Initial Muscle Activity Research Articles

Precise cortical contributions to sensorimotor feedback control during reactive balance.

The role of the cortex in shaping automatic whole-body motor behaviors such as walking and balance is poorly understood. Gait and balance are typically mediated through subcortical circuits, with the cortex becoming engaged as needed on an individual basis by task difficulty and complexity. However, we lack a mechanistic understanding of how increased cortical contribution to whole-body movements shapes motor output. Here we use reactive balance recovery as a paradigm to identify relationships between hierarchical control mechanisms and their engagement across balance tasks of increasing difficulty in young adults. We hypothesize that parallel sensorimotor feedback loops engaging subcortical and cortical circuits contribute to balance-correcting muscle activity, and that the involvement of cortical circuits increases with balance challenge. We decomposed balance-correcting muscle activity based on hypothesized subcortically- and cortically-mediated feedback components driven by similar sensory information, but with different loop delays. The initial balance-correcting muscle activity was engaged at all levels of balance difficulty. Its onset latency was consistent with subcortical sensorimotor loops observed in the lower limb. An even later, presumed, cortically-mediated burst of muscle activity became additionally engaged as balance task difficulty increased, at latencies consistent with longer transcortical sensorimotor loops. We further demonstrate that evoked cortical activity in central midline areas measured using electroencephalography (EEG) can be explained by a similar sensory transformation as muscle activity but at a delay consistent with its role in a transcortical loop driving later cortical contributions to balance-correcting muscle activity. These results demonstrate that a neuromechanical model of muscle activity can be used to infer cortical contributions to muscle activity without recording brain activity. Our model may provide a useful framework for evaluating changes in cortical contributions to balance that are associated with falls in older adults and in neurological disorders such as Parkinson's disease.

Acute Responses Of A Drop-Set Session On Muscular Activation And Its Applicability In Resistance- Trained Individuals

We investigated whether performing repetitions to muscular failure (FAIL) during a drop-set would affect muscle activation in trained individuals. Twelve young men performed a drop-set session consisting of 3 sets of two intensity drops (80 to 60 and to 40% of one-repetition maximum [1-RM]) load in a leg press machine. Linear regression between the quadriceps femoris root mean square of surface electromyography (EMGRMS) was employed to observe the initial muscle activation (intercept) and its behavior over the repetitions (slope). The EMGRMS intercept of the first set decreased (p<0.05) according to load reduction (136.8±4.8 at 80%1-RM to 119.3±5.5 and 110.6±5.5 at 60 and 40%1-RM, respectively). Slopes different from zero (p<0.05) were observed at 80 and 60%1-RM during the first set. Remarkably, during the second and third sets, we observed an increased EMGRMS intercept at 60%1-RM (p<0.05), leading to non-significant (p>0.05) differences compared to 80%1-RM. The maximum initial muscle activation occurred at higher loads only, but low loads performed to FAIL may be necessary for increasing and maintaining muscle activation at higher loads. Understanding these acute responses may support coaches and athletes in optimizing strength training responses during drop-set sessions into their periodization.

A simulation-based study for optimizing proportional-integral-derivative controller gains for different control strategies of an active upper extremity model using experimental data

This study investigates the effect of PID controller gains, reaction time, and initial muscle activation values on active human model behavior while comparing three different control strategies. The controller gains and reaction delays were optimized using published experimental data focused on the upper extremity. The data describes the reaction of five male subjects in four tests based on two muscle states (relaxed and tensed) and two states of awareness (open and closed eye). The study used a finite element model of the left arm isolated from the Global Human Body Models Consortium (GHBMC) average male simplified occupant model for simulating biomechanical simulations. Major skeletal muscles of the arm were modeled as 1D beam elements and assigned a Hill-type muscle material. Angular position control, muscle length control, and a combination of both were used as a control strategy. The optimization process was limited to 4 variables; three Proportional-Integral-Derivative (PID) controller gains and one reaction delay time. The study assumed the relaxed and tensed condition require distinct sets of controller gains and initial activation and that the closed-eye simulations can be achieved by increasing the reaction delay parameter. A post-hoc linear combination of angle and muscle length control was used to arrive at the final combined control strategy. The premise was supported by variation in the controller gains depending on muscle state and an increase in reaction delay based on awareness. The CORA scores for open-eye relaxed, closed-eye relaxed, open-eye tensed, and closed-eye tensed was 0.95, 0.90, 0.95, and 0.77, respectively using the combined control strategy.

