Stretch Reflex Gain Research Articles

Stretch reflex gain scaling at the shoulder varies with synergistic muscle activity.

The unique anatomy of the shoulder allows for expansive mobility but also sometimes precarious stability. It has long been suggested that stretch-sensitive reflexes contribute to maintaining joint stability through feedback control, but little is known about how stretch-sensitive reflexes are coordinated between the muscles of the shoulder. The purpose of this study was to investigate the coordination of stretch reflexes in shoulder muscles elicited by rotations of the glenohumeral joint. We hypothesized that stretch reflexes are sensitive to not only a given muscle's background activity but also the aggregate activity of all muscles crossing the shoulder based on the different groupings of muscles required to actuate the shoulder in three rotational degrees of freedom. We examined the relationship between a muscle's background activity and its reflex response in eight shoulder muscles by applying rotational perturbations while participants produced voluntary isometric torques. We found that this relationship, defined as gain scaling, differed at both short and long latencies based on the direction of voluntary torque generated by the participant. Therefore, gain scaling differed based on the aggregate of muscles that were active, not just the background activity in the muscle within which the reflex was measured. Across all muscles, the consideration of torque-dependent gain scaling improved model fits (ΔR2) by 0.17 ± 0.12. Modulation was most evident when volitional torques and perturbation directions were aligned along the same measurement axis, suggesting a functional role in resisting perturbations among synergists while maintaining task performance.NEW & NOTEWORTHY Careful coordination of muscles crossing the shoulder is needed to maintain the delicate balance between the joint's mobility and stability. We provide experimental evidence that stretch reflexes within shoulder muscles are modulated based on the aggregate activity of muscles crossing the joint, not just the activity of the muscle in which the reflex is elicited. Our results reflect coordination through neural coupling that may help maintain shoulder stability during encounters with environmental perturbations.

Voluntary suppression of neck reflexes during passive head-on-trunk rotations: reflex gain control versus proprioceptive feedback.

Normal subjects can completely eliminate resistance upon imposed head-on-trunk rotations when they are asked to relax. It is not, however, clear how neck reflexes to stretch can be voluntarily suppressed. Reflexive responses might be modified by adjusting the gain of the reflex loop through descending control. Theoretically, necessary corrections upon interfering disturbances during coordinated motor performance requiring the interplay of relaxation/activation may be missing if muscle relaxation is taking place exclusively by this mechanism. It has been alternatively proposed that sensory information from the periphery may be allowed to "neutralize" neck reflexes if it is fed back with opposite sign to the structures driving the reflexes. Six healthy subjects were asked to relax while subjected to head-on-trunk rotations generated by a head motor. After any initial resistance had completely subsided, the head was unexpectedly exposed to "ramp-and-hold" perturbations of up to 2° amplitude and 0.7 s duration. Resistance to stretch consistently reappeared thereupon, suggesting that stretch reflex gain had not been set to zero during the previously achieved complete relaxation. Resistance to perturbations under these circumstances was compared with the forces generated when the same ramp-and-hold displacements were delivered unpredictably to the head held stationary. A quantitative model of neck proprioceptive reflexes suppression has been thus constructed. Gain scheduling or "motor set" cannot sufficiently account for the voluntary reflex suppression during slow passive head rotations. Instead, we propose as underlying mechanism, the "neutralization" of the controlling servo by means of continuous feedback tracking displacement and force signals from the periphery.NEW & NOTEWORTHY Head stabilizing neck reflexes can be voluntarily suppressed or activated depending on the task at hand. By applying brief perturbations unexpectedly, both during passive head-on-trunk movements and at rest, we investigated the mechanism of voluntary suppression of resistance to stretch. A physiologically plausible, neuromechanical model of voluntary/reflexive interactions was constructed favoring feedback over reflex gain adjustments. Accordingly, muscle relaxation during imposed head movements is based on sensory feedback similarly to muscle contractions during purposeful movements.

Characterization of Differences in the Time Course of Reflex and Voluntary Responses Following Botulinum Toxin Injections in Chronic Stroke Survivors.

Spasticity is a major impairment that can occur following a hemispheric stroke and is often treated with injections of botulinum toxin, a neurotoxin that impairs transmission at the neuromuscular junction. Hyperreflexia is a defining feature of spasticity. Our main objective here was to quantify the time course of changes in the deep tendon reflex (DTR) responses and voluntary activation capacity following BT injection as well as to track changes in a clinical assessment of spasticity. Four chronic stroke survivors, scheduled to receive BT in their Biceps Brachii(BB) as part of their clinical care plan, were recruited for repeated testing sessions over the course of 4 months post injection. Both surface BB EMG reflex response to bicipital tendon taps as well as signals of applied tendon tap forces were recorded before and up to 18 weeks post-BT. Voluntary force and biceps EMG signals were also recorded during maximum voluntary (isometric) contractions (MVC) at each testing session. Our results show major reductions (up to 75%) in voluntary sEMG and force arising between 11 to 35 days post-BT-injection. The stretch reflex gain declined two weeks after the maximal reductions in voluntary EMG and force. Paradoxically, there was a short-term increase in stretch reflex gain, in three out of four participants, approximately 11-35 days post BT. The time course of recovery of voluntary MVC and reflex responses varied considerably with a longer recovery time for the reflex responses.

Effects of stretch reflex on back muscle response during sinusoidal whole body vibration in sitting posture: A model study

This study seeks to examine human vibration response using a musculoskeletal model that appropriately considers stretch reflex. The stretch reflex is modeled with a feedback control approach, and integrated into a generic musculoskeletal model to study the active muscle forces during seated whole body vibration. The model is used to investigate the effects of stretch reflex gain, vibration frequency and vibration magnitude on transmissibility from the seat to upper body and lower body and on muscle activations.The overall model is validated by comparison with thoracic and lumbar muscle activities measured in human participants during whole body vibration. The simulation results were consistent with the experimental results that the peak transmissibility occurred at resonance frequency of 5–6 Hz, and were in line with other experimental studies that found a primary resonance of 4–6 Hz. Furthermore, the peak normalized Electromyography (EMG) level accorded with the activation level for both thoracic and lumbar regions. What's more, an increase of primary resonance frequency was observed with increasing gains of stretch reflex. In contrary, the peak seat transmissibility of the upper body and lower body had a significant reduction.The major contribution of this model is that the proposed stretch reflex model provides a useful method to consider muscle active response in whole body vibration simulation. This may be used in future studies to better understand how stretch reflex affects spinal loading in a variety of conditions.

Muscle disuse caused by botulinum toxin injection leads to increased central gain of the stretch reflex in the rat.

Botulinum toxin (Btx) is used in children with cerebral palsy and in other neurological patients to diminish spasticity and reduce the risk of development of contractures. We investigated changes in the central gain of the stretch reflex circuitry in response to Btx injection in the triceps surae muscle in rats. Experiments were performed in 21 rats. Eight rats were a control group, and 13 rats were injected with 6 IU of Btx in the left triceps surae muscle. Two weeks after Btx injection, larger monosynaptic reflexes (MSR) were recorded from the left (injected) than the right (noninjected) L4 + L5 ventral roots following stimulation of the corresponding dorsal roots. A similar increase on the left side was observed in response to stimulation of descending motor tracts, suggesting that increased excitability of spinal motor neurons may at least partly explain the increased reflexes. However, significant changes were also observed in postactivation depression of the MSR, suggesting that plastic changes in transmission from Ia afferent to the motor neurons also may be involved. The data demonstrate that muscle paralysis induced by Btx injection is accompanied by plastic adaptations in the central stretch reflex circuitry, which counteract the antispastic effect of Btx.NEW & NOTEWORTHY Injection of botulinum toxin into ankle muscles causes increased gain of stretch reflex. This is caused by adaptive changes in regulation of transmitter release from Ia afferents and increased excitability of spinal motor neurons.

Impaired H-Reflex Gain during Postural Loaded Locomotion in Individuals Post-Stroke

ObjectiveSuccessful execution of upright locomotion requires coordinated interaction between controllers for locomotion and posture. Our earlier research supported this model in the non-impaired and found impaired interaction in the post-stroke nervous system during locomotion. In this study, we sought to examine the role of the Ia afferent spinal loop, via the H-reflex response, under postural influence during a locomotor task. We tested the hypothesis that the ability to increase stretch reflex gain in response to postural loads during locomotion would be reduced post-stroke.MethodsFifteen individuals with chronic post-stroke hemiparesis and 13 non-impaired controls pedaled on a motorized cycle ergometer with specialized backboard support system under (1) seated supported, and (2) non-seated postural-loaded conditions, generating matched pedal force outputs of two levels. H-reflexes were elicited at 90°crank angle.ResultsWe observed increased H-reflex gain with postural influence in non-impaired individuals, but a lack of increase in individuals post-stroke. Furthermore, we observed decreased H-reflex gain at higher postural loads in the stroke-impaired group.ConclusionThese findings suggest an impaired Ia afferent pathway potentially underlies the defects in the interaction between postural and locomotor control post-stroke and may explain reduced ability of paretic limb support during locomotor weight-bearing in individuals post-stroke.SignificanceThese results support the judicious use of bodyweight support training when first helping individuals post-stroke to regain locomotor pattern generation and weight-bearing capability.

Mechanical and neural changes in plantar-flexor muscles after spinal cord injury in humans.

Cross-sectional study. To determine the effect of injury duration on plantar-flexor elastic properties in individuals with chronic spinal cord injury (SCI) and spasticity. National Rehabilitation Center for Persons with Disabilities, Japan. A total of 16 chronic SCI patients (age, 33±9.3 years; injury localization, C6-T12; injury duration, 11-371 months) participated. Spasticity of the ankle plantar-flexors was assessed using the Modified Ashworth Scale (MAS). The calf circumference and muscle thickness of the medial gastrocnemius (MG), lateral gastrocnemius and soleus were assessed using tape measure and ultrasonography. In addition, the ankle was rotated from 10° plantar-flexion to 20° dorsiflexion at 5 deg s(-1) with a dynamometer, and the ankle angle and torque were recorded. After normalizing the data (the initial points of angle and torque were set to zero), we calculated the peak torque and energy. Furthermore, angle-torque data (before and after normalization) were fitted with a second- and fourth-order polynomial, and exponential (Sten-Knudsen) models, and stiffness indices (SISOP, SIFOP, SISK) and AngleSLACK (the angle at which plantar-flexor passive torque equals zero) were calculated. The stretch reflex gain and offset were determined from 0-10° dorsiflexion at 50, 90, 120 and 150 deg s(-1). After logarithmic transformation, Pearson's correlation coefficients were calculated. MAS, calf circumference, MG thickness, peak torque and SIFOP significantly decreased with injury duration (r log-log=-0.63, -0.69, -0.63, -0.53 and -0.55, respectively, P<0.05). The peak torque and SIFOP maintained significant relationships even after excluding impacts from muscle morphology. Plantar-flexor elasticity in chronic SCI patients decreased with increased injury duration.

Characterizations of reflex and nonreflex changes in spastic multiple sclerosis

Spasticity, an increased resistance of a limb to movement, is associated with functional limitations and a major source of disability in neurological disorders, including multiple sclerosis (MS) and stroke. Despite the clinical significance of spasticity in brain and spinal cord injuries, it is often not clear whether the spasticity is due to reflex or non-reflex changes. Reflex and nonreflex properties of the human knee joint were studied in eight MS patients with spasticity and ten healthy subjects. A digitally controlled joint driving device was used to apply small-amplitude, and band-limited white-noise perturbations to the knee to manifest the reflex and nonreflex properties. The subjects were asked to maintain a steady level of background muscle torque during the perturbation. A nonlinear delay differential equation model was used to characterize the reflex and intrinsic properties of the knee in terms of phasic stretch reflex gain, tonic stretch reflex gain, joint elastic stiffness, and coefficient of viscosity. It was found that joint coefficient of viscosity and tonic stretch reflex gain of the spastic MS patients were significantly lower than those of normal controls. On the other hand, spastic MS patients showed higher phasic stretch reflex gains than normal controls and a trend of increased joint stiffness. Simultaneous characterizations of changes in tonic and phasic reflexes and nonreflex changes in joint elastic stiffness and viscosity in neurological disorders may help us gain insight into mechanisms underlying spasticity and develop impairment-specific treatment.

Simultaneous characterizations of reflex and nonreflex dynamic and static changes in spastic hemiparesis.

This study characterizes tonic and phasic stretch reflex and stiffness and viscosity changes associated with spastic hemiparesis. Perturbations were applied to the ankle of 27 hemiparetic and 36 healthy subjects under relaxed or active contracting conditions. A nonlinear delay differential equation model characterized phasic and tonic stretch reflex gains, elastic stiffness, and viscous damping. Tendon reflex was characterized with reflex gain and threshold. Reflexively, tonic reflex gain was increased in spastic ankles at rest (P < 0.038) and was not regulated with muscle contraction, indicating impaired tonic stretch reflex. Phasic-reflex gain in spastic plantar flexors was higher and increased faster with plantar flexor contraction (P < 0.012) than controls (P < 0.023) and higher in dorsi-flexors at lower torques (P < 0.038), primarily because of its increase at rest (P = 0.045), indicating exaggerated phasic stretch reflex especially in more spastic plantar flexors, which showed higher phasic stretch reflex gain than dorsi-flexors (P < 0.032). Spasticity was associated with increased tendon reflex gain (P = 0.002) and decreased threshold (P < 0.001). Mechanically, stiffness in spastic ankles was higher than that in controls across plantar flexion/dorsi-flexion torque levels (P < 0.032), and the more spastic plantar flexors were stiffer than dorsi-flexors at comparable torques (P < 0.031). Increased stiffness in spastic ankles was mainly due to passive stiffness increase (P < 0.001), indicating increased connective tissues/shortened fascicles. Viscous damping in spastic ankles was increased across the plantar flexion torque levels and at lower dorsi-flexion torques, reflecting increased passive viscous damping (P = 0.033). The more spastic plantar flexors showed higher viscous damping than dorsi-flexors at comparable torque levels (P < 0.047). Simultaneous characterizations of reflex and nonreflex changes in spastic hemiparesis may help to evaluate and treat them more effectively.

Neural correlates of task-related changes in physiological tremor

Appropriate control of muscle contraction requires integration of command signals with sensory feedback. Sensorimotor integration is often studied under conditions in which muscle force is controlled with visual feedback. While it is known that alteration of visual feedback can influence task performance, the underlying changes in neural drive to the muscles are not well understood. In this study, we characterize the frequency content of force fluctuations and neural drive when production of muscle force is target guided versus self guided. In the self-guided condition, subjects performed isometric contractions of the first dorsal interosseous (FDI) muscle while slowly and randomly varying their force level. Subjects received visual feedback of their own force in order to keep contractions between 6% and 10% of maximum voluntary contraction (MVC). In the target-guided condition, subjects used a display of their previously generated force as a target to track over time. During target tracking, force tremor increased significantly in the 3-5 and 7-9 Hz ranges, compared with self-guided contractions. The underlying changes in neural drive were assessed by coherence analysis of FDI motor unit activity. During target-guided force production, pairs of simultaneously recorded motor units showed less coherent activity in the 3-5 Hz frequency range but greater coherence in the 7-9 Hz range than in the self-guided contractions. These results show that the frequency content of common synaptic input to motoneurons is altered when force production is visually guided. We propose that a change in stretch-reflex gain could provide a potential mechanism for the observed changes in force tremor and motor unit coherence.

Tonic Stretch Reflex Threshold as a Measure of Spasticity: Implications for Clinical Practice

Lance’s definition of spasticity states: (1) the excitability of the tonic stretch reflex threshold is the conceptual unit of measure of spasticity; (2) because spasticity is a velocity-dependent phenomenon, different velocities of stretch should be used to evaluate spasticity; and (3) measures should provide insight into the role of spasticity in disordered motor control. This article reviews studies of clinical and laboratory-based methods to evaluate spasticity. There is a lack of consensus regarding the conceptual unit that best captures spasticity. Several biomechanical variables and parameters such as stretch reflex gain, stretch reflex threshold, and/or suprathreshold phenomena are often measured alone or in combination without a unifying conceptual framework. Most studies do not establish links between spasticity and other motor deficits and adhere only partly to Lance’s definition. A promising alternative to current measures is offered by the lambda model that uses the tonic stretch reflex threshold as the descriptor of spasticity. The lambda model also provides a framework in which spasticity and the presence of disorders in muscle activation can be described and explained. We introduce a portable device to measure spasticity, based on the measurement of the tonic stretch reflex threshold, which is more closely related to Lance’s definition.

