this effect was greater in elbow flexor muscles (brachioradialis, biceps brachii). Flexor SRTs correlated with clinical spasticity in elbow flexors only when elbow muscles were at mid-length (90°). These findings support the notion that motor impairments after CNS damage are related to deficits in the specification and regulation of SRTs, resulting in the occurrence of spasticity zones in the space of elbow-shoulder configurations. It is suggested that the presence of spatial spasticity zones might be a major cause of motor impairments in general and deficits in inter-joint coordination in particular in patients with spasticity.     

A re-examination of the effects of instruction on the long-latency stretch reflex response of the flexor pollicis longus muscle

We re-examined the issue of how a subject’s intention to react to a joint perturbation may modulate the long-latency M2 stretch reflex response. The experiments were done on the flexor pollicis longus muscle (FPL) of the human thumb, for which there is evidence that its M2 reflex response is mediated, at least in part, by a pathway that traverses the motor cortex. The participation of the cerebral cortex in the genesis of the M2 reflex response may allow for a modulation of its amplitude, based on the intention of the subject. To test whether the M2 response is genuinely modulated by the subject’s intention, we examined the magnitude of this response as a function of the FPL background level of activation, measured by the surface rectified and filtered EMG. The subject was instructed either to oppose the perturbation as quickly as possible, not to react, or to relax as quickly as possible after the onset of the perturbation. The time integral of the long latency FPL EMG response, computed between 40 and 70 ms following the onset of stretch, was plotted against the mean torque produced by the distal inter-phalangeal joint of the thumb, or against the mean background FPL EMG. There were no significant differences in the FPL M2 EMG responses for different instructions. The amplitude of the reflex response was dependent only - in an approximately linear manner - on the background level of muscle activation. The total joint stiffness (intrinsic plus reflex) was also calculated for each combination of instruction and background torque. This variable was calculated over a time interval (from 75 to 105 ms) that included the torque due to the M2 reflex response superimposed on the background torque, but was well before any voluntary reaction. Again, there were no significant differences in joint stiffness as a result of the instruction. We therefore conclude that, despite a cortical contribution to the M2 stretch reflex response, this response is not influenced by the intention of the subject on how to react to a perturbation.     

A stretch reflex in extraocular muscles of species purportedly lacking muscle spindles

It is generally assumed that proprioceptive feedback plays a crucial role in limb posture and movement. However, the role of afferent signals from extraocular muscles (EOM) in the control of eye movement has been a matter of continuous debate. These muscles have atypical sensory receptors in several species and it has been proposed that they are not supported by stretch reflexes. We recorded electromyographic activity of EOM during passive rotations of the eye in sedated rats and squirrel monkeys and observed typical stretch reflexes in these muscles. Results suggest that there is a similarity in the reflexive control of limb and eye movement, despite substantial differences in their biomechanics and sensory receptors. Like in some limb skeletal muscles, the stretch reflex in EOM in the investigated species might be mediated by other length-sensitive receptors, rather than muscle spindles.     

A re-examination of the effects of instruction on the long-latency stretch reflex response of the flexor pollicis longus muscle

We re-examined the issue of how a subject's intention to react to a joint perturbation may modulate the long-latency M2 stretch reflex response. The experiments were done on the flexor pollicis longus muscle (FPL) of the human thumb, for which there is evidence that its M2 reflex response is mediated, at least in part, by a pathway that traverses the motor cortex. The participation of the cerebral cortex in the genesis of the M2 reflex response may allow for a modulation of its amplitude, based on the intention of the subject. To test whether the M2 response is genuinely modulated by the subject's intention, we examined the magnitude of this response as a function of the FPL background level of activation, measured by the surface rectified and filtered EMG. The subject was instructed either to oppose the perturbation as quickly as possible, not to react, or to relax as quickly as possible after the onset of the perturbation. The time integral of the long latency FPL EMG response, computed between 40 and 70 ms following the onset of stretch, was plotted against the mean torque produced by the distal inter-phalangeal joint of the thumb, or against the mean background FPL EMG. There were no significant differences in the FPL M2 EMG responses for different instructions. The amplitude of the reflex response was dependent only — in an approximately linear manner — on the background level of muscle activation. The total joint stiffness (intrinsic plus reflex) was also calculated for each combination of instruction and background torque. This variable was calculated over a time interval (from 75 to 105 ms) that included the torque due to the M2 reflex response superimposed on the background torque, but was well before any voluntary reaction. Again, there were no significant differences in joint stiffness as a result of the instruction. We therefore conclude that, despite a cortical contribution to the M2 stretch reflex response, this response is not influenced by the intention of the subject on how to react to a perturbation.     

