Can the cross-education of strength attenuate the impact of detraining after a period of strength training? A quasi-randomized trial.

PURPOSE: Unilateral strength training may attenuate the decline in muscle strength and size in homologous, contralateral muscles. This study aimed to determine whether the cross-education of strength could specifically attenuate the effects of detraining immediately after a short (prehabilitation-type) period of strength training. METHODS: Twenty-six strength-trained participants were assigned to either four weeks of unilateral strength training of the stronger arm (UNI) or detraining (Detrain). Motor evoked potential (MEP) and cortical silent period (cSP) responses, muscle cross-sectional area (CSAFlexor; peripheral quantitative computed tomography) and maximal strength, rate of force development (RFD) and muscle activation (EMG) were examined in both elbow flexors before and after the intervention period. RESULTS: In UNI, one-repetition maximum (1-RM) strength improved in both the trained (∆ = 2.0 ± 0.9 kg) and non-trained (∆ = 0.8 ± 0.9 kg) arms despite cessation of training of the weaker arm, whereas 1-RM strength was unchanged in Detrain. Maximal voluntary isometric contraction, isokinetic peak torque, and RFD did not change in either group. No neural changes were detected in UNI, but cSP increased in Detrain (∆ = 0.010 ± 0.015 s). CSAFlexor increased in the trained arm (∆ = 51 ± 43 mm2) but decreased in the non-trained arm (∆ = -53 ± 50 mm2) in UNI. CSAFlexor decreased in both arms in Detrain and at a similar rate to the non-trained arm in UNI. CONCLUSION: UNI attenuated the effects of detraining in the weaker arm as shown by the improvement in 1-RM strength. However, the cross-education of strength did not attenuate the decline in muscle size in the contralateral arm.

Reduction and recovery of self-sustained muscle activity after fatiguing plantar flexor contractions.

PURPOSE: Persistent inward calcium and sodium currents (PICs) are crucial for initiation and maintenance of motoneuron firing, and thus muscular force. However, there is a lack of data describing the effects of fatiguing exercise on PIC activity in humans. We simultaneously applied tendon vibration and neuromuscular electrical stimulation (VibStim) before and after fatiguing exercise. VibStim induces self-sustained muscle activity that is proposed to result from PIC activation. METHODS: Twelve men performed 5-s maximal isometric plantar flexor contractions (MVC) with 5-s rests until joint torque was reduced to 70%MVC. VibStim trials consisted of five 2-s trains of neuromuscular electrical stimulation (20 Hz, evoking 10% MVC) of triceps surae with simultaneous Achilles tendon vibration (115 Hz) without voluntary muscle activation. VibStim was applied before (PRE), immediately (POST), 5-min (POST-5), and 10-min (POST-10) after exercise completion. RESULTS: Sustained torque (Tsust) and soleus electromyogram amplitudes (EMG) measured 3 s after VibStim were reduced (Tsust: -59.0%, p < 0.001; soleus EMG: -38.4%, p < 0.001) but largely recovered by POST-5, and changes in MVC and Tsust were correlated across the four time points (r = 0.69; p < 0.001). After normalisation to values obtained at the end of the vibration phase to control for changes in fibre-specific force and EMG signal characteristics, decreases in Tsust (-42.9%) and soleus EMG (-22.6%) remained significant and were each correlated with loss and recovery of MVC (r = 0.41 and 0.46, respectively). CONCLUSION: The parallel changes observed in evoked self-sustained muscle activity and force generation capacity provide motivation for future examinations on the potential influence of fatigue-induced PIC changes on motoneuron output.

Physiological effects of cathodal electrode configuration for transspinal stimulation in humans.