LaDIVA: A neurocomputational model providing laryngeal motor control for speech acquisition and production.

Many voice disorders are the result of intricate neural and/or biomechanical impairments that are poorly understood. The limited knowledge of their etiological and pathophysiological mechanisms hampers effective clinical management. Behavioral studies have been used concurrently with computational models to better understand typical and pathological laryngeal motor control. Thus far, however, a unified computational framework that quantitatively integrates physiologically relevant models of phonation with the neural control of speech has not been developed. Here, we introduce LaDIVA, a novel neurocomputational model with physiologically based laryngeal motor control. We combined the DIVA model (an established neural network model of speech motor control) with the extended body-cover model (a physics-based vocal fold model). The resulting integrated model, LaDIVA, was validated by comparing its model simulations with behavioral responses to perturbations of auditory vocal fundamental frequency (fo) feedback in adults with typical speech. LaDIVA demonstrated capability to simulate different modes of laryngeal motor control, ranging from short-term (i.e., reflexive) and long-term (i.e., adaptive) auditory feedback paradigms, to generating prosodic contours in speech. Simulations showed that LaDIVA's laryngeal motor control displays properties of motor equivalence, i.e., LaDIVA could robustly generate compensatory responses to reflexive vocal fo perturbations with varying initial laryngeal muscle activation levels leading to the same output. The model can also generate prosodic contours for studying laryngeal motor control in running speech. LaDIVA can expand the understanding of the physiology of human phonation to enable, for the first time, the investigation of causal effects of neural motor control in the fine structure of the vocal signal.

Human Response to Longitudinal Perturbations of Standing Passengers on Public Transport During Regular Operation.

This study investigates the response of standing passengers on public transport who experience balance perturbations during non-collision incidents. The objective of the study was to analyse the effects of the perturbation characteristics on the initial responses of the passengers and their ability to maintain their balance. Sled tests were conducted on healthy volunteers aged 33.8 ± 9.2 years (13 males, 11 females) standing on a moving platform, facilitating measurements of the initial muscle activity and stepping response of the volunteers. The volunteers were exposed to five different perturbation profiles representing typical braking and accelerating manoeuvres of a public transport bus in the forward and backward direction. The sequence of muscle activations in lower-extremity muscles was consistent for the perturbation pulses applied. For the three acceleration pulses combining two magnitudes for acceleration (1.5 and 3.0 m/s2) and jerk (5.6 and 11.3 m/s3), the shortest muscle onset and stepping times for the passengers to recover their balance were observed with the higher jerk value, while the profile with the higher acceleration magnitude and longer duration induced more recovery steps and a higher rate of safety-harness deployment. The tendency for a shorter response time was observed for the female volunteers. For the two braking pulses (1.0 and 2.5 m/s2), only the lower magnitude pulse allowed balance recovery without compensatory stepping. The results obtained provide a reference dataset for human body modelling, the development of virtual test protocols, and operational limits for improving the safety of public transportation vehicles and users.

Hard-wired Epimysial Recordings from Normal and Reinnervated Muscle Using a Bone-anchored Device.

A bone-anchored device was implanted trans-tibially in n = 8 sheep with a bipolar recording electrode secured epimysially to the peroneus tertius muscle. TMR was carried out in a single animal: the peroneus tertius was deinnervated and the distal portion of the transected nerve to the peroneus muscle was coapted to a transected nerve branch previously supplying the tibialis anterior muscle. For 12 weeks (TMR) or 19 weeks (standard procedure), epimysial muscle signals were recorded while animals walked at 2 km·h-1. After 19 weeks implantation following standard procedure, epimysial recording signal-to-noise ratio (SNR) was 18.7 dB (± 6.4 dB, 95% CI) with typical recordings falling in the range 10-25 dB. Recoveries in gait and muscle signals were coincident 6 weeks post-TMR; initial muscle activity was identifiable 3 weeks post-TMR though with low signal amplitude and signal-to-noise ratio compared with normal muscle recordings. Following recovery, muscle signals were recorded reliably over 19 weeks following implantation. In this study, targeted reinnervation was successful in parallel with bone-anchor implantation, with recovery identified 6 weeks after surgery.

Relationship Between Muscle Activation and Force Recovery Following Sustained Maximal Voluntary Isometric Contractions

Previously we observed dissociation of skeletal muscle activation and force recovery following sustained maximal voluntary isometric contractions (MVIC). Fatigue was specifically related to reduced muscle activation within bouts; yet, incomplete recovery of force between bouts occurred with maximal muscle activation, suggesting interference in excitation-contraction coupling. PURPOSE: to investigate time-dependency of nervous system recovery following MVIC. METHODS: Men (n=29) performed two bouts (B1, B2) of sustained handgrip MVIC preceded/followed by 10-min recovery periods. Force (dynamometer) and surface EMG (sEMG) from the brachioradialis (BR), flexor carpi radialis (FCR), flexor carpi ulnaris (FCU), and flexor digitorum profundus (FDP) were collected continuously (1000 Hz) during bouts. sEMG signals were band pass filtered, rectified, and integrated (iEMG), then normalized (nEMG) to initial B1 iEMG. Force and sEMG were analyzed at 0.5 second intervals every 15 seconds. RESULTS: Recovery (B2 initial force >90% of B1) response fell into two groups; recovered (R, n=13) and not recovered (NR; n=16). Force decreased similarly in B1 (R: 77%; NR: 78%) and B2 (R: 79%; NR: 80%), yet initial B2 force was less (22%) than B1 in NR. Fatigue progressed in two-phases; B1 fast-phase decreased more rapidly with slow phase inflection occurring earlier (60 sec; 35% initial force) in R compared to NR (90 sec; 26% initial force). In R, B2 had a similar rate of decline in force and inflection (60 sec; 32% initial force). NR B2 showed a similar rate of decline in force, but inflection occurred sooner (75 sec) at the same level of initial B1 force (22%). Muscle activation (iEMG) during B1 was reduced similarly in R and NR (R: BR: 68%; FCR: 63%; FCU: 73%; FDP: 75%; NR: BR: 61%; FCR: 67%; FCU: 43%; FDP: 57%). During B2, R and NR showed similar decreases as B1, but all muscles except FCR showed lower initial B2 muscle activation compared to B1. CONCLUSIONS: Fatigue manifested in two phases; fast and slow. Recovery of force following sustained MVIC appears to be related to initial rate of decline of force (fast phase) with earlier onset of phase two. Earlier onset of phase shift may be related to changes in external compressive force and blood flow through the muscle, reducing metabolic perturbation and reflex inhibition of activation.

Carbonic Anhydrase Inhibition Does Not Impact Force Generation or Fatigue Following Sustained Voluntary Maximal Isometric Contractions

BackgroundPreviously we observed a two‐phase decline in force generation during sustained maximal voluntary isometric contractions (MVIC) suggestive of impaired Ca2+ kinetics. Carbonic anhydrase inhibition (CAI) increases fatigue in vitro due to altered Ca2+ kinetics. CAI impairs sensory transmission in vivo, which could also impact fatigue. Our purpose was to investigate the muscle activation and fatigue response during sustained MVIC in vivo following CAI.MethodsFollowing provision of informed consent to participate in this University approved study, men (n=9) performed two bouts (B1, B2) of sustained handgrip MVICs preceded/followed by 10‐min recovery periods, with and without acetazolamide (A); CA inhibitor. Using repeated measures, randomized, crossover design, A (250 mg) or placebo were ingested 14, 8, and 2 hours prior to contractions. HR (Lead II ECG) and BP (auscultation) were collected throughout the 35‐minute experiment. Force (dynamometer) and surface EMG from the brachioradialis (BR), flexor carpi radialis (FCR), flexor carpi ulnaris (FCU), and flexor digitorum profundus (FDP) were collected continuously (1000 Hz) during bouts. sEMG signals were band pass filtered, rectified, and integrated (iEMG).ResultsBody weight (C: 87.3±18.6; A: 86.3±18.3 kg) decreased and urine pH (C: 5.57±0.43; A: 7.56±0.20) increased with A. Resting HR (C: 60±11; A: 60±10 b.min−1) and BP (C: 119±6/75±5; A: 120±7/75±6) were similar. Isometric force declined similarly in B1 and B2 respectively (C:76 and 81%; A:79 and 78%); yet B2 initial force was less than B1 (21%) with A. Fatigue progressed in two‐phases; fast phase (C B1: y=−0.38x+25.1 kg; A B1: y=−0.41x+26.8 kg; C B2: y=−0.28x+23.1 kg; A B2: y=−0.25+20.4 kg) and slow phase (C B1: y=−0.05x+11.2 kg; A B1: y=−0.06x+12.9 kg; C B2: y=−0.04x+9.9 kg; A B2: y=−0.03x+8.1 kg) were similar in B1 and B2. Slow‐phase inflection occurred at 45‐sec during B1 and 60‐sec during B2 in both treatments. Muscle activation (iEMG) showed a similar biphasic reduction in A (BR: 84%; FCR: 72%; FCU: 76%; FDP: 75%) and C (BR: 80%; FCR: 62%; FCU: 70%; FDP: 72%), as over 70% of this reduction was expressed in the initial 30–45 sec of B1. iEMG during B2 showed a similar pattern of decrease in both conditions. HR and BP increased rapidly during each bout and returned to pre‐contraction levels by 1‐min post contraction; this response was not altered by A.ConclusionsIn agreement with previous studies, A resulted in typical loss of body weight and elevated urine pH presumably due to increased urine output and Na+ excretion. CAI had no effect on initial force generation, muscle activation (iEMG), or fatigue response. The reduced recovery of force without a change in iEMG prior to B2 indicates that CAI may impact both feedback inhibition and recovery of excitation‐contraction following the initial bout.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Evaluation of electromyographic signals in children with bruxism before and after therapy with Melissa Officinalis L-a randomized controlled clinical trial.

[Purpose] Bruxism is a repetitive muscle activity involving the clenching or grinding of one’s teeth during sleep or waking hours. Melissa officinalis L. may be employed as a natural therapy due to the sedative, anxiolytic, anti-inflammatory, and anti-spasm properties of the chemical constituents of the essential oil obtained from its leaves. The aim of the present study was to evaluate electromyographic signals in the temporal muscle using the BiteStrip® test on children with sleep bruxism before and after therapy with Melissa officinalis L. [Subjects and Methods] The subjects were randomly allocated to two groups. Group 1 (n = 12) ingested a tincture containing Melissa officinalis L. for 30 days. Group 2 (n = 12) received a placebo solution with the same dose and frequency as Group 1. The Wilcoxon and Mann-Whitney tests were employed for statistical analysis. [Results] The sample was made up of 24 children aged 6 to 10 years. No statistically significant differences were found between initial and final muscle activity in either group or in an intergroup comparison. [Conclusion] Use of the Melissa officinalis L. tincture at the dose employed did not lead to a reduction in muscle activity in children with bruxism.

The early use of botulinum toxin in post-stroke spasticity: study protocol for a randomised controlled trial

BackgroundPatients surviving stroke but who have significant impairment of function in the affected arm are at more risk of developing pain, stiffness and contractures. The abnormal muscle activity, associated with post-stroke spasticity, is thought to be causally associated with the development of these complications. Treatment of spasticity is currently delayed until a patient develops signs of these complications.Methods/DesignThis protocol is for a phase II study that aims to identify whether using OnabotulinumtoxinA (BoNT-A) in combination with physiotherapy early post stroke when initial abnormal muscle activity is neurophysiologically identified can prevent loss of range at joints and improve functional outcomes.The trial uses a screening phase to identify which people are appropriate to be included in a double blind randomised placebo-controlled trial. All patients admitted to Sandwell and West Birmingham NHS Trust Hospitals with a diagnosis of stroke will be screened to identify functional activity in the arm. Those who have no function will be appropriate for further screening. Patients who are screened and have abnormal muscle activity identified on EMG will be given electrical stimulation to forearm extensors for 3 months and randomised to have either injections of BoNT-A or normal saline. The primary outcome measure is the action research arm test - a measure of arm function. Further measures include spasticity, stiffness, muscle strength and fatigue as well as measures of quality of life, participation and caregiver strain.Trial registrationsISRCTN57435427, EudraCT2010-021257-39, NCT01882556

Lip Competence in Class III Patients Undergoing Orthognathic Surgery: An Electromyographic Study

The aim of this study was to compare the presurgical and postsurgical electromyographic (EMG) activities of the lips in patients with skeletal Class III treated with combined orthognathic surgery and contrast these data with those obtained from a control group with skeletal Class I. Ten patients with skeletal Class III underwent the registration of EMG activity before an orthognathic surgical procedure and 4 months after surgery. The results were compared with a control group of 11 healthy patients with skeletal Class I and clinical and EMG lip competence. EMG activity was recorded from the upper orbicularis oris and mentalis muscles during swallowing, lips in contact (LC), and lips apart (LA) using bipolar surface electrodes. The competence condition was assessed by determining the difference in the EMG activity of the mentalis muscle (LC-LA ≤0 for lip competence). Patients with skeletal Class III showed greater EMG activity than the control group before and after surgery. Patients with skeletal Class III showed a significantly greater difference in LC-LA than the control group before surgery for the 2 muscles (P < .05). No significant difference was found between the skeletal Class III group after surgery and the control group for the mentalis muscle (P > .05). Four months after treatment with orthognathic surgery, patients with skeletal Class III and an initial muscle activity pattern of lip incompetence different from the control group (P < .05) showed EMG values compatible with lip competence. These values were similar to the control group.

An extended motor network generates beta and gamma oscillatory perturbations during development

This study examines the time course and neural generators of oscillatory beta and gamma motor responses in typically-developing children. Participants completed a unilateral flexion–extension task using each index finger as whole-head magnetoencephalography (MEG) data were acquired. These MEG data were imaged in the frequency-domain using spatial filtering and the resulting event-related synchronizations and desynchronizations (ERS/ERD) were subjected to voxel-wise statistical analyses to illuminate time–frequency specific activation patterns. Consistent with adult data, these children exhibited a pre-movement ERD that was strongest over the contralateral post-central gyrus, and a post-movement ERS response with the most prominent peak being in the contralateral precentral gyrus near premotor cortices. We also observed a high-frequency (∼80 Hz) ERS response that coincided with movement onset and was centered on the contralateral precentral gyrus, slightly superior and posterior to the beta ERS. In addition to pre- and post-central gyri activations, these children exhibited beta and gamma activity in supplementary motor areas (SMA) before and during movement, and beta activation in cerebellar cortices before and after movement. We believe the gamma synchronization may be an excellent candidate signal of basic cortical motor control, as the spatiotemporal dynamics indicate the primary motor cortex generates this response (and not the beta oscillations) which is closely yoked to the initial muscle activation. Lastly, these data suggest several additional neural regions including the SMA and cerebellum are involved in basic movements during development.

Application of singular spectrum-based change-point analysis to EMG-onset detection

While many approaches have been proposed to identify the signal onset in EMG recordings, there is no standardized method for performing this task. Here, we propose to use a change-point detection procedure based on singular spectrum analysis to determine the onset of EMG signals. This method is suitable for automated real-time implementation, can be applied directly to the raw signal, and does not require any prior knowledge of the EMG signal’s properties. The algorithm proposed by Moskvina and Zhigljavsky (2003) was applied to EMG segments recorded from wrist and trunk muscles. Wrist EMG data was collected from 9 Parkinson’s disease patients with and without tremor, while trunk EMG data was collected from 13 healthy able-bodied individuals. Along with the change-point detection analysis, two threshold-based onset detection methods were applied, as well as visual estimates of the EMG onset by trained practitioners. In the case of wrist EMG data without tremor, the change-point analysis showed comparable or superior frequency and quality of detection results, as compared to other automatic detection methods. In the case of wrist EMG data with tremor and trunk EMG data, performance suffered because other changes occurring in these signals caused larger changes in the detection statistic than the changes caused by the initial muscle activation, suggesting that additional criteria are needed to identify the onset from the detection statistic other than its magnitude alone. Once this issue is resolved, change-point detection should provide an effective EMG-onset detection method suitable for automated real-time implementation.

Temporal Evolution of “Automatic Gain-Scaling”

The earliest neural response to a mechanical perturbation, the short-latency stretch response (R1: 20-45 ms), is known to exhibit "automatic gain-scaling" whereby its magnitude is proportional to preperturbation muscle activity. Because gain-scaling likely reflects an intrinsic property of the motoneuron pool (via the size-recruitment principle), counteracting this property poses a fundamental challenge for the nervous system, which must ultimately counter the absolute change in load regardless of the initial muscle activity (i.e., show no gain-scaling). Here we explore the temporal evolution of gain-scaling in a simple behavioral task where subjects stabilize their arm against different background loads and randomly occurring torque perturbations. We quantified gain-scaling in four elbow muscles (brachioradialis, biceps long, triceps lateral, triceps long) over the entire sequence of muscle activity following perturbation onset-the short-latency response, long-latency response (R2: 50-75 ms; R3: 75-105 ms), early voluntary corrections (120-180 ms), and steady-state activity (750-1250 ms). In agreement with previous observations, we found that the short-latency response demonstrated substantial gain-scaling with a threefold increase in background load resulting in an approximately twofold increase in muscle activity for the same perturbation. Following the short-latency response, we found a rapid decrease in gain-scaling starting in the long-latency epoch ( approximately 75-ms postperturbation) such that no significant gain-scaling was observed for the early voluntary corrections or steady-state activity. The rapid decrease in gain-scaling supports our recent suggestion that long-latency responses and voluntary control are inherently linked as part of an evolving sensorimotor control process through similar neural circuitry.

P105 A comparison of hamstring and patellar bone tendon autografts for ACL reconstruction in terms of quantitative gait data

Despite the ongoing evolution of anterior cruciate ligament injury prevention methods, injury rates and the associated sex-disparity remain. Strategies capable of successfully countering key control parameters existent within the injury mechanism thus remain elusive. Forward dynamics model simulations afford an expedited means to study realistic injury causing scenarios, while controlling all facets of the movement control strategy. Utilizing these methods, the current study examined the potential for perturbations in key initial contact neuromuscular parameters to injure the anterior cruciate ligament during the stance phase of sidestep cutting maneuvers.Controlled experiments were performed on optimized and validated subject-specific forward dynamic musculoskeletal sidestep models generated from 10 male and 10 female data sets. Random perturbations (n = 5000) were applied to initial contact kinematic and muscle activation parameters in these baseline models and then to those with prescribed systematic modifications in initial hip and knee flexion, hip internal rotation and hip internal rotation velocity postures. The number of injuries via an isolated anterior tibial shear (>2000 N) or knee valgus load (>125 Nm) mechanism was determined for each of the seven model conditions and subsequently compared.Neuromuscular control perturbations produced peak stance phase (0–100 ms) knee valgus loads large enough to induce anterior cruciate ligament injury. Decreases and increases in combined initial contact hip and knee flexion postures and hip internal rotation velocity produced significant increases and decreases in these valgus-induced ACL injury rates respectively.Anterior cruciate ligament injury via a valgus load mechanism is more likely during sidestepping when landing in a more extended posture, or with increased hip external rotation velocity. The fact that injury rates are reduced when these control parameters are reversed suggests they should be central to ongoing prevention strategy developments.

Investigating isolated neuromuscular control contributions to non-contact anterior cruciate ligament injury risk via computer simulation methods

Background Despite the ongoing evolution of anterior cruciate ligament injury prevention methods, injury rates and the associated sex-disparity remain. Strategies capable of successfully countering key control parameters existent within the injury mechanism thus remain elusive. Forward dynamics model simulations afford an expedited means to study realistic injury causing scenarios, while controlling all facets of the movement control strategy. Utilizing these methods, the current study examined the potential for perturbations in key initial contact neuromuscular parameters to injure the anterior cruciate ligament during the stance phase of sidestep cutting maneuvers. Methods Controlled experiments were performed on optimized and validated subject-specific forward dynamic musculoskeletal sidestep models generated from 10 male and 10 female data sets. Random perturbations ( n = 5000) were applied to initial contact kinematic and muscle activation parameters in these baseline models and then to those with prescribed systematic modifications in initial hip and knee flexion, hip internal rotation and hip internal rotation velocity postures. The number of injuries via an isolated anterior tibial shear (>2000 N) or knee valgus load (>125 Nm) mechanism was determined for each of the seven model conditions and subsequently compared. Findings Neuromuscular control perturbations produced peak stance phase (0–100 ms) knee valgus loads large enough to induce anterior cruciate ligament injury. Decreases and increases in combined initial contact hip and knee flexion postures and hip internal rotation velocity produced significant increases and decreases in these valgus-induced ACL injury rates respectively. Interpretation Anterior cruciate ligament injury via a valgus load mechanism is more likely during sidestepping when landing in a more extended posture, or with increased hip external rotation velocity. The fact that injury rates are reduced when these control parameters are reversed suggests they should be central to ongoing prevention strategy developments.

Threshold control of motor actions prevents destabilizing effects of proprioceptive delays

It is usually assumed that proprioceptive feedback comes to motoneurons too late to contribute to the initial activity of agonist muscles during fast arm movements, leading to the suggestion that this feedback is only efficient in slow movements and postural control. The argument does not take into account that the changes in the motoneuronal membrane potentials and the associated changes in the state of spinal neurons preceding the initial activity of muscles deeply affect, in a forward way, the state of reflex systems by shifting their thresholds, as suggested in the lambda model for motor control. As a result, the initial muscle activity emerges with full contribution of these systems so that the effects of reflex delays become negligible. We tested the hypothesis that threshold control of muscle activation may be instrumental in preventing destabilizing effects of proprioceptive delays in spinal and trans-cortical pathways to motoneurons. The analysis was made by recording fast elbow movements (peak velocity approximately 300-500 degrees/s) and simulating them in a dynamic model that incorporates the notion of threshold control of intrinsic and reflex muscle properties. The model was robust in reproducing experimental movement patterns (R (2)>0.95). It generated stable output despite substantial proprioceptive (up to 100 ms) and electromechanical (40 ms) delays. Stability was thus ensured for delays not only in segmental (about 25-50 ms) but also in trans-cortical loops (50-70 ms). Our study illustrates that a natural physiological process--threshold control--may manifest feed-forward properties hitherto attributed to hypothetical internal neural models.

Muscle Activation Deficits During Fatigue after Limb Disuse

1890 PURPOSE: To determine the extent of plantarflexor muscle activation deficits during fatigue in patients after immobilization. METHODS: Six patients with surgically stabilized, unilateral ankle fractures and 6 healthy subjects participated. Patients were immobilized for 8 weeks, followed by 10 weeks of rehabilitation. Isometric plantarflexion torque was measured at 1 week (1w-R), 5 weeks (5w-R) and 10 weeks (10w-R) of rehabilitation. Subjects performed maximal voluntary isometric contractions (MVIC) with burst superimposition (100ms; 100pps) to assess muscle activation. Fatigue testing involved a 90 second, sustained MVIC of the plantarflexors, with burst superimposition at the beginning, middle, and end. Muscle activation was quantified using the central activation ratio (CAR), which was calculated by dividing the maximum voluntary force by the maximum force produced with electrical stimulation. A CAR of 1.0 indicates full muscle activation by the central nervous system. A fatigue index (final/initial force) was used quantify the extent of muscle fatigue. T-tests were used for all comparisons. RESULTS: At 1 wk-R, the involved leg fatigued less than 5%, while the uninvolved leg fatigued almost 50% (p<0.05). At 5w-R and 10w-R, the involved leg fatigued between 20 and 25%. During the nonfatigued state at 1wk-R, there were significant differences in muscle activation between the involved and uninvolved limbs (CAR = 0.98 vs. 0.79) (p<0.05), which resolved by 5w-R (0.93) and 10w-R (0.96). Decreases in CAR during the fatigue test were minimal (<0.1) for all subjects for both the involved and uninvolved legs. Torque deficits present in the involved legs at 1w-R, recovered to normal by 10w-R (p<0.05). CONCLUSION: Patients experienced less muscle fatigue in their involved leg, early after limb disuse. Fatigability did not recover to normal levels even after 10 weeks of rehabilitation, despite the complete restoration of torque and muscle activation deficits. Initial muscle activation deficits can only account for some of the decreased fatigue in patients early after limb disuse because activation deficits resolved by 5w-R. Clinically, these results suggest that traditional measures of strength may not completely reflect the resolution of a patient's impairments. Supported by NIH-RO1HD37645, NIHRO1HD40850, 2P41RR02305.

Muscle Activation Deficits During Fatigue after Limb Disuse

1890 PURPOSE: To determine the extent of plantarflexor muscle activation deficits during fatigue in patients after immobilization. METHODS: Six patients with surgically stabilized, unilateral ankle fractures and 6 healthy subjects participated. Patients were immobilized for 8 weeks, followed by 10 weeks of rehabilitation. Isometric plantarflexion torque was measured at 1 week (1w-R), 5 weeks (5w-R) and 10 weeks (10w-R) of rehabilitation. Subjects performed maximal voluntary isometric contractions (MVIC) with burst superimposition (100ms; 100pps) to assess muscle activation. Fatigue testing involved a 90 second, sustained MVIC of the plantarflexors, with burst superimposition at the beginning, middle, and end. Muscle activation was quantified using the central activation ratio (CAR), which was calculated by dividing the maximum voluntary force by the maximum force produced with electrical stimulation. A CAR of 1.0 indicates full muscle activation by the central nervous system. A fatigue index (final/initial force) was used quantify the extent of muscle fatigue. T-tests were used for all comparisons. RESULTS: At 1 wk-R, the involved leg fatigued less than 5%, while the uninvolved leg fatigued almost 50% (p<0.05). At 5w-R and 10w-R, the involved leg fatigued between 20 and 25%. During the nonfatigued state at 1wk-R, there were significant differences in muscle activation between the involved and uninvolved limbs (CAR = 0.98 vs. 0.79) (p<0.05), which resolved by 5w-R (0.93) and 10w-R (0.96). Decreases in CAR during the fatigue test were minimal (<0.1) for all subjects for both the involved and uninvolved legs. Torque deficits present in the involved legs at 1w-R, recovered to normal by 10w-R (p<0.05). CONCLUSION: Patients experienced less muscle fatigue in their involved leg, early after limb disuse. Fatigability did not recover to normal levels even after 10 weeks of rehabilitation, despite the complete restoration of torque and muscle activation deficits. Initial muscle activation deficits can only account for some of the decreased fatigue in patients early after limb disuse because activation deficits resolved by 5w-R. Clinically, these results suggest that traditional measures of strength may not completely reflect the resolution of a patient's impairments. Supported by NIH-RO1HD37645, NIHRO1HD40850, 2P41RR02305.

Intent-Related Differences in Surface EMG of Maximum Eccentric and Concentric Contractions

For this study it was hypothesized that when participants intended to perform a maximum voluntary concentric (or eccentric) contraction but had an eccentric (or concentric) contraction imposed upon them, the initial EMG measured during the isometric phase preceding the onset of the dynamometer motion would reflect the intended contraction condition. The surface EMG of the vastus lateralis muscle was measured in 24 participants performing isokinetic concentric and eccentric maximum voluntary knee extensor contractions. The contractions were initiated from rest and from the same knee flexion angle and required the same level of external force to trigger the onset of dynamometer motion. Vastus lateralis EMG were quantified during the isometric phase preceding the onset of the dynamometer motion. When participants intended to perform a concentric contraction but had an eccentric contraction imposed upon them, the initial EMG resembled that of a concentric contraction. When they intended to perform an eccentric contraction but had a concentric contraction imposed upon them, the initial EMG resembled that of an eccentric contraction. Overall, the difference between concentric and eccentric contractions observed during the period of the initial muscle activation implies that descending signals include information that distinguishes between eccentric and concentric contractions.