Stretch shortening cycle fatigue: interactions among joint stiness,reflex, and muscle mechanical performance in the drop jump

The purpose of the present study was to investigate the effect of strenuous stretch-shortening cycle exercise on the relationship between reflex and stiffness regulation during the drop jump. Ten healthy male subjects performed submaximal stretch-shortening cycle exercise on a special sledge apparatus. Exhaustion occurred on average within 3 min. A drop jump test from a 50-cm height was performed immediately before and after the sledge exercise, as well as 2 h, 2 days and 4 days later. The fatigue exercise showed relatively high blood lactate concentrations 12.5 (SD 2.6) mmol·l^–1 and a 2-day delayed increase of serum cretaine kinase concentration. In drop jumps, the short latency M1 component of the vastus lateralis muscle electromyogram (EMG) response showed a continuous decline throughout the entire follow-up period after fatigue (NS), whereas the medium latency EMG component increased 2 days after the postfatigue sessions (P < 0.05). Immediately after the fatigue exercise a positive correlation (P < 0.05) was found between the changes in the short latency EMG response and in the amount of knee joint stiffness during the early post-landing phase of the drop jump. This suggests that the M1 response was closely related to the stiffness changes during the initial braking phase of the drop jump. Increase of creatine kinase concentration on the 2nd day correlated negatively with the changes in the drop jump performance (P < 0.05). Since the short latency EMG component has almost recovered on the 2nd day, impairment of the mechanical function of the muscle might have taken place. In conclusion, exhausting stretch-shortening cycle exercise induced local muscle impairment, which resulted in modulation of the reflex and stiffness interaction in the drop jump as well as compensation by central motor command.     

Movements modulate the reflex responses of human flexor pollicis longus to stretch

The reflex responses to brisk, ramp stretch perturbations of the human flexor pollicis longus muscle (FPL) were recorded during isometric and slow concentric or eccentric contractions at similar levels of muscle excitation. The subjects flexed their thumb to push down against a thumb-rest, whose position was controlled by a servo-controlled motor. In different runs, the stretch perturbations were imposed when the thumb-rest was stationary (isometric) or was flexing or extending the interphalangeal joint of the thumb at a constant velocity, i.e. during concentric or eccentric contractions of FPL. The latency of the most prominent component of the electromyographic reflex in the isometrically contracting muscle was about 60 ms, measured from the command signal. The amplitude of this response was sharply reduced during the non-isometric contractions. While not dependent on the direction, this modulation of the reflex response increased with the speed of active movement of the interphalangeal joint (flexion or extension). The response was greatly reduced during concentric or eccentric movements as slow as 1.6 mm·s^–1 (approximately 5°·s^–1 at the joint). When the force rather than the position of the thumb-rest was servo-controlled, the stretch response to perturbation again diminished with speed in a self-paced flexion task, compared with an isometric “hold” condition. Received: 25 April 1996 / Accepted: 2 June 1997     

Behaviour space of a stretch reflex model and its implications for the neural control of voluntary movement