Transspinal stimulation modulates neuronal excitability and promotes recovery in upper motoneuron lesions. The recruitment input-output curves of transspinal evoked potentials (TEPs) recorded from knee and ankle muscles, and their susceptibility to spinal inhibition, were recorded when the position, size, and number of the cathode electrode were arranged in four settings or protocols (Ps). The four Ps were the following: 1) one rectangular electrode placed at midline (KNIKOU-LAB4Recovery or K-LAB4Recovery; P-KLAB), 2) one square electrode placed at midline (P-2), 3) two square electrodes 1 cm apart placed at midline (P-3), and 4) one square electrode placed on each paravertebral side (P-4). P-KLAB and P-3 required less current to reach TEP threshold or maximal amplitudes. A rightward shift in TEP recruitment curves was evident for P-4, whereas the slope was increased for P-2 and P-4 compared with P-KLAB and P-3. TEP depression upon single and paired transspinal stimuli was pronounced in ankle TEPs but was less prominent in knee TEPs. TEP depression induced by single transspinal stimuli at 1.0 Hz was similar for most TEPs across protocols, but TEP depression induced by paired transspinal stimuli was different between protocols and was replaced by facilitation at 100-ms interstimulus interval for P-4. Our results suggest that P-KLAB and P-3 are preferred based on excitability threshold of motoneurons. P-KLAB produced more TEP depression, thereby maximizing the engagement of spinal neuronal pathways. We recommend P-KLAB to study neurophysiological mechanisms underlying transspinal stimulation or when used as a neuromodulation method for recovery in neurological disorders.NEW & NOTEWORTHY Transspinal stimulation with a rectangular cathode electrode (P-KLAB) requires less current to produce transspinal evoked potentials and maximizes spinal inhibition. We recommend P-KLAB for neurophysiological studies or when used as a neuromodulation method to enhance motor output and normalize muscle tone in neurological disorders.

Brain and spinal cord paired stimulation coupled with locomotor training facilitates motor output in human spinal cord injury.

Combined interventions for neuromodulation leading to neurorecovery have gained great attention by researchers to resemble clinical rehabilitation approaches. In this randomized clinical trial, we established changes in the net output of motoneurons innervating multiple leg muscles during stepping when transcranial magnetic stimulation (TMS) of the primary motor cortex was paired with transcutaneous spinal (transspinal) stimulation over the thoracolumbar region during locomotor training. TMS was delivered before (TMS-transspinal) or after (transspinal-TMS) transspinal stimulation during the stance phase of the less impaired leg. Ten individuals with chronic incomplete or complete SCI received at least 20 sessions of training. Each session consisted of 240 paired stimuli delivered over 10-min blocks for 1 h during robotic assisted step training on a motorized treadmill. Body weight support, leg guidance force and treadmill speed were adjusted based on each subject's ability to step without knee buckling or toe dragging. Most transspinal evoked potentials (TEPs) recorded before and after each intervention from ankle and knee muscles during assisted stepping were modulated in a phase-dependent pattern. Transspinal-TMS and locomotor training affected motor neuron output of knee and ankle muscles with ankle TEPs to be modulated in a phase-dependent manner. TMS-transspinal and locomotor training increased motor neuron output for knee but not for ankle muscles. Our results support that targeted brain and spinal cord stimulation alters responsiveness of neurons over multiple spinal segments in people with chronic SCI. Noninvasive stimulation of the brain and spinal cord along with locomotor training is a novel neuromodulation method that can become a promising modality for rehabilitation in humans after SCI.

Brain and spinal cord paired stimulation coupled with locomotor training affects polysynaptic flexion reflex circuits in human spinal cord injury.

Neurorecovery from locomotor training is well established in human spinal cord injury (SCI). However, neurorecovery resulting from combined interventions has not been widely studied. In this randomized clinical trial, we established the tibialis anterior (TA) flexion reflex modulation pattern when transcranial magnetic stimulation (TMS) of the primary motor cortex was paired with transcutaneous spinal cord (transspinal) stimulation over the thoracolumbar region during assisted step training. Single pulses of TMS were delivered either before (TMS-transspinal) or after (transspinal-TMS) transspinal stimulation during the stance phase of the less impaired leg. Eight individuals with chronic incomplete or complete SCI received at least 20 sessions of paired stimulation during assisted step training. Each session consisted of 240 paired stimuli delivered over 10-min blocks for 1 h during robotic-assisted step training with the Lokomat6 Pro®. Body weight support, leg guidance force and treadmill speed were adjusted based on each participant's ability to step without knee buckling or toe dragging. Both the early and late TA flexion reflex remained unaltered after TMS-transspinal and locomotor training. In contrast, the early and late TA flexion reflexes were significantly depressed during stepping after transspinal-TMS and locomotor training. Reflex changes occurred at similar slopes and intercepts before and after training. Our findings support that targeted brain and spinal cord stimulation coupled with locomotor training reorganizes the function of flexion reflex pathways, which are a part of locomotor networks, in humans with varying levels of sensorimotor function after SCI.Trial registration number NCT04624607; Registered on November 12, 2020.

Transspinal stimulation and step training alter function of spinal networks in complete spinal cord injury.

STUDY DESIGN: Pilot study (case series). OBJECTIVE: The objective of this study was to establish spinal neurophysiological changes following high-frequency transspinal stimulation during robot-assisted step training in individuals with chronic motor complete spinal cord injury (SCI). SETTING: University research laboratory (Klab4Recovery). METHODS: Four individuals with motor complete SCI received an average of 18 sessions of transspinal stimulation over the thoracolumbar region with a pulse train at 333 Hz during robotic-assisted step training. Each session lasted ~1 h, with an average of 240 stimulations delivered during each training session. Before and after the combined intervention, we evaluated the amplitude modulation of the long-latency tibialis anterior (TA) flexion reflex and transspinal evoked potentials (TEP) recorded from flexors and extensors during assisted stepping, and the TEP recruitment curves at rest. RESULTS: The long-latency TA flexion reflex was depressed in all phases of the step cycle and the phase-dependent amplitude modulation of TEPs was altered during assisted stepping, while spinal motor output based on TEP recruitment curves was increased after the combined intervention. CONCLUSION: This is the first study documenting noninvasive transspinal stimulation coupled with locomotor training depresses flexion reflex excitability and concomitantly increases motoneuron output over multiple spinal segments for both flexors and extensors in people with motor complete SCI. While both transspinal stimulation and locomotor training may act via similar activity-dependent neuroplasticity mechanisms, combined interventions for rehabilitation of neurological disorders has not been systematically assessed. Our current findings support locomotor training induced neuroplasticity may be augmented with transspinal stimulation.

Neurophysiological Changes After Paired Brain and Spinal Cord Stimulation Coupled With Locomotor Training in Human Spinal Cord Injury.

Neurophysiological changes that involve activity-dependent neuroplasticity mechanisms via repeated stimulation and locomotor training are not commonly employed in research even though combination of interventions is a common clinical practice. In this randomized clinical trial, we established neurophysiological changes when transcranial magnetic stimulation (TMS) of the motor cortex was paired with transcutaneous thoracolumbar spinal (transspinal) stimulation in human spinal cord injury (SCI) delivered during locomotor training. We hypothesized that TMS delivered before transspinal (TMS-transspinal) stimulation promotes functional reorganization of spinal networks during stepping. In this protocol, TMS-induced corticospinal volleys arrive at the spinal cord at a sufficient time to interact with transspinal stimulation induced depolarization of alpha motoneurons over multiple spinal segments. We further hypothesized that TMS delivered after transspinal (transspinal-TMS) stimulation induces less pronounced effects. In this protocol, transspinal stimulation is delivered at time that allows transspinal stimulation induced action potentials to arrive at the motor cortex and affect descending motor volleys at the site of their origin. Fourteen individuals with motor incomplete and complete SCI participated in at least 25 sessions. Both stimulation protocols were delivered during the stance phase of the less impaired leg. Each training session consisted of 240 paired stimuli delivered over 10-min blocks. In transspinal-TMS, the left soleus H-reflex increased during the stance-phase and the right soleus H-reflex decreased at mid-swing. In TMS-transspinal no significant changes were found. When soleus H-reflexes were grouped based on the TMS-targeted limb, transspinal-TMS and locomotor training promoted H-reflex depression at swing phase, while TMS-transspinal and locomotor training resulted in facilitation of the soleus H-reflex at stance phase of the step cycle. Furthermore, both transspinal-TMS and TMS-transspinal paired-associative stimulation (PAS) and locomotor training promoted a more physiological modulation of motor activity and thus depolarization of motoneurons during assisted stepping. Our findings support that targeted non-invasive stimulation of corticospinal and spinal neuronal pathways coupled with locomotor training produce neurophysiological changes beneficial to stepