Muscle Stretch Velocity Research Articles

Applying Stretch to Evoke Hyperreflexia in Spasticity Testing: Velocity vs. Acceleration.

In neurological diseases, muscles often become hyper-resistant to stretch due to hyperreflexia, an exaggerated stretch reflex response that is considered to primarily depend on the muscle's stretch velocity. However, there is still limited understanding of how different biomechanical triggers applied during clinical tests evoke these reflex responses. We examined the effect of imposing a rotation with increasing velocity vs. increasing acceleration on triceps surae muscle repsonse in children with spastic paresis (SP) and compared the responses to those measured in typically developing (TD) children. A motor-operated ankle manipulator was used to apply different bell-shaped movement profiles, with three levels of maximum velocity (70, 110, and 150°/s) and three levels of maximum acceleration (500, 750, and 1,000°/s2). For each profile and both groups, we evaluated the amount of evoked triceps surae muscle activation. In SP, we evaluated two additional characteristics: the intensity of the response (peak EMG burst) and the time from movement initiation to onset of the EMG burst. As expected, the amount of evoked muscle activation was larger in SP compared to TD (all muscles: p < 0.001) and only sensitive to biomechanical triggers in SP. Further investigation of the responses in SP showed that peak EMG bursts increased in profiles with higher peak velocity (lateral gastrocnemius: p = 0.04), which was emphasized by fair correlations with increased velocity at EMG burst onset (all muscles: r > 0.33–0.36, p ≤ 0.008), but showed no significant effect for acceleration. However, the EMG burst was evoked faster with higher peak acceleration (all muscles p < 0.001) whereas it was delayed in profiles with higher peak velocity (medial gastrocnemius and soleus: p < 0.006). We conclude that while exaggerated response intensity (peak EMG burst) seems linked to stretch velocity, higher accelerations seem to evoke faster responses (time to EMG burst onset) in triceps surae muscles in SP. Understanding and controlling for the distinct effects of different biological triggers, including velocity, acceleration but also length and force of the applied movement, will contribute to the development of more precise clinical measurement tools. This is especially important when aiming to understand the role of hyperreflexia during functional movements where the biomechanical inputs are multiple and changing.

Diverse and complex muscle spindle afferent firing properties emerge from multiscale muscle mechanics.

Despite decades of research, we lack a mechanistic framework capable of predicting how movement-related signals are transformed into the diversity of muscle spindle afferent firing patterns observed experimentally, particularly in naturalistic behaviors. Here, a biophysical model demonstrates that well-known firing characteristics of mammalian muscle spindle Ia afferents - including movement history dependence, and nonlinear scaling with muscle stretch velocity - emerge from first principles of muscle contractile mechanics. Further, mechanical interactions of the muscle spindle with muscle-tendon dynamics reveal how motor commands to the muscle (alpha drive) versus muscle spindle (gamma drive) can cause highly variable and complex activity during active muscle contraction and muscle stretch that defy simple explanation. Depending on the neuromechanical conditions, the muscle spindle model output appears to 'encode' aspects of muscle force, yank, length, stiffness, velocity, and/or acceleration, providing an extendable, multiscale, biophysical framework for understanding and predicting proprioceptive sensory signals in health and disease.

Modification of Spastic Stretch Reflexes at the Elbow by Flexion Synergy Expression in Individuals With Chronic Hemiparetic Stroke