A nonlinear model for the stretch reflex has recently been used to study the interactions between voluntary and reflex controls during fast, targeted movements. The present study explores the topography of a ‘behaviour space’ generated by computer simulations of this model under various combinations of values for the gain parameters and time constants in the model's feedback loops. In general, we define a behaviour space to be any set of behavioural characteristics of the simulated movement, such as movement time, peak acceleration or peak velocity. The mathematical model can therefore be viewed as an M×N dimensional map from its parameter space N to a behaviour space M. Here, a one-dimensional behaviour space is explored. This provides a method for quantitatively comparing the different control strategies that might be employed by the nervous system for integrating reflex and descending signals during fast, voluntary movements. The results indicate that an optimal strategy will employ proprioceptive feedback as a means of fine-tuning the braking and clamping activities of fast, goal-directed movements and that descending signals are primarily important for initiating the movement and for controlling reciprocal patterns of muscle activity during the end phase of the movement.     

Prolonged time course for vibratory suppression of stretch reflex in the decerebrate cat

Summary We studied the effects of longitudinal tendon vibration on the stretch reflex of the soleus and gastrocnemius muscles in 11 decerebrate cats. Vibration was applied at amplitudes (40–80 m) and frequencies (120–250 Hz) sufficient to provide a strong tonic vibration reflex. In keeping with previous reports, we found that during an established tonic vibration reflex, the force and emg response to superimposed ramp and hold stretch are largely suppressed. This suppression is most obvious during the dynamic phase of stretch where it gives rise to a complex force response resembling that of active areflexic muscle.If stretch initiation is delayed until after vibration is terminated, the suppressive effects of vibration persist for 5 s or more. These suppressive effects are marked in the first 200 ms, and then decay gradually over the ensuing time period, paralleling the decline in emg and force which follows vibration offset. Simultaneous recordings from homonymous Ia afferents showed that this suppression persists even though the stretch responsiveness of primary spindle endings has returned to normal immediately following the end of vibration.When stretch is initiated shortly after vibration commences, the suppressive effects are first evident at 50–100 ms latency, but are not well established until 1 s or more after vibration onset.Tests of monosynaptic transmission using small amplitude tendon taps or electrical stimulation of synergist nerves to activate Ia fibers revealed that reductions in the magnitude of the response following vibration are usually modest (12% mean reduction at 50 ms, n = 5), and they are quite sensitive to the initial level of excitation of the motoneuron pool. These reductions were also rather shortlived, being largely completed within 500 ms of vibration offset. Although the relative contributions of presynaptic and postsynaptic inhibition are not readily dissociated in this type of experiment, it is likely that the magnitude of presynaptic inhibition is quite small.We argue that the effects of vibration on the stretch reflex are best explained by invoking an excitatory autogenetic projection from Ia interneurons to extensor motor neurons, which lies in parallel with the Ia monosynaptic projection. In order to account for the vibratory suppression, we propose that these interneurons are driven to saturation by vibration. When vibration ceases, the discharge rate of these interneurons declines with a prolonged time-course that coincides with the recovery of stretch responsiveness. This recovery would contribute to the return of stretch reflex force.     

The role of cocontraction in the impairment of movement accuracy with fatigue

The present experiment was designed to test the hypothesis that fatigue-induced impairment in movement accuracy is caused by a decrease in muscle cocontraction rather than a reduced ability to produce muscular force. Seven participants performed fast and accurate elbow extensions aimed at a target, before and after a fatigue protocol. The inertia of the manipulandum was decreased after the fatigue protocol so that the ratio of required to available force during movements was identical pre- and post-fatigue. After the fatigue protocol, movement endpoint accuracy decreased and movement endpoint variability increased. These alterations were associated with a decrease in cocontraction. We concluded that the impairment of movement accuracy during fatigue could not be explained by the lack of available force, but was likely to be due to a fatigue-induced decrease in muscular cocontraction. We then speculate that fatigue influences the relative weights of accuracy and energy economy in the optimisation of sensorimotor control.     

