Segmental reflexes and ankle joint stiffness during co-contraction of antagonistic ankle muscles in man

The size of soleus H-reflexes and short-latency stretch reflexes was measured at different levels of plantar flexion or co-contraction (simultaneous activation of dorsi- and plantar flexors) in seven healthy subjects. In four of seven subjects the short-latency stretc reflex was smaller during weak co-contraction than during isolated plantar flexion at matched background electromyogram (EMG) levels in the soleus muscle. In three of these four subjects the stretch reflex was larger during strong co-contraction than during plantar flexion, whereas it had the same size during the two tasks in the last subject. In the remaining subjects the stretch reflex either had the same size or was larger at all levels of co-contraction than at similar levels of plantar flexion. In contrast, the H-reflex was found to decrease with co-contraction at all contraction levels in all subjects. The decrease in the reflexes during weak co-contraction might be caused by presynaptic inhibition of Ia afferents. It is unclear why only the H-reflex decreased during strong co-contraction. The stiffness of the ankle joint was measured from the torque increment following the stretch of the plantar flexors divided by the stretch amplitude. In all subjects the total stiffness of the ankle joint was larger during strong co-contraction than during plantar flexion of similar strength. The stiffness was smaller during weak co-contraction than during weak plantar flexion in three out of seven subjects. The medial gastrocnemius muscle was more active at a given level of soleus activity during the co-contraction task than during the isolated plantar flexion task. It is suggested that the increase in the stiffness during co-contraction as compared to isolated plantar flexion was mainly due to the mechanical contribution of the activity in the tibialis anterior and medial gastrocnemius muscles. The decrease in stiffness during weak co-contraction was, in contrast, most likely mainly caused by modulation of reflex stiffness.     

Spatial and temporal modulation of joint stiffness during multijoint movement

Joint stiffness measurements during small transient perturbations have suggested that stiffness during movement is different from that observed during posture. These observations are problematic for theories like the classical equilibrium point hypothesis, which suggest that desired trajectories during movement are enforced by joint stiffness. We measured arm impedances during large, slow perturbations to obtain detailed information about the spatial and temporal modulation of stiffness and viscosity during movement. While our measurements of stiffness magnitudes during movement generally agreed with the results of measurements using fast perturbations, they revealed that joint stiffness undergoes stereotyped changes in magnitude and aspect ratio which depend on the direction of movement and show a strong dependence on joint angles. Movement simulations using measured parameters show that the measured modulation of impedance acts as an energy conserving force field to constrain movement. This mechanism allows for a computationally simplified account of the execution of multijoint movement. While our measurements do not rule out a role for afferent feedback in force generation, the observed stereotyped restoring forces can allow a dramatic relaxation of the accuracy requirements for forces generated by other control mechanisms, such as inverse dynamical models.     

Adaptation to destabilizing dynamics by means of muscle cocontraction

Adaptive control of wrist mechanics was investigated by means of destabilizing dynamics created by a torque motor. Subjects performed a 20 degrees movement to a 3 degrees target under the constraint that no motion should occur outside of the target zone once 800 ms had elapsed from movement onset. This constraint served as the minimum acceptable level of postural stability. The ability of subjects to modify their muscle activation patterns in order to successfully achieve this stability was investigated by creating three types of destabilizing dynamics with markedly different features: negative stiffness, negative damping, and square-wave vibration. Subjects performed sets of trials with the first type of destabilizing dynamics and were then required to adapt to the second and third. The adaptive response was quantified in terms of the rms electromyographic (EMG) activity recorded during various phases of the task. Surface EMG activity was recorded from three muscles contributing to wrist flexion and three muscles contributing to wrist extension. With negative stiffness, a significant compensatory increase in cocontraction of wrist flexor and extensor muscles was observed for slow movements, but there was little change in the muscle activity for rapid movements. With negative damping, muscle cocontraction was elevated to stabilize rapid movements, declining only gradually after the target was reached. For slow movements, cocontraction occurred only when negative damping was high. The response to square-wave vibration (10 Hz, +/-0.5 Nm), beginning at movement onset, was similar to that of negative damping, in that it resulted in elevated cocontraction. However, because the vibration persisted after the target was reached, there was no subsequent decrease in muscle activity. When the frequency was reduced to 5.5 Hz, but with the same torque impulse, cocontraction increased. This is consistent with greater mechanical instability. In summary, agonist-antagonist cocontraction was adapted to the stability of the task. This generally resulted in less of a change in muscle activity during the movement phase, when the task was performed quickly compared with slowly. On the other hand, the change in muscle activity during stabilization depended more on the nature of the instability than the movement speed.     