Reflex regulation of antagonist muscles for control of joint equilibrium position

A systems model of spinal neuro-musculo-skeletal system (alpha - gamma model) is developed to investigate the plausible roles of spinal proprioceptive feedback in movement control. The model is composed of a joint, a pair of antagonist muscles, length and velocity feedback from muscle spindle, as well as spinal stretch reflex, reciprocal inhibition and recurrent inhibition of Renshaw cells. A descending command modulates the background activation of alpha motoneuron pools in combination with these reflex activities. A static gamma command controls the fusimotor contraction of the spindle. Simulation results reveal that the equilibrium joint angle is linearly correlated to the level of static gamma fusimotor activity of the spindle for a wide range of external loading conditions and reflex gains, suggesting that these spinal reflexes may contribute to regulate the equilibrium position of the joint. Sensitivity analysis further shows that reflex gains and other central commands alter the quasi-linear relation in regular fashions. The reciprocal inhibition gain changes the slope of the linear theta(eq) - gamma curve; and the descending alpha excitation, the stretch reflex gain, and the external load all shift the theta(eq) - gamma curve in parallel. These results imply that reflex gains and descending alpha commands may be coordinated to maintain a unique theta(eq) - gamma curve while providing the flexibility to counteract external loads, to execute a movement, or to regulate additional muscle variables. Dynamic simulation suggests that control of a class of movements can be achieved with a triphasic, alpha pulse and a continuous gamma signal. The model study supports the notion of a dual strategy for controlling trajectories via a feedforward alpha command and for regulating the final equilibrium positions via a feedback gamma command.

Stretch reflex excitability of the anti-gravity ankle extensor muscle in elderly humans.

To examine whether the stretch reflex excitability of the soleus muscle changes with age, stretch reflexes at rest (REST) and during weak voluntary contractions (ACT) were elicited in 18 older and 14 younger subjects. The amplitude of the stretch reflex responses and gain, defined as the gradient of the regression line for the relation between stretch reflex responses against the angular velocity of the applied perturbation, were evaluated in each short-latency (M1) and two long-latency components (M2 and M3). It was found that in the older group, both the amplitude and gain of the M1 component did not change from the REST to the ACT conditions, whereas in the younger group both variables significantly increased from the REST to ACT conditions. The latency of the M1 component was significantly shorter under the REST condition (older vs. younger: 51.8 +/- 7.37 vs. 55.1 +/- 8.69 ms), while no group differences were found in those variables under the ACT condition, suggesting that the muscle-tendon complexes of SOL muscles of the older subjects were less elastic and had less slack, probably due to age-related histochemical alterations. Further, the Hoffman reflex (H-reflex), elicited during the REST condition in 10 older and 11 younger subjects showed no significant differences, suggesting that the soleus motoneuron response to the Ia input was comparable between the two subject groups. The histochemical alterations occurring with the ageing process might augment the short-latency stretch reflex in the SOL muscle without enhancement of motoneuronal excitability, and this effect might be masked when the muscle is voluntarily activated.

Stretch reflex gain in cat triceps surae muscles with compliant loads.

The triceps surae (TS) stretch reflex was measured in decerebrate cats during crossed extensor stimulation (tonic contractions) and after spinalization during rhythmic locomotor activity. The TS reflex force in response to a short pulse stretch measured during tonic contractions at low level of background activity was greater than when more background activity was present at the time of application of stretch. In contrast, the reflex force measured during rhythmic contractions was very small at low level of background force (flexion phase) and increased at moderate and high levels of background activity (extension phase). Thus, even in reduced preparations, a task modulation of the stretch reflex occurs. Throughout the experimental procedure, the torque motor used to stretch the muscles behaved like a spring of a preset compliance (from isometric to very compliant). A reflex model was used to simulate the responses obtained experimentally. The gain of the stretch reflex loop was estimated for each load condition and both behavioural tasks. The reflex loop gain was significantly larger as the compliance of the external load increased for both tonic and rhythmic contractions, although to a lesser extent in the phasically activated muscles. During rhythmic locomotor contractions the gain was less than 1, assuring stability of the system. In contrast, during tonic contractions against a compliant load the gain exceeded 1, consistent with the instability (oscillations, clonus) seen at times under these load conditions. However, the high gain and instability was only transient, since repeated stretch reduced the gain. Thus, non-linearities in the system assured vigorous responses at the onset of perturbations, but then weaker responses to ongoing perturbations to reduce the chance of feedback instability (clonus).

Interaction of pre-programmed control and natural stretch reflexes in human landing movements.

Pre-programmed mechanisms of motor control are known to influence the gain of artificially evoked stretch reflexes. However, their interaction with stretch reflexes evoked in the context of unimpeded natural movement is not understood. We used a landing movement, for which a stretch reflex is an integral part of the natural action, to test the hypothesis that unpredicted motor events increase stretch reflex gain. The unpredicted event occurred when a false floor, perceived to be solid, collapsed easily on impact, allowing the subjects to descend for a further 85 ms to a solid floor below. Spinal stretch reflexes were measured following solid floor contact. When subjects passed through the false floor en route to the solid floor, the amplitude of the EMG reflex activity was double that found in direct falls. This was not due to differences in joint rotations between these conditions. Descending pathways can modify H- and stretch-reflex gain in man. We therefore manipulated the time between the false and real floor contacts and hence the time available for transmission along these pathways. With 30 ms between floors, the enhancement of the reflex was extinguished, whereas with 50 ms between floors it reappeared. This excluded several mechanisms from being responsible for the doubling of the reflex EMG amplitude. It is argued that the enhanced response is due to the modulation of reflex gain at the spinal level by signals in descending pathways triggered by the false platform. The results suggest the future hypothesis that this trigger could be the absence of afferent signals expected at the time of false floor impact and that salient error signals produced from a comparison of expected and actual sensory events may be used to reset reflex gains.

Increased reflex activation of the peroneus longus following application of an ankle brace declines over time

Two experiments were performed to document the time-dependent characteristics of the peroneus longus short latency stretch reflex amplitude following application of an ankle brace. In Experiment 1, stretch reflexes were induced in 15 weightbearing subjects during an unbraced condition and braced condition. In Experiment 2, stretch reflexes were induced in 15 weightbearing subjects before and after 3 h of wearing the brace. In Experiment 1, the amplitude of the stretch reflex increased in the braced condition by about 25% relative to the non-braced condition ( p=0.006). In Experiment 2 the amplitude of the stretch reflex increased about 18% immediately after application of the brace relative to the non-braced condition ( p=0.037). After 3 h, the stretch reflex amplitude was not different from that of initial non-braced condition. Given the importance of the peroneus longus muscle in ankle complex stability, further attention should be directed to whether the increased stretch reflex gain can be exploited during rehabilitation from ankle complex injuries. The findings provide a framework by which the effect of ankle braces on ankle joint proprioception, muscle activation profiles and balance may be physiologically interpreted.

Reflex and intrinsic changes induced by fatigue of human elbow extensor muscles.

Fatigue-induced changes in intrinsic and reflex properties of human elbow extensor muscles and the underlying mechanisms for fatigue compensation were investigated. The elbow joint was perturbed using small-amplitude and pseudorandom movement patterns while subjects maintained steady levels of mean joint extension torque. Intrinsic and reflex properties were identified simultaneously using a nonlinear delay differential equation model. Intrinsic joint properties were characterized by measures of joint stiffness, viscous damping, and limb inertia and reflex properties characterized by measures of dynamic and static reflex gains. Fatigue was induced using 15 min of intermittent voluntary isometric (submaximal) exercise, and a rest period of 10 min was taken to allow the fatigued muscles to recover from acute fatigue effects. Identical experimental and data analysis procedures were used before and after fatigue. Our findings were that after fatigue, joint stiffness was significantly reduced at higher torque levels, presumably reflecting the reduced force-generating capacity of fatigued muscles. Conversely, joint viscosity was increased after fatigue potentially because of the reduced crossbridge detachment rate and prolonged relaxation associated with intracellular acidosis accompanying fatigue. Static stretch reflex gain decreased significantly at higher torque levels after fatigue, indicating that the isometric fatiguing exercise might be associated with a preferential change in properties of spindle chain fibers and bag(2) fibers. For matched pre- and postfatigue torque levels, dynamic reflexes contributed relatively more torque after fatigue, displaying higher dynamic reflex gains and larger dynamic electromyographic responses elicited by the controlled small-amplitude position perturbations. These changes appear to counteract the fatigue-induced reductions in joint stiffness and static reflex gain. The compensatory responses could be partly due to the effects of increasing the number of active motoneurons innervating the fatiguing muscles. This shift in operating point gave rise to significant compensation for the loss of contractile force. The compensation could also be due to fusimotor adjustment, which could make the dynamic reflex gain much less sensitive to fatigue than intrinsic stiffness. In short, the reduced contribution from intrinsic stiffness to joint torque was compensated by increased contribution from dynamic stretch reflexes after fatigue.

Adaptive changes in locomotor control after partial denervation of triceps surae muscles in the cat.

This report concerns a test of the hypothesis that gain in the stretch reflex pathway of cat medial gastrocnemius (MG) muscle during locomotion increases after denervation of its synergists, lateral gastrocnemius (LG), soleus (SOL) and plantaris (PL) muscles. In four cats, MG, tibialis anterior (TA) and vastus lateralis (VL) muscles were implanted with electromyogram (EMG) electrodes. The cats walked on a row of elevated pegs, some of which were spring-loaded and could be triggered to pop up at the moment of foot touchdown, rapidly dorsiflexing the foot. Pre-stretch EMG activity in MG as well as short-, medium- and long-latency responses to the dorsiflexions were compared before and after unilateral denervation of synergists. Short- and medium-latency responses of MG to perturbations increased in proportion to the increase in pre-stretch EMG in the days and weeks after partial denervation. This argues against an adaptive increase in stretch reflex gain independent of centrally generated extensor drive. Local anaesthesia of the skin of the paw did not significantly change the sizes of the stretch responses of MG before or after partial denervation. We conclude that pre-stretch EMG activity as well as stretch reflexes in MG muscle increased substantially after denervation of synergistic muscles. The data were consistent with an adaptive increase in central locomotor drive, causing more motoneuronal activity, which in turn resulted in an increase in the size of stretch reflexes.

Voluntary and reflex control of human back muscles during induced pain.

1. Back pain is known to change motor patterns of the trunk. The purpose of this study was to examine the motor output of the erector spinae (ES) muscles during pain in the lumbar region. First, their voluntary activation was assessed during flexion and re-extension of the trunk. Second, effects of cutaneous and muscle pain on the ES stretch reflex were measured, since increased stretch reflex gain has been suggested to underlie increased muscle tone in painful muscles. 2. The trunk movement and electromyographical (EMG) signals from the right and left ES during pain were compared with values before pain. Controlled muscle pain was induced by infusion of 5 % saline into the right lumbar ES. Cutaneous pain was elicited by mechanical or electrical stimulation of the dorsal lumbar skin. The stretch reflex was evoked by rapidly indenting the right lumbar ES with a servo-motor prodder. 3. The results from the voluntary task show that muscle pain decreased the modulation depth of ES EMG activity. This pattern was associated with a decreased range and velocity of motion of the painful body segment, which would normally serve to avoid further injury. Interestingly, when subjects overcame this guarding tendency and made exactly the same movements during pain as before pain, the EMG modulation depth was still reduced. The results seem to reconcile the controversy of previous studies, in which both hyper- and hypoactivity of back muscles in pain have been reported. 4. In the tapped muscle, the EMG response consisted of two peaks (latency 19.3 +/- 2.1 and 44.6 +/- 2.5 ms, respectively) followed by a trough. On the contralateral side the first response was a trough (26.2 +/- 3.2 ms) while the second (46.4 +/- 4.3 ms) was a peak, similar to the second peak on the tapped side. Cutaneous pain had no effect on the short-latency response but significantly increased the second response on the tapped side. Surprisingly, deep muscle pain had no effect on the stretch reflex. A short-latency reciprocal inhibition exists between the right and left human ES. 5. It is concluded that deep back pain does not influence the stretch reflexes in the back muscles but modulates the voluntary activation of these muscles.

H-REFLEX SIZE IN WEIGHT TRAINED OLD AND YOUNG ADULTS

1967 H-reflex size is lower in elite sprinters & volleyball players (1) and in rats following plyometric training (2), compared to controls. It is unknown if the elderly or young varsity power athletes who weight train have a lower H-reflex size than peers who do not weight train. A reduced stretch reflex gain may be detrimental due to the role of the stretch reflex in enhancing force output during ankle extension while walking, running or doing plyometric movements. Bilateral 1RM strength of the ankle extensor muscles, divided by body weight (BW), and soleus H-reflex size (Hmax/Mmax ratio) was measured in weight trained (minimum 2 yrs training) and not weight trained old (71±5.7 yrs, mean±SD) and young (24±4.2 yrs) subjects. (Table)TableOld subjects and young varsity athletes with greater muscle strength following regular weight training have a H-reflex size similar to age matched controls.