The suppression of the long-latency stretch reflex in the human tibialis anterior muscle by transcranial magnetic stimulation

The purpose of this study was to investigate the transcortical nature of the long-latency stretch reflex (M3) in the human tibialis anterior muscle. This was achieved by applying a single pulse of subthreshold (90% motor threshold) transcortical magnetic stimulation (subTMS) at the site of the motor cortex. Such a stimulus is able to activate intracortical inhibitory circuits and thereby depress motor cortical output. We hypothesized that it would also suppress a transcortical reflex loop. The stretch reflex was elicited using a pedal attached to an electric motor. SubTMS was applied at several intervals prior to M3. Recordings were repeated 20–40 times. The reflex components were quantified using 20-ms windows in the averaged rectified electromyogram (EMG). SubTMS evoked significantly larger depression of M3 than of the background EMG in the same time frame when applied 55–85 ms prior to M3 (P<0.05, n=10). Furthermore, the effect on M3 was significantly larger than the effect on the spinal M2 (P<0.01, n=7). Our results provide evidence that the long-latency stretch reflex in the tibialis anterior muscle is at least partly transcortical.     

Modulation by horizontal eye position of the vestibulo-collic reflex induced by tilting in the frontal plane in the alert cat

Summary In alert cats, during sinusoidal rotations of head and trunk en bloc around a longitudinal axis, in darkness or in light, the vestibulo-collic reflex induces neck muscle contractions. The phase and gain diagrams are consistent, in the frequency range 0.2 to 1.2 Hz, with previous results from anesthetized or decerebrate cats. In addition, neck muscle contractions are modulated by horizontal eye position, as is the case for rotations in the horizontal plane, around the vertical (Z) axis. Neck muscle contraction is consequently under control of both eye position and head tilt angle. This synergy of eye and head could suppress the effects of vestibulo-collic reflex during orienting reactions.     

Heart rate at the onset of muscle contraction and during passive muscle stretch in humans: a role for mechanoreceptors

Previous evidence suggests that the heart rate (HR) increase observed with isometric exercise is dependent on different afferent mechanisms to those eliciting the increase in blood pressure (BP). Central command and muscle metaboreceptors have been shown to contribute to this differential effect. However, in experimental animals passive stretch of the hindlimb increases HR suggesting that small fibre mechanoreceptors could also have a role. This has not been previously shown in humans and was investigated in this study. Healthy human volunteers were instrumented to record BP, ECG, respiration, EMG of rectus femoris and gastrocnemius and contraction force of triceps surae. Voluntary isometric contraction of triceps surae elicited a significant HR change in the first three respiratory cycles at 40 % of maximum voluntary contraction whereas BP did not change significantly until after 30 s. This suggests that different mechanisms are involved in the initiation of the cardiovascular changes. Sustained passive stretch of triceps surae for 1 min, by dorsiflexion of the foot, caused a significant (   P < 0.05  ) increase in HR (5 ± 2.6 beats min⁻¹) with no significant change in BP. A time domain measure of cardiac vagal activity was reduced significantly during passive stretch from 69.7 ± 12.9 to 49.6 ± 8.9 ms. Rapid rhythmic passive stretch (0.5 Hz for 1 min) was without significant effect suggesting that large muscle proprioreceptors are not involved. We conclude that in man small fibre muscle mechanoreceptors responding to stretch, inhibit cardiac vagal activity and thus increase HR. These afferents could contribute to the initial cardiac acceleration in response to muscle contraction.     

Sensitivity of monosynaptic test reflexes to facilitation and inhibition as a function of the test reflex size: a study in man and the cat

Summary In parallel experiments on humans and in the cat it was investigated how the sensitivity of monosynaptic test reflexes to facilitation and inhibition varies as a function of the size of the control test reflex itself. In man the monosynaptic reflex (the Hoffmann reflex) was evoked in either the soleus muscle (by stimulation of the tibial nerve) or the quadriceps muscle (by stimulation of the femoral nerve). In the decerebrate cat monosynaptic reflexes were recorded from the nerves to soleus and medial gastrocnemius muscles; they were evoked by stimulation of the proximal ends of the sectioned L7 and S1 dorsal roots. Various excitatory and inhibitory spinal reflex pathways were used for conditioning the test reflexes (e.g. monosynaptic Ia excitation, disynaptic reciprocal inhibition, cutaneous inhibition, recurrent inhibition, presynaptic inhibition of the Ia fibres mediating the test reflex). It was shown that the additional number of motoneurones recruited in a monosynaptic test reflex by a constant excitatory conditioning stimulus was very much dependent on the size of the test reflex itself. This dependency had the same characteristic pattern whatever the conditioning stimulus. With increasing size of the test reflex the number of additionally recruited motoneurones first increased, then reached a peak (or plateau) and finally decreased. A similar relation was also seen with inhibitory conditioning stimuli. The basic physiological factors responsible for these findings are discussed. Finally, the implications for the interpretation of experiments in man with the H-reflex technique are considered.     

Effects of knee joint angles and fatigue on the neuromuscular control of vastus medialis oblique and vastus lateralis muscle in humans

The effects of different knee joint angles and fatigue on the neuromuscular control of the vastus medialis oblique (VMO) and vastus lateralis (VL) muscles were investigated in 17 (11 men, 6 women) young subjects. The electromyogram (EMG) activities and the force generation capacities were monitored before and after a fatigue protocol at three different knee joint angles, 90°, 150°, 175° of knee extension, on three occasions. In response to randomly triggered light signals, the subjects performed three isometric maximal voluntary contraction (IMVC) that lasted for 4 to 8 s. This was then followed by the fatigue protocol which consisted of six bursts of contractions fixed at 30 s on and 10 s off. Immediately after the exercise to fatigue, the subjects performed another three IMVC in response to the light signals. Repeated measures ANOVA were performed to examine the effects of fatigue at these three positions on the electromechanical delay (EMD), median frequency (f _med), peak force (F _peak) and root mean square (rms)-EMG:F _peak quotient of VMO and VL. The results revealed a significant effect of the three knee joint angles on the EMD before the fatigue (P < 0.05). The fatigue protocol induced a significant decrease in F _peak at all the three positions (P < 0.01). However, the fatigue induced a significant decrease of f _med at only 90° and 150° of knee extension (P < 0.01). This occurred in parallel with the lengthening of EMD at these two joint angles (P < 0.01 and P < 0.05). The effects of fatigue on the f _med and EMD were not significant between VMO and VL at all three angles. The insignificant difference in f _med and EMD between VMO and VL at the three knee positions before and after fatigue indicated that no preferential onset activation between VMO and VL had occurred. Accepted: 1 September 2000     

An IFN-{gamma}-dependent pathway plays a critical role in the pathogenesis of murine immunodeficiency syndrome induced by LP-BM5 murine leukemia virus

The murine acquired immunodeficiency syndrome (MAIDS) causedby a defective murine leukemia virus produces severe immunodeficiencywith abnormal lymphoproliferation and hypergammaglobulinemia.The presence of both CD4⁺ T cells and B cells is critical forthe development of this disease. Remarkably elevated mRNA expressionfor IFN- and IL-10 was observed in spleen cells of C67BU6 micestarting from the early phase of viral infection. IFN- productionwas induced by spleen cells from virus-infected mice upon stimulationwith concanavalln A or lipopolysaccharide in both the earlyand late phases of MAIDS progression. When mice that had beenpassively administered anti-IFN- mAb were infected with thevirus, the development and progression of lymphadenopathy, immunodeficiencyand elevated levels of serum lgG2a associated with MAIDS weredelayed. Treatment with anti-IL-4 or anti-IL-10 mAb in placeof anti-IFN- mAb did not induce the delayed progression of MAIDS.These data support the concept that IFN--dependent pathway maybe involved in the development of MAIDS.