ObjectiveTo systematically characterize the effect of flexion synergy expression on the manifestation of elbow flexor stretch reflexes poststroke, and to relate these findings to elbow flexor stretch reflexes in individuals without neurologic injury. DesignControlled cohort study. SettingAcademic medical center. ParticipantsParticipants (N=20) included individuals with chronic hemiparetic stroke (n=10) and a convenience sample of individuals without neurologic or musculoskeletal injury (n=10). InterventionsParticipants with stroke were interfaced with a robotic device that precisely manipulated flexion synergy expression (by regulating shoulder abduction loading) while delivering controlled elbow extension perturbations over a wide range of velocities. This device was also used to elicit elbow flexor stretch reflexes during volitional elbow flexor activation, both in the cohort of individuals with stroke and in a control cohort. In both cases, the amplitude of volitional elbow flexor preactivation was matched to that generated involuntarily during flexion synergy expression. Main Outcome MeasuresThe amplitude of short- and long-latency stretch reflexes in the biceps brachii, assessed by electromyography, and expressed as a function of background muscle activation and stretch velocity. ResultsIncreased shoulder abduction loading potentiated elbow flexor stretch reflexes via flexion synergy expression in the paretic arm. Compared with stretch reflexes in individuals without neurologic injury, paretic reflexes were larger at rest but were approximately equal to control muscles at matched levels of preactivation. ConclusionsBecause flexion synergy expression modifies stretch reflexes in involved muscles, interventions that reduce flexion synergy expression may confer the added benefit of reducing spasticity during functional use of the arm.

Modeling of Stretch Reflex Activation Considering Muscle Type.

Although the stretch reflex plays an important role in spasticity, so far the stretch reflex has not been sufficiently investigated. Previous stretch reflex activation models have some limitations, whereby they are not able to predict outcomes of some stretch reflex cases and do not consider uneven distribution of muscle length and stretch velocity on reflex activation. The purpose of this study was: 1) to develop a modified stretch reflex activation model employing a new muscle length threshold and weighting factors for slow-twitch fiber and fast-twitch fiber, and 2) to validate the model using pendulum experiments of the lower and upper limbs. The new muscle length threshold was defined using the optimal muscle fiber length. Based on the optimal fiber length, the new threshold allows for prediction of the stretch reflex activation at muscle lengths shorter than have been possible with previous models. The muscle type weighting factors realized unequal contributions between the muscle length and stretch velocity. We proved the validity of the proposed reflex activation model by using pendulum tests to induce patellar tendon and biceps brachii reflexes. Unknown parameters employed in the proposed model were obtained by minimizing differences in motion obtained with the proposed model and experiments. The proposed model can predict stretch reflex activation at shorter muscle lengths. In addition, the proposed model reflected nonhomogeneous characteristics related to the unequal contributions between muscle length and stretch velocity. As a result, patellar tendon and biceps brachii reflex phenomena were shown to be predicted more accurately in this study.

Stretch speed-dependent myofiber damage and functional deficits in rat skeletal muscle induced by lengthening contraction.

Exercise involving lengthening contraction (LC) often results in delayed myofiber damage and functional deficits over the ensuing days. The present study examined whether the stretch speed of LC is a determinant of damage severity. Under isoflurane anesthesia, LC was repeatedly induced in rat ankle extensor muscles at different stretch speeds (angular velocities of 50, 100, 200, and 400 deg/sec) over a fixed stretch range of motion (90°). The number of muscle fibers labeled with Evans blue dye, a marker of muscle fiber damage associated with increased membrane permeability, increased with the angular velocity of LC (by 20% of all myofibers at 400 deg/sec). Muscle fibers with cross‐sectional areas in the range of 3600–4800 μm2, corresponding to type IIb fiber size, exhibited the most severe damage as revealed by the largest decrease in the number of fibers 3 days after LC at 200 deg/sec, suggesting that muscle damage occurred preferentially in type IIb myofibers. Isometric torque of dorsiflexion measured 2 days after LC decreased progressively with LC angular velocity (by 68% reduction at 400 deg/sec). The angular velocity of muscle stretch during LC is thus a critical determinant of the degree of damage, and LC appears to damage type IIb fibers preferentially, resulting in a disproportionate reduction in isometric torque. This LC response is an important consideration for the design of physical conditioning and rehabilitation regimens.

Effects of Dorisflexion Perturbation Velocity and Amplitude on Sex Comparisons of Soleus Spinal Stretch Reflexes

1133 Variability in velocity and amplitude of muscle stretch, and background EMG may contaminate spinal stretch reflex (SSR) data. Servo-controlled perturbation devices and EMG biofeedback have been used to control these factors. Spring-loaded perturbation devices and static muscle loading methods reduce experimental complexity, but may introduce measurement error. PURPOSE: To determine the efficacy of a springloaded dorsiflexion perturbation device (PD) designed to stretch the soleus and a static muscle loading method in evaluating sex differences in SSR latency and amplitude. METHODS: Subjects (20 males, 20 females) were seated with the hip and knee of the right leg at 90°, and the right foot on the PD. A static load was placed on the distal thigh via a custom device, resisting plantarflexion. The forefoot was placed on a block fixed to the PD such that plantarflexion brought the calcaneus out of contact with the PD. The static load was standardized at ∼15% soleus MVC. Ankle position was maintained at 90°, making the contraction isometric. SSR amplitude was standardized to the maximal soleus motor response (S/M ratio). RESULTS: While S/M ratio did not differ across sex (P>.05), SSR latency was significantly shorter in females (t38 = 2.16, p = .01). However, SSR latency and leg length were related (r = .57, p<.01), and the sex difference in SSR latency was not significant when variance in leg length was accounted for (ANCOVA;F1,37 = .03, p = .45). Due to inter-subject differences in angular inertia and the fact that the calcaneus was not in contact with the PD, perturbation amplitude varied from 2 to 7°, and perturbation velocity varied from 55 to 177°/s. Perturbation amplitude did not differ across sex, and was not related to S/M ratio (r = .06) or SSR latency (r = .20). Perturbation velocity was significantly greater in females, but was not significantly related to S/M ratio (r = .05) or SSR latency (r = .21). The sex difference in background soleus EMG was not significant, and did not demonstrate significant relationships with S/M ratio (r = .31) or SSR latency (r = .19). Activity of the tibialis anterior and knee fiexors and extensors was negligible. CONCLUSIONS: Though spring-loaded platforms and static loading mechanisms do introduce variation to perturbation characteristics between individuals, the effects on SSR characteristics are limited and do not have significant implications for group comparisons. Additionally, it is necessary to account for differences in the distance traveled by the neural impulse (leg length) when comparing SSR latencies between individuals. These results suggest that this methodology is effective for comparing SSR characteristics between groups.

Effects of Dorisflexion Perturbation Velocity and Amplitude on Sex Comparisons of Soleus Spinal Stretch Reflexes

1133 Variability in velocity and amplitude of muscle stretch, and background EMG may contaminate spinal stretch reflex (SSR) data. Servo-controlled perturbation devices and EMG biofeedback have been used to control these factors. Spring-loaded perturbation devices and static muscle loading methods reduce experimental complexity, but may introduce measurement error. PURPOSE: To determine the efficacy of a springloaded dorsiflexion perturbation device (PD) designed to stretch the soleus and a static muscle loading method in evaluating sex differences in SSR latency and amplitude. METHODS: Subjects (20 males, 20 females) were seated with the hip and knee of the right leg at 90°, and the right foot on the PD. A static load was placed on the distal thigh via a custom device, resisting plantarflexion. The forefoot was placed on a block fixed to the PD such that plantarflexion brought the calcaneus out of contact with the PD. The static load was standardized at ∼15% soleus MVC. Ankle position was maintained at 90°, making the contraction isometric. SSR amplitude was standardized to the maximal soleus motor response (S/M ratio). RESULTS: While S/M ratio did not differ across sex (P>.05), SSR latency was significantly shorter in females (t38 = 2.16, p = .01). However, SSR latency and leg length were related (r = .57, p<.01), and the sex difference in SSR latency was not significant when variance in leg length was accounted for (ANCOVA;F1,37 = .03, p = .45). Due to inter-subject differences in angular inertia and the fact that the calcaneus was not in contact with the PD, perturbation amplitude varied from 2 to 7°, and perturbation velocity varied from 55 to 177°/s. Perturbation amplitude did not differ across sex, and was not related to S/M ratio (r = .06) or SSR latency (r = .20). Perturbation velocity was significantly greater in females, but was not significantly related to S/M ratio (r = .05) or SSR latency (r = .21). The sex difference in background soleus EMG was not significant, and did not demonstrate significant relationships with S/M ratio (r = .31) or SSR latency (r = .19). Activity of the tibialis anterior and knee fiexors and extensors was negligible. CONCLUSIONS: Though spring-loaded platforms and static loading mechanisms do introduce variation to perturbation characteristics between individuals, the effects on SSR characteristics are limited and do not have significant implications for group comparisons. Additionally, it is necessary to account for differences in the distance traveled by the neural impulse (leg length) when comparing SSR latencies between individuals. These results suggest that this methodology is effective for comparing SSR characteristics between groups.

