Effect of combined electrical stimulation and brief muscle lengthening on torque development.

This study aimed to evaluate torque production in response to the application of a brief muscle lengthening during neuromuscular electrical stimulation (NMES) applied over the posterior tibial nerve. Fifteen participants took part in three experimental sessions, where wide-pulse NMES delivered at 20 and 100 Hz (pulse duration of 1 ms applied during 15 s at an intensity evoking 5-10% of maximal voluntary contraction) was either applied alone (NMES condition) or in combination with a muscle lengthening at three distinct speeds (60, 180, or 300°/s; NMES + LEN condition). The torque-time integral (TTI) and the muscle activity following the stimulation trains [sustained electromyography (EMG)] were calculated for each condition. Results show that TTI and sustained EMG activity were higher for the NMES + LEN condition only when using 100-Hz stimulation, regardless of the lengthening speed (P = 0.029 and P = 0.007 for the two parameters, respectively). This indicates that superimposing a muscle lengthening to high-frequency NMES can enhance the total torque production, partly due to neural mechanisms, as evidenced by the higher sustained EMG activity. This finding has potential clinical relevance, especially when it comes to finding ways to enhance torque production to optimize the effectiveness of NMES training programs.NEW & NOTEWORTHY This study showed, for the first time, that the combined application of a brief muscle lengthening and wide-pulse neuromuscular electrical stimulation (NMES) delivered over the posterior tibial nerve can entail increased torque production as compared with the sole application of NMES. This observation, present only for high stimulation frequencies (100 Hz) and independently of the lengthening speed, is attributed to neural mechanisms, most probably related to increased afferents' solicitation, although muscular phenomena cannot be excluded.

Specific modulation of presynaptic and recurrent inhibition of the soleus muscle during lengthening and shortening submaximal and maximal contractions.

The study analyzed neural mechanisms mediating spinal excitability modulation during eccentric (ECC) movement (passive muscle lengthening, submaximal, and maximal ECC contractions) as compared with concentric (CON) conditions. Twenty-two healthy subjects participated in three experiments. Experiment A (n = 13) examined D1 presynaptic inhibition (D1 PI) and recurrent inhibition (RI) modulation during passive muscle lengthening and shortening, by conditioning the soleus (SOL) H-reflex with common peroneal nerve submaximal and tibial nerve maximal stimulation, respectively. Experiment B (n = 13) analyzed the effect of passive muscle lengthening on D1 PI and heteronymous Ia facilitation (HF, conditioning the SOL H-reflex by femoral stimulation). Experiment C (n = 13) focused on the effect of muscle contraction level (20%, 50%, and 100% of maximal voluntary contraction) on D1 PI and RI. Results showed a significantly higher level of D1 PI during passive muscle lengthening than shortening (P < 0.01), whereas RI and HF were not affected by passive muscle movement. D1 PI and RI were both higher during ECC as compared with CON contractions (P < 0.001). However, the amount of D1 PI was independent of the torque level, whereas RI was reduced as the torque level increased (P < 0.05). The decreased spinal excitability induced by muscle lengthening during both passive and active conditions is mainly attributed to D1 PI, whereas RI also plays a role in the control of the specific motoneuron output during ECC contractions. Both inhibitory mechanisms are centrally controlled, but the fact that they evolve differently with torque increases, suggests a distinct supraspinal control.NEW & NOTEWORTHY Presynaptic (PI) and recurrent inhibitions (RI) were studied during passive muscle lengthening and eccentric contractions. Results indicate that the increased PI during passive muscle lengthening accounts for the decreased spinal excitability at rest. During eccentric contraction both mechanisms contribute to spinal excitability modulation. The same amount of PI was observed during eccentric contractions, while RI decreased as developed torque increased. This distinct modulation according to torque level suggests a distinct supraspinal control of these mechanisms.

Mechanisms modulating spinal excitability after nerve stimulation inducing extra torque.

The study included three experiments aiming to examine the mechanisms responsible for spinal excitability modulation, as assessed by the H-reflex, following stimulation trains delivered at two different frequencies (20 and 100 Hz) inducing extra torque (ET). A first experiment (n = 15) was conducted to evaluate changes in presynaptic inhibition acting on Ia afferents induced by these electrical stimulation trains, assessed by conditioning the soleus H-reflex (tibial nerve stimulation) with stimulation of the common peroneal nerve (D1 inhibition) and of the femoral nerve (heteronymous Ia facilitation, HF). A second experiment (n = 12) permitted to investigate homosynaptic postactivation depression (HPAD) changes after the stimulation trains. A third experiment (n = 14) analyzed changes in motoneuron intrinsic properties after the stimulation trains, by electrically stimulating the descending corticospinal tract at the thoracic level, evoking thoracic motor-evoked potentials (TMEP). Main results showed that in all experiments, spinal excitability decreased after the 20-Hz train (P < 0.05), whereas this parameter significantly increased after the 100-Hz stimulation (P < 0.05). D1 and HF were not significantly modified after either stimulation. HPAD was significantly decreased only after the 20-Hz train, whereas TMEP was significantly increased only after the 100-Hz train (P < 0.05). It is concluded that the decreased spinal excitability observed after the 20-Hz train cannot be attributed to D1 presynaptic inhibition but rather to increased HPAD of the Ia afferents terminals, whereas the increase of this parameter obtained after the 100-Hz train can be assigned to changes in intrinsic motoneuron properties allowing to maintain Ia-α-motoneurons transmission efficacy.NEW & NOTEWORTHY Using different electrophysiological techniques, results show that the downregulation of spinal excitability observed after the 20-Hz train could be ascribed to homosynaptic postactivation depression of the Ia afferents terminals, whereas changes in intrinsic motoneuron properties could explain the increased spinal excitability observed after the 100-Hz train. A novel methodology for assessing soleus D1 presynaptic inhibition and heteronymous Ia facilitation, accounting for eventual modulations of test reflex amplitude throughout the session, was developed.

Impact of stimulation frequency on neuromuscular fatigue.

PURPOSE: The aim of the present study was to examine the frequency effects (20 Hz and 100 Hz) on neuromuscular fatigue using stimulation parameters favoring an indirect motor unit recruitment through the afferent pathway. METHODS: Nineteen subjects were divided into two groups: 20 Hz (n = 10) and 100 Hz (n = 9). The electrical stimulation session consisted of 25 stimulation trains (20 s ON/20 s OFF, pulse width: 1 ms) applied over the tibial nerve and delivered at an intensity evoking 10% maximal voluntary isometric contraction (MVIC). Before and after these protocols, MVIC was assessed, while neural changes were evaluated by the level of activation (VAL) and muscle changes were evaluated by the twitch associated with the maximal M-wave (Pt). For all stimulation trains, the real and the theoretical values of the torque-time integral (TTIr and TTIth, respectively) were calculated. The TTIr/TTIth ratio of the first train was calculated to evaluate the presence of extra torque. RESULTS: The main results showed a similar decrease in MVIC torque after both protocols accompanied by neural and muscle changes, as evidenced by the decrease in VAL and Pt. TTIr values across the 20-Hz trains remained constant, whereas they significantly decreased during the 100-Hz stimulation trains. The relative MVIC decrease was negatively correlated with TTIr/TTIth. CONCLUSION: Results give evidence of an identical neuromuscular fatigue development between protocols, while lower stimulation frequency permitted preservation of a given torque level during the stimulation trains. The negative correlation between this fatigue development and TTIr/TTIth suggests that extra torque production induces greater voluntary torque losses.

Torque gains and neural adaptations following low-intensity motor nerve electrical stimulation training.

The purpose of the study was to assess neural adaptations of the plantar-flexors induced by an electrical stimulation training applied over the motor nerve at low intensity using two different stimulation frequencies. Thirty subjects were randomly assigned into 3 groups: 20 Hz, 100 Hz, and control group. The training consisted of 15 sessions of 25 stimulation trains applied over the tibial nerve and delivered at an intensity evoking 10% maximal voluntary isometric contraction (MVIC). Before and after training, MVIC was assessed and neural adaptations were evaluated by the voluntary activation level (VAL) and the V-wave (normalized by the superimposed muscle compound action potential, V/MSUP). H-reflex and motor-evoked potential (MEP) recorded during MVIC were studied to assess spinal and corticospinal excitabilities [i.e., maximal H-reflex during maximal voluntary isometric contraction (HSUP)/MSUP and maximal motor-evoked potential during maximal voluntary isometric contraction (MEPSUP)/MSUP]. MVIC significantly increased after training only for the two training groups (P = 0.017). This increase was accompanied by a significant increase of VAL only for these groups (P = 0.014), whereas statistical analysis revealed a time effect for V/MSUP (P = 0.022). HSUP/MSUP and MEPSUP/MSUP were significantly increased at post conditions only for the 100 Hz group (P = 0.021 and P = 0.029). Results show that low-intensity electrical stimulation training applied over the motor nerve can induce torque gains, accompanied by neural adaptations. Stimulation frequency differentially affected spinal and corticospinal excitabilities, indicating that neural adaptations could have a supraspinal origin for the 20-Hz protocol, whereas spinal and supraspinal mechanisms were implicated in the torque increases after the 100-Hz training.NEW & NOTEWORTHY This study brings new insights into the neurophysiological mechanisms responsible for torque gains after electrical stimulation training using wide pulse duration and low stimulation intensity applied over the motor nerve. Stimulation frequency had a distinct impact on spinal and/or supraspinal origins of the observed neural adaptations. The use of the aforementioned stimulation parameters in rehabilitation settings can be proved beneficial in terms of strength gains while avoiding any serious discomfort because of stimulation.

Effect of reflexive activation of motor units on torque development during electrically-evoked contractions of the triceps surae muscle.

The aim of the study was to identify stimulation conditions permitting the occurrence of extra torque (ET) and to examine their impact on spinal and corticospinal excitabilities. Twelve subjects received stimulation trains over the tibial nerve (20 s duration, 1 ms pulse duration) that were delivered at 3 stimulation frequencies (20, 50, and 100 Hz) and at 5 intensities (110%, 120%, 130%, 140%, and 150% of the motor threshold). Torque-time integral (TTI) of each stimulation train was calculated. Spinal [maximum H-reflex (Hmax)/maximal M-wave (Mmax)] and corticospinal [maximal motor evoked potential amplitude (MEPmax)/Mmax] excitabilities were assessed at rest before and after each stimulation train by tibial nerve stimulation and by transcranial magnetic stimulation, respectively. Moreover, a twitch at each stimulation intensity was delivered before and after each stimulation train. The EMG activity associated with this twitch was analyzed to identify the initial motor unit (MU) recruitment pathway before each stimulation train and discriminate trials to H-trials (indirect recruitment) and M-trials (direct recruitment). TTI was higher for H-trials compared with M-trials for all tested frequencies. There was a decrease in Hmax/Mmax for the 20 Hz-H trials and an increase for the 100 Hz-H trials, whereas MEPmax/Mmax remained unchanged at post measurements. Present results demonstrate that the initial MU recruitment pattern plays a main role in the ET occurrence, with the indirect recruitment via the afferent volley being substantial for its development. The modulations of Hmax/Mmax without changes in MEPmax/Mmax suggest that the ET development affects spinal excitability and that these changes are frequency dependent. NEW & NOTEWORTHY This study brings new insights into the stimulation conditions permitting the development of extra torque. An initial indirect recruitment of motor units, inducing reflex activation of spinal neurons through Ia afferent solicitation, appears a prerequisite for extra torque development. Under these conditions, spinal excitability modulations were frequency dependent.

Cutaneous Recording and Stimulation of Muscles Using Organic Electronic Textiles.

Electronic textiles are an emerging field providing novel and non-intrusive solutions for healthcare. Conducting polymer-coated textiles enable a new generation of fully organic surface electrodes for electrophysiological evaluations. Textile electrodes are able to assess high quality muscular monitoring and to perform transcutaneous electrical stimulation.

Spinal and supraspinal mechanisms affecting torque development at different joint angles.

INTRODUCTION: We examined the neural mechanisms responsible for plantar flexion torque changes at different joint positions. METHODS: Nine subjects performed maximal voluntary contractions (MVC) at 6 ankle-knee angle combinations [3 ankle angles (dorsiflexion, anatomic position, plantar flexion) and 2 knee angles (flexion, full extension)]. Neural mechanisms were determined by V-wave, H-reflex (at rest and during MVC), and electromyography during MVC (RMS), normalized to the muscle compound action potential (V/Msup, Hmax/Mmax, Hsup Msup and RMS/Msup) and voluntary activation (VA), while muscle function was assessed by doublet amplitude. RESULTS: MVC and doublet amplitude were significantly lower at plantar flexion (P < 0.01), while VA was significantly lower at dorsiflexion and full knee extension (P < 0.05). V/Msup and RMS/Msup were significantly lower at knee extension (P < 0.01), while Hsup/Msup was not affected by joint angle. CONCLUSIONS: These results indicate that joint positions leading to muscle lengthening produce reduced neural drive, due mainly to supraspinal mechanisms.

Electrically induced torque decrease reflects more than muscle fatigue.

The aim of the study was to compare the fatigue induced by different electrical stimulation (ES) protocols. The triceps surae muscle of 8 healthy subjects was fatigued with 4 protocols (30 Hz-500 µs, 30 Hz-1 ms, 100 Hz-1 ms, and 100 Hz-500 µs), composed of 60 trains (4 s on-6 s off), delivered at an intensity evoking 30% of maximal voluntary contraction (MVC). Fatigue was quantified by ES and MVC torque decreases. The amplitude of the twitch delivered at the intensity and pulse width used in each fatiguing protocol (twitch at Istim ) was analyzed. All parameters decreased significantly after all protocols. The ES torque decrease correlated positively with the twitch decrease elicited at Istim only for the 30-Hz protocols. Results show that, during the 100-Hz protocols, phenomena not related to the fatigue of the solicited motor units may occur, including changes in the excitability threshold of the axonal terminal branches.

Neuromuscular fatigue is not different between constant and variable frequency stimulation.

This study compared fatigue development of the triceps surae induced by two electrical stimulation protocols composed of constant and variable frequency trains (CFTs, VFTs, 450 trains, 30 Hz, 167 ms ON, 500 ms OFF and 146 ms ON, 500 ms OFF respectively). For the VFTs protocol a doublet (100 Hz) was used at the beginning of each train. The intensity used evoked 30% of a maximal voluntary contraction (MVC) and was defined using CFTs. Neuromuscular tests were performed before and after each protocol. Changes in excitation-contraction coupling were assessed by analysing the M-wave [at rest (Mmax) and during MVC (Msup)] and associated peak twitch (Pt). H-reflex [at rest (Hmax) and during MVC (Hsup)] and the motor evoked potential (MEP) during MVC were studied to assess spinal and corticospinal excitability of the soleus muscle. MVC decrease was similar between the protocols (-8%, P<0.05). Mmax, Msup and Pt decreased after both protocols (P<0.01). Hmax/Mmax was decreased (P<0.05), whereas Hsup/Msup and MEP/Msup remained unchanged after both protocols. The results indicate that CFTs and VFTs gave rise to equivalent neuromuscular fatigue. This fatigue resulted from alterations taking place at the muscular level. The finding that cortical and spinal excitability remained unchanged during MVC indicates that spinal and/or supraspinal mechanisms were activated to compensate for the loss of spinal excitability at rest.

A new method for muscle fatigue assessment: Online model identification techniques.

INTRODUCTION: The purpose of this study was to propose a method that allows extraction of the current muscle state under electrically induced fatigue. METHODS: The triceps surae muscle of 5 subjects paralyzed by spinal cord injury was fatigued by intermittent electrical stimulation (5 × 5 trains at 30 Hz). Classical fatigue indices representing muscle contractile properties [peak twitch (Pt) and half-relaxation time (HRT)] were assessed before and after each 5-train series and were used to identify 2 relevant parameters (Fm , Ur ) of a previously developed mathematical model using the Sigma-Point Kalman Filter. RESULTS: Pt declined significantly during the protocol, whereas HRT remained unchanged. Identification of the model parameters with experimental data yielded a model-based fatigue assessment that gave a more stable evaluation of fatigue than classical parameters. CONCLUSIONS: This work reinforces clinical research by providing a tool that clinicians can use to monitor fatigue development during stimulation.

Torque prediction using stimulus evoked EMG and its identification for different muscle fatigue states in SCI subjects.

Muscle fatigue is an unavoidable problem when electrical stimulation is applied to paralyzed muscles. The detection and compensation of muscle fatigue is essential to avoid movement failure and achieve desired trajectory. This work aims to predict ankle plantar-flexion torque using stimulus evoked EMG (eEMG) during different muscle fatigue states. Five spinal cord injured patients were recruited for this study. An intermittent fatigue protocol was delivered to triceps surae muscle to induce muscle fatigue. A hammerstein model was used to capture the muscle contraction dynamics to represent eEMG-torque relationship. The prediction of ankle torque was based on measured eEMG and past measured or past predicted torque. The latter approach makes it possible to use eEMG as a synthetic force sensor when force measurement is not available in daily use. Some previous researches suggested to use eEMG information directly to detect and predict muscle force during fatigue assuming a fixed relationship between eEMG and generated force. However, we found that the prediction became less precise with the increase of muscle fatigue when fixed parameter model was used. Therefore, we carried out the torque prediction with an adaptive parameters using the latest measurement. The prediction of adapted model was improved with 16.7%-50.8% comparing to the fixed model.

Does central fatigue exist under low-frequency stimulation of a low fatigue-resistant muscle?

The aim of the present study was to determine whether central fatigue occurs when fatigue is electrically induced in the abductor pollicis brevis muscle. Three series of 17 trains (30 Hz, 450 µs, 4 s on/6 s off, at the maximal tolerated intensity) were used to fatigue the muscle. Neuromuscular tests consisting of electrically evoked and voluntary contractions were performed before and after every 17-train series. Both the force induced by the stimulation trains and maximal voluntary force generation capacity significantly decreased throughout the protocol (-27 and -20%, respectively, at the end of the protocol, P < 0.001). These decreases were accompanied by failure in muscle excitability (P < 0.01), as assessed by the muscle compound action potential (M-wave or Mmax), leading to significant impairment in the muscle contractile properties (P < 0.05), as assessed by the muscle mechanical response (Pt). Central fatigue indices (level of activation, RMS/Mmax and H reflex) were not significantly changed at any point in the protocol. This gives evidence of preserved motor command reaching the motor neurons and preserved spinal excitability. The results indicate that this low-frequency stimulation protocol entails purely peripheral fatigue development when applied to a low fatigue-resistant muscle.

Kinetics of neuromuscular changes during low-frequency electrical stimulation.

The purpose of the study was to examine the time course of neuromuscular fatigue components during a low-frequency electrostimulation (ES) session. Three bouts of 17 trains of stimulation at 30 HZ (4 s on, 6 s off) were used to electrically induce fatigue in the plantar flexor muscles. Before and after every 17-train bout, torque, electromyographic activity [expressed as root mean square (RMS) and median frequency (MF) values], evoked potentials (M-wave and H-reflex), and the level of voluntary activation (LOA, using twitch interpolation technique) were assessed. Torque during maximal voluntary contraction decreased significantly from the very first stimulation bout (-6.6 +/- 1.11%, P < 0.001) and throughout the session (-10.32 +/- 1.68% and -11.53 +/- 1.27%, for the second and third bouts, respectively). The LOA and RMS/Mmax values were significantly decreased during the ES session (-2.9 +/- 1.07% and -17.5 +/- 6.14%, P < 0.01 and P< 0.001, respectively, at the end of the protocol), while MF showed no changes. The Hmax/Mmax ratio and Mmax were not significantly modified during the session. All twitch parameters were significantly potentiated after the first bout and throughout the session (P < 0.001). The maximal torque decrease was evident from the early phase of a low-frequency ES protocol, with no concomitant inhibition of motoneuron excitability or depression of muscle contractile properties. These results are consistent with an early failure of the central drive to the muscle.