Contribution of peripheral afferents to the activation of the soleus muscle during walking in humans

Summary Small, rapid stretches were applied to the soleus muscle during the stance phase of walking by lifting the forefoot with a pneumatic device. Stretch responses were induced in the soleus muscle by the disturbance. The amplitude and time course of the responses from the soleus muscle were a function of both the kinematics of the disturbance and the time in the step cycle when the disturbance was applied. The step cycle was divided into 16 equal time parts, and data obtained within each of these parts were averaged together. The electromyographic (EMG) response of the soleus muscle showed a time course that was similar to the time course of the angular velocity induced by the disturbance at the ankle. Three linear equations were used to predict the EMG response from the soleus muscle as a function of the angular kinematics of the disturbance: 1) velocity, 2) velocity and displacement, 3) velocity, displacement and acceleration. Introduction of a pure delay between the EMG and the kinematics substantially improved the predictions. Most of the variance (70%) in the EMG response could be accounted for by the velocity of the disturbance alone with an optimal delay (average 38 ms). Inclusion of a displacement term significantly increased the variance accounted for (85%), but further addition of an acceleration term did not. Since the velocity of the disturbance accounted for most of the variance, the reflex gain was estimated from the velocity coefficient. This coefficient increased in a ramp-like fashion through the early part of the stance phase, qualitatively similar to the increase in the H-reflex. Based on these identified gains, this reflex pathway was estimated to contribute substantially (30% to 60%) to the activation of the soleus muscle particularly during the early part of the stance phase.     

Characterisation of the quadriceps stretch reflex during the transition from swing to stance phase of human walking

The main objective of this study was to characterize the stretch reflex response of the human thigh muscles to an unexpected knee flexion at the transition from stance to swing during walking. Eleven healthy subjects walked on a treadmill at their preferred speed. Reliable and constant knee flexions (6–12° amplitude, 230–350°/s velocity, 220 ms duration) were applied during the late swing and early stance phase of human walking by rotating the knee joint with a specifically designed portable stretch apparatus affixed to the left knee. Responses from rectus femoris (RF), vastus lateralis (VL), vastus medialis (VM), biceps femoris (BF), medial hamstrings (MH) and medial gastrocnemius (GM) were recorded via bipolar surface electromyograms (EMG). The onset of the response in the RF, VL and VM, remained stable and independent of the time in the step cycle when the stretch was applied. Across all subjects the response onset (mean ± SD) occurred at 23±1, 24±1 and 23±1 ms for RF, VL and VM, respectively. The duration of the initial response was 90–110 ms, at which time the EMG signal returned towards baseline levels. Three reflex response windows, labelled the short latency reflex (SLR), the medium latency reflex (MLR) and the late latency reflex response (LLR), were analysed. The medium and late reflex responses of all knee extensors increased significantly (p=0.008) as the gait cycle progressed from swing to stance. This was not related to the background EMG activity. In contrast, during standing at extensor EMG levels similar to those attained during walking the reflex responses were dependent on background EMG. During walking, LLR amplitudes expressed as a function of the background activity were on average two to three times greater than SLR and MLR reflex amplitudes. Distinct differences in SLR and LLR amplitude were observed for RF, VL and VM but not in the MLR amplitude. This may be related to the different pathways mediating the SLR, MLR and LLR components of the stretch response. As for the knee extensor antagonists, they exhibited a response to the stretch of the quadriceps at latencies short enough to be monosynaptic. This is in agreement with the suggestion by Eccles and Lundberg (1958) that there may be functional excitatory connections between the knee extensors and flexors in mammals.     

Time-varying stiffness of human elbow joint during cyclic voluntary movement

Summary The objective of this study was to determine the extent to which subjects modulate their elbow joint mechanical properties during ongoing arm movement. Small pseudo-random force disturbances were applied to the wrist with an airjet actuator while subjects executed large (1 rad) elbow joint movements. Using a lumped parameter model of the muscle, tendom and proprioceptive feedback dynamics, a time-varying system identification technique was developed to analyze the phasic changes in the elbow joint's mechanical response. The mechanical properties were found to be time-varying, and well approximated by a quasi-linear second-order model. The stiffness of the arm was found to drop during movement. The arm was always underdamped, with the damping ratio changing during movement. Inertia estimates were constant and consistent with previous measurements. Overall, the moving arm was found to be very compliant, with a peak stiffness value less than the lowest value measured during posture, and a natural frequency of less than 3 Hz. Changing the speed of movement, or the load from gravity, changed the stiffness measured, but not in strict proportion to the change in net muscle torque.     

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.     

Passive visco-elastic properties of the structures spanning the human elbow joint

Summary The passive elastic torque function and the passive viscous torque function of the muscles and connective tissues spanning the elbow joint have been determined in three adult male subjects. The procedure for estimating the passive elastic torque involved measurement of the torque required to passively move the forearm-hand segment, at a constant angular velocity, throughout a complete range of elbow joint motion. The suspension method (Hatze, 1975) was used to obtain the estimate of passive viscous torque. Both of these torque functions were shown to be nonlinear functions of the angular displacement of the joint. In order to assess whether myotatic reflex activity was contributing to the damping of the segment, and thereby biasing the value of the torque contributed by passive viscous elements, the surface electromyograms of the biceps brachii and brachioradialis muscles were examined while the suspended body segment was oscillated. In one subject there was firm evidence of involuntary muscle activity in the brachioradialis muscle which tended to distort the oscillogram. This activity was enhanced when the subject maintained a voluntary isometric contraction in a remote muscle group (Jendrassik's manoeuvre). Based upon these observations, recommendations have been made for reducing unwanted myotatic reflex activity while using the suspension method to obtain estimates of various biomechanical parameters.On leave from the National Research Institute for Mathematical Sciences, CSIR, Pretoria 0001     

The mechanical response of active human muscle during and after stretch

Summary Five subjects contracted forearm supinator muscles which were stretched after development of maximal isometric torque. The ratio of torque at the end of stretch over isometric torque at that position was calculated as excess torque. Excess torque increased with stretch velocity and decreased with stretch amplitude, and it was not dependent upon final muscle length. The rate of decay of torque following stretch could not be shown to depend upon stretch variables.The absence of significant changes in myoelectric activity suggested that with high initial forces, reflex activity did not account for the observed changes. Time-constants of decay (0.15 s to 1.8 s) were much greater than time-constants of rise (approx. 0.07 s) of isometric torque at the same muscle length. This indicates that interaction of series elastic and contractile elements is not the sole cause of prolonged torque following stretch. It is concluded that stretch temporarily enhances the intrinsic contractile properties of a group of human muscles in a manner similar to, but quantitatively different from that seen in isolated muscle preparations.     

Habituation and conditioning of the human long latency stretch reflex

Summary The effects of stretch repetition rate, prior warning stimuli and self administered stretch were examined on the size of the short and long latency components of the stretch reflex electromyographic EMG response in flexor pollicis longus and the flexor muscles of the wrist and fingers. Stretches of constant velocity and extent were given every 10 s, 5 s, 2 s, or 1 s to either the wrist or thumb during a small background contraction of the flexor muscles. The size of the long latency component of the stretch reflex (measured as the area under the averaged rectified EMG responses) declined dramatically at faster repetition rates, especially in the wrist and finger flexors. The size of the short latency component was relatively unaffected. The size of the electrically elicited H-reflex in forearm muscles also failed to habituate under the same conditions. If each individual trial of a series was examined, the long latency component of the stretch reflex EMG could be seen to decrease in size over the first three to six stretches if stretches were given every 1 s, but not if stretches were given every 10 s. When stretches were given every 5 s to either wrist or thumb, an electrical stimulus applied to the digital nerves of the opposite hand 1 s before stretch reduced the size of the long latency component of the reflex EMG response. The short latency component was unaffected. Self triggering of wrist or thumb stretch by the subject pressing the stimulator button himself with his opposite hand, also decreased the size of the long latency component of the reflex EMG response without affecting the short latency component. It is concluded that factors other than stretch size or velocity can have marked effects on the size of the long latency component of the stretch reflex. These factors must be taken into account when comparing values of reflex size obtained with different stretching techniques and in different disease states in man.     

Phasic and tonic stretch reflexes in muscles with few muscle spindles: human jaw-opener muscles

 We investigated phasic and tonic stretch reflexes in human jaw-opener muscles, which have few, if any, muscle spindles. Jaw-unloading reflexes were recorded for both opener and closer muscles. Surface electromyographic (EMG) activity was obtained from left and right digastric and superficial masseter muscles, and jaw orientation and torques were recorded. Unloading of jaw-opener muscles elicited a short-latency decrease in EMG activity (averaging 20 ms) followed by a short-duration silent period in these muscles and sometimes a short burst of activity in their antagonists. Similar behavior in response to unloading was observed for spindle-rich jaw-closer muscles, although the latency of the silent period was statistically shorter than that observed for jaw-opener muscles (averaging 13 ms). Control studies suggest that the jaw-opener reflex was not due to inputs from either cutaneous or periodontal mechanoreceptors. In the unloading response of the jaw openers, the tonic level of EMG activity observed after transition to the new jaw orientation was monotonically related to the residual torque and orientation. This is consistent with the idea that the tonic stretch reflex might mediate the change in muscle activation. In addition, the values of the static net joint torque and jaw orientation after the dynamic phase of unloading were related by a monotonic function resembling the invariant characteristic recorded in human limb joints. The torque-angle characteristics associated with different initial jaw orientations were similar in shape but spatially shifted, consistent with the idea that voluntary changes in jaw orientation might be associated with a change in a single parameter, which might be identified as the threshold of the tonic stretch reflex. It is suggested that functionally significant phasic and tonic stretch reflexes might not be mediated exclusively by muscle spindle afferents. Thus, the hypothesis that central modifications in the threshold of the tonic stretch reflex underlie the control of movement may be applied to the jaw system. Received: 11 October 1996 / Accepted: 17 March 1997     

Symmetric force response of human masticatory muscles to stretch and unloading

 During chewing, the force exerted by the jaw-closing muscles must constantly adapt to changing resistances between the teeth, as the food is broken down. In the present study, the changes in biting force resulting from small, controlled displacements imposed on isometrically contracting jaw-closing muscles were measured. We found that the force changes resulting from small loading and unloading movements were normally highly symmetrical. The initial force change was linear, and preceded the onset of reflex changes in muscle activity. Later changes in force were the result of both short- and long-latency reflexes in the jaw-closing muscles, the long-latency component being quantitatively greater. The long-latency unloading reflex in the jaw-closing muscles has not been described hitherto. The symmetry of force increase with loading and decrease with unloading was absent in one subject with atypical stretch and H-reflexes. Received: 2 June 1995 / 30 September 1996     

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.     

Electromyographic responses to constant position errors imposed during voluntary elbow joint movement in human

The role of reflexes in the control of stiffness during human elbow joint movement was investigated for a wide range of movement speeds (1.5–6 rad/s). The electromyographic (EMG) responses of the elbow joint muscles to step position errors (step amplitude 0.15 rad; rise time 100 ms) imposed at the onset of targeted flexion movements (1.0 rad amplitude) were recorded. For all speeds of movement, the step position disturbance produced large modulations of the usual triphasic EMG activity, both excitatory and inhibitory, with an onset latency of 25 ms. In the muscles stretched by the perturbation, the early EMG response (25–60 ms latency) magnitude was greater than 50% of the activity during the unperturbed movements (background activity). In all muscles the EMG responses integrated over the entire movement were greater than 25% of the background activity. The responses were relatively greater for slower movements. Perturbations assisting the movement caused a short-latency (25–60 ms) reflex response (in the antagonist muscle) that increased with movement speed and was constant as a percentage of the background EMG activity. In contrast, perturbations resisting the movement caused a reflex response (in the agonist muscle) that was of the same absolute magnitude at all movement speeds, and thus decreased with movement speed as a percentage of the background EMG activity. There was a directional asymmetry in the reflex response, which produced an asymmetry in the mechanical response during slow movements. When the step perturbation occurred in a direction assisting the flexion movement, the antagonist muscle activity increased, but the main component of this response was delayed until the normal time of onset of the antagonist burst. When the step perturbation resisted the movement the agonist muscles responded briskly at short latency (25 ms). A reflex reversal occurred in two of six subjects. A fixed reflex response occurred in the antagonist muscle, regardless of the perturbation direction. For the extension direction perturbations (resisting movement), this response represented a reflex reversal (50 ms onset latency) and it caused the torque resisting the imposed step (stiffness) to drop markedly (below zero for one subject). Reflex responses were larger when the subject was prevented from reaching the target. That is, when the perturbation remained on until after the normal time of reaching the target, the EMG activity increased, with a parallel increase in stiffness. Similarly, when the perturbations prevented the subject from reaching the target during a 1-rad voluntary cyclic movement, the EMG and stiffness increased markedly. Coactivation of the antagonist muscle with the agonist muscle was not prominent (<30% of antagonist activity) during unperturbed movements. The perturbations were resisted with reciprocal activity, and thus reflex action did not increase the coactivation. However, as a result of the low-pass properties of muscle, substantial cocontraction of the agonist and antagonists muscle forces may have occurred during rapid movements, thus leading to increased stiffness. As the relative changes in normal EMG activity produced by the perturbation were often comparable with the changes in mean muscle torque (stiffness) reported in the first paper of this series, we conclude that the action of reflexes produced a significant portion of the resistance to perturbations. This reflexive portion was greater for slower movements, it was greater when the subject neared the target, and it was variable according to the perturbation direction and the particular subject. Given that the perturbations were of similar frequency content to the movement itself (though of smaller amplitude) and that the reflexes contributed substantially to the resistance to these perturbations, we suggest that in normal unperturbed movements the observed EMG is likewise substantially determined by the reflex activity.     

Torques generated at the human elbow joint in response to constant position errors imposed during voluntary movements

The stiffness of the human elbow joint was investigated during targeted, 1.0-rad voluntary flexion movements at speeds ranging from slow (1.5 rad/s) to very fast (6.0 rad/s). A torque motor produced controlled step position errors in the execution of the movements. The steps began at the onset of movement, rose to an amplitude of 0.15 rad in 100 ms, and had a duration equal to movement duration. The net joint torque (muscle torque) resisting the step perturbation was computed from the applied torque, the joint acceleration, and the limb inertia. Subjects resisted the imposed step changes with approximately step changes in the net muscle torque. The mean resistance torque divided by the step amplitude was computed and is referred to as the stiffness. The stiffness increased with the voluntary movement speed, over the range of speeds (1.5–6 rad/s). The stiffness increased linearly with the magnitude of the net muscle torque on the unperturbed trials (referred to as background torque). The stiffness changed by only 20% when the step amplitude ranged from 0.05 to 0.15 rad. The mechanical resonant frequency (f _r), estimated from the average stiffness estimates, ranged from 0.8 to 3.0 Hz. The resonant frequency approximately equaled the principal frequency component of the movement f _m. On average: f _r = 0.96 f _m+0.46. During the fixed, 100-ms rise time of the step, the resistance was not linearly related to the background torque. At slower speeds the resistance was relatively greater during this rise time. However, when the imposed step perturbation was modified so that its rise time occurred in a time proportional to the movement duration (rather than in the fixed, 100-ms, time), the muscle torque resisting the motor during this rise time was proportional to the background torque. When these modified step responses were plotted on a time scale normalized to the movement duration, they all had approximately the same shape. Apparently the muscle viscosity scaled with the stiffness so as to maintain the constant response shape (constant damping ratio). The observed tuning of the mechanical properties to the movement speed is suggested to be important in the robust generation of smooth stereotyped voluntary movements.     

Acute passive stretching alters the mechanical properties of human plantar flexors and the optimal angle for maximal voluntary contraction

The purpose of this study was to investigate whether acute passive stretching (APS) reduced maximal isometric voluntary contraction (MVC) of the plantar flexors (PF) and if so, by what mechanisms. The PF in 15 female volunteers were stretched for 10 min (5×120 s) by a torque motor to within 2° of maximum dorsiflexion (D) range of motion (ROM). MVC with twitch interpolation, maximal Hoffmann reflex (H_max) and compound action potentials (M_max) were recorded at 20° D. Stretch reflexes (SR) were mechanically induced at 200° s^–1 between 0° and 10° D and SR torque and EMG amplitude were determined. All tests were assessed pre- (pre) and post-APS (post-test₁). MVC, SR, and M_max were again assessed after additional stretch was applied [mean 26 (1)° D; post-test₂] to test if the optimal angle had been altered. EMG was recorded from soleus (SOL), medial gastrocnemius (MG) and tibialis anterior (TA) using bipolar surface electrodes. APS resulted in a 27% decrease in mean peak passive torque (P<0.05). MVC and SR torque were 7% (P<0.05) and 13% lower at post-test₁ (P<0.05), respectively. SR EMG amplitude of SOL and MG was reduced by 27% (P<0.05) and 22% (P<0.05), respectively. The H_max/M_max EMG and H_max/M_max torque ratios were unchanged at post-test₁. At post-test₂, MVC and SR EMG recovered to pre-APS values, while the SR and M_max torque increased by 19% and 13%, respectively (P<0.05). The decrease in MVC during post-test₁ was attributed to changes in the mechanical properties of PF and not to reduced muscle activation.     

Evidence for a supraspinal contribution to the human quadriceps long-latency stretch reflex

In sitting humans a rapid unexpected lengthening of the knee extensors elicits a stretch reflex (SR) response as recorded by the electromyogram (EMG) which comprises multiple bursts. These are termed short latency responses (SLR), medium latency responses (MLR) and long latency responses (LLR). The aim of this study was to determine if a transcortical pathway contributes to any of these bursts. Flexion perturbations (amplitude =4°, velocity=150°/s) were imposed on the right knee joint of sitting subjects (n=11). The effect of the perturbation on the electromyographic (EMG) response of the pre-contracted quadriceps muscle to magnetic stimulation of the contralateral motor cortex was quantified. Transcranial magnetic stimulation (TMS) was applied to elicit a compound motor evoked potential (MEP) in the target muscle rectus femoris (RF), in the vastus lateralis (VL), vastus medialis (VM) and biceps femoris (BF). The MEP and SR were elicited either in combination or separately. When applied in combination the delay between the SR and the MEP varied from 0 to 150 ms in steps of 4, 5 and 10 ms. Somatosensory evoked potentials (SEPs) were recorded from four subjects during the imposed stretch to quantify the latency of the resulting afferent volley. Onset latencies of responses in RF were 25±2 ms for the SR and 20±4 ms for the MEP. The average SEP latency was 24±2 ms. A transcortical pathway thus has the potential to contribute to the RF SR no earlier than 54±6 ms (SEP + MEP + 10 ms central processing delay) following the stretch onset. The duration of the total reflex burst was 85±6 ms. Significant facilitation of the MEP commenced at 78 ms, coinciding with the LLR component of the stretch response. No such facilitation was observed in the synergists VL and VM, or in the antagonist BF. Our results indicate that the LLR of the RF likely involves supraspinal pathways. More importantly, of the investigated muscles, this involvement of higher centers in the shaping of the LLR is specific to the RF muscle during the investigated task.     

Independent control of reflex and volitional EMG modulation during sinusoidal pursuit tracking in humans