Neural control: novel evaluation of stretch reflex sensitivity.

We evaluated the stretch reflex activities of the elbow flexor and extensor muscles considering the relationship between the reflex electromyographic (EMG) responses and their corresponding standardized muscle stretch velocities. Specifically, muscular stretch velocity was estimated by using ultrasonograms. Stretch reflex EMG responses were elicited in the biceps brachii, brachioradialis and triceps brachii with a ramp-and-hold rotation at the elbow joint, which consisted of various angular velocities for the extension- or flexion-direction. The whole muscle stretch velocity induced by each ramp-and-hold rotation was calculated on the basis of fibre length changes associated with the elbow joint angle. A linear regression equation was fitted to the relation between the whole muscle stretch velocity and the reflex EMG responses, and the variables from the equation were used to quantify sensitivity of each reflex EMG component. The reflex EMG responses were increased as the ramp-and-hold rotational velocity increased. There were no significant differences in the recorded magnitudes of reflex EMG responses with equivalent joint rotational velocity between the brachioradialis and the triceps brachii medial head. These muscles showed the highest reflex responses in the flexor and extensor muscles, respectively. To the contrary, the reflex EMG response elicited by the standardized muscle stretches was significantly greater in the extensor muscles, indicating a higher reflex sensitivity. This was because of the lower muscle stretch velocity of the triceps brachii with an equivalent elbow joint rotation. The stretch reflex sensitivity in both the elbow flexor and extensor muscles might be regulated so as to make the reflex responses the same when the equivalent joint rotational velocity is applied to these muscles.

Two identified afferent neurones entrain a central locomotor rhythm generator

Sensory feedback can modulate the intensity and timing of the central rhythms underlying locomotion and adjust them to compensate for natural or experimental perturbations1–4. However, because of the complexity of the neural systems involved, the role of specific sense organs and the function of individual afferent neurones are poorly understood. The thoracic-coxal muscle receptor organ (TCMRO), a proprioceptor of the crayfish walking leg, has only two afferent neurones, the non-spiking S and T fibres. Their receptor potentials encode, respectively, the magnitude and velocity of receptor muscle stretch, which occurs during limb remotion (retraction). Rhythmically stretching the TCMRO entrains a central locomotor rhythm, produced by the thoracic ganglia, in which remotor and promotor motoneurones of the leg discharge in alternation. Intracellular stimulation of the S and T fibres can trigger promotor and remotor bursts, respectively. Here we propose a mechanism for proprioceptive entrainment in terms of the opposite feedback effects of these two afferents. The possible role of these effects in the feedback control of locomotion is also discussed.

Cerebellar cortical activity during stretch of antagonist muscles.

Single unit activity was recorded from the anterior lobe of the cerebellum during ramp and hold stretches of limb muscles in chloralose anesthetized cats. The activity of 95 "phasic" units showed a transient response during dynamic stretch of at least one muscle usually lasting for less than 350 ms following the stimulus onset. The activity of 59 phasic-tonic units was modified not only during dynamic stretch but also during the 1 s of maintained muscle length. All Purkinje cells, identified by their complex spikes, that responded to muscle stretch demonstrated exclusively phasic changes in discharge. Fourteen of 25 Purkinje cells (56%) responded to stretch of both antagonist muscles and these responses were always similar rather than reciprocal. From the 129 units without complex spikes, 70 demonstrated phasic discharge patterns whereas 59 had tonic responses. Seventy-five (59%) of these unidentified units revealed convergent responses to stretch of both antagonists, compared with 54 which responded to stretch of one muscle only. Of the unidentified units receiving convergent afferents from antagonist muscles, 62 (83%) had similar responses and only 13 (17%) had reciprocal reactions. There appeared to be no evidence that muscle afferents alone can induce reciprocal discharge patterns in Purkinje neurons of the cerebellar cortex. The firing frequency of some phasic-tonic units was correlated with both the velocity and amplitude of muscle stretch. No Purkinje cells were found with activity related to either velocity or amplitude of muscle stretch. One phasic and seven phasic-tonic unidentified units were activated at fixed latencies following trains of electrical stimulation applied to the thoracic spinal cord at frequencies exceeding 200 Hz, implying they were terminal portions of mossy fibers originating from direct spinocerebellar tracts. A few recordings of compound potentials were presumed to arise from the cerebellar glomeruli. The changing form of one of these potentials suggested that the glomerulus might be a site at which somatosensory peripheral information is modified by the cerebellar cortex.

Modification of spastic gait through mechanical damping

The effect of dissipative mechanical loads on spastic gait has been studied, to evaluate the feasibility of using mechanically damped orthoses to effect functional improvements in the gait of spastic patients. This concept is based on a hypothesis citing uninhibited, velocity-dependent stretch reflexes as a possible causal factor in spastic gait abnormalities, such as equinus and back-kneeing. In order to screen potential experimental subjects and to quantify velocity-dependent reflex behaviour, ankle rotation experiments and filmed gait analysis were performed. The results supported the existence of a velocity threshold. Orthosis simulation experiments were performed with one spastic subject, using a wearable, computer-controlled, electromechanical, below-knee orthosis simulator to apply a variety of damping loads to the ankle as the subject walked. Results indicated that appropriate damping can improve local joint kinematics. The damping causes a reduction in muscle stretch velocity which apparently results in reduced spastic reflex activity.

Activity patterns in individual hindlimb primary and secondary muscle spindle afferents during normal movements in unrestrained cats

1. Chronically implanted microelectrode wires in the L7 and S1 dorsal root ganglia were used to record unit activity from cat hindlimb primary and secondary muscle spindle afferents. Units could be reliably recorded for several days, permitting comparison of their activity with homonymous muscle EMG and length during a variety of normal, unrestrained movements. 2. The general observation was that among both primary and secondary endings there was a broad range of different patterns of activity depending on the type of muscle involved and the type of movement performed. 3. During walking, the activity of a given spindle primary was usually consistent among similar step cycles. However, the activity was usually poorly correlated with absolute muscle length, apparently unrealted to velocity of muscle stretch, and could change markedly for similar movements performed under different conditions. 4. Spindle activity modulation not apparently related to muscle length changes was assumed to be influenced by fusimotor activity. In certain muscles, this presumption leads to the conclusion that gamma-motoneurons may be activated out of phase with homonymous alpha-motoneurons as well as by more conventional alpha-gamma-motoneuron coactivation. 5. Simultaneous recordings of two spindle primary afferents from extensor digitorum longus indicated that spindles within the same muscle may differ considerably with respect to this presumed gamma-motoneuron drive. 6. Spindle secondary endings appeared to be predominantly passive indicators of muscle length during walking, but could demonstrate apparently strong fusimotor modulation during other motor activities such as postural changes and paw shaking. 7. Both primary and secondary endings were observed to undergo very rapid modulation of firing rates in response to presumed reflexly induced intrafusal contractions. 8. It is suggested that the pattern of fusimotor control of spindles may be tailored to the specific muscle and task being performed, rather than necessarily dominated by rigid alpha-gamma coactivation.