It is well known that during volitional sinusoidal tracking the long-latency reflex modulates in parallel with the volitional EMG activity. In this study, a series of experiments are reported demonstrating several conditions in which an uncoupling of reflex from volitional activity occurs. The paradigm consists of a visually guided task in which the subject tracked a sinusoid with the wrist. The movement was perturbed by constant torque or controlled velocity perturbations at 45° intervals of the tracking phase. Volitional and reflex-evoked EMG and wrist displacement as functions of the tracking phase were recorded. The relationship of both short-latency (30–60 ms) and longer-latency (60–100 ms) reflex components to the volitional EMG was evaluated. In reflex tracking, the peak reflex amplitude occurs at phases of tracking which correspond to a maximum of wrist joint angular velocity in the direction of homonymous muscle shortening and a minimum of wrist compliance. Uncoupling of the reflex and volitional EMG was observed in three situations. First, during passive movement of the wrist through the sinusoidal tracking cycle perturbation-evoked long-latency stretch reflex peak is modulated as for normal, volitional tracking. However, with passive joint movement the volitional EMG modulation is undetectable. Second, a subset of subjects demonstrate a normally modulated and positioned long-latency reflex with a single peak. However, these subjects have distinct bimodal peaks of volitional EMG. Third, the imposition of an anti-elastic load (positive position feedback) shifts the volitional EMG envelope by as much as 180° along the tracking phase when compared with conventional elastic loading. Yet the long-latency reflex peak remains at its usual phase in the tracking cycle, corresponding to the maximal velocity in the direction of muscle shortening. Furthermore, comparison of the results from elastic and anti-elastic loads reveals a dissociation of short- and long-latency reflex activity, with the short-latency reflex shifting with the volitional EMG envelope. Comparable results were also obtained for controlled velocity perturbations used to control for changes in joint compliance. The uncoupling of the reflex and volitional EMG activity in the present series of experiments points to a flexible relationship between reflex and volitional control systems, altered by peripheral input and external load.     

Mechanical and electromyographic responses to stretch of the human anterior tibial muscle at different levels of contraction

Summary The EMG response and the mechanical response to 2 degree stretch of the human anterior tibial muscle was studied during contractions ranging from 0% to 80% of maximal voluntary contraction (MVC). The EMG response showed three distinct peaks M1, M2, and M3 with peak latencies of 59 ms, 86 ms, and 120 ms respectively. At low background torques M1 dominated while M2 and M3 were small or absent. M2 and M3 dominated above 40% of MVC and M2 in particular showed automatic gain compensation, i.e. it constituted a — more or less — constant proportion of the background EMG for all contraction levels. The ratio between M1 amplitude and background EMG steadily decreased with contraction level. Even though the summed contributions of M1, M2, and M3 to some degree showed automatic gain compensation, this was not the case for the mechanical response to stretch. Between 0% and 30% of MVC the reflex mediated mechanical response increased approximately in proportion to the contraction level, but the reflex mediated mechanical response peaked at 40% of MVC and declined to zero at 80% of MVC. This discrepancy between EMG and mechanical response was explained by a simple model. The regression line between rectified and filtered tibialis anterior EMG and torque was used to predict the mechanical response from the EMG response. At increasing contraction levels the twitch elicited by supramaximal electrical stimulation decreases, and we reduced the predicted mechanical response by the same factor as the twitch. This simple model predicted the mechanical response for all contraction levels, making it possible to assess the functionality of reflexes even when accurate measurements of muscle force or intrinsic muscle properties are not possible.     

Reflex and non-reflex torque responses to stretch of the human knee extensors

Reflex responses to unexpected stretches are well documented for selected muscles in both animal and human. Moreover, investigations of their possible functional significance have revealed that stretch reflexes can contribute substantially to the overall stiffness of a joint. In the lower extremity only the muscles spanning the human ankle joint have been investigated in the past. This study implemented a unique hydraulic actuator to study the contributions of the knee extensor stretch reflex to the overall knee joint torque. The quadriceps muscles were stretched at various background torques, produced either voluntarily or by electrical stimulation, and thus the purely reflex mediated torque could be calculated. The stretch had a velocity of 67°/s and an amplitude of 20°. A reflex response as measured by electromyography (EMG) was observed in all knee extensors at latencies of 26 – 36 ms. Both phasic and tonic EMG stretch responses increased with increasing background torques. Lines of best fit produced correlation coefficients of 0.59 – 0.78. This study is the first to examine the reflex contribution of the knee extensors to the total torque at background torques of 0 – 90% MVC. The contribution of the reflex mediated torque is initially low and peaked at background torques of 20 – 40% MVC. In terms of the total torque the reflex contributed 16 – 52% across all levels of background torque. It is concluded that during medium background torque levels such as those obtained during walking, the stretch reflex of the quadriceps muscle group contributes substantially to the total torque around the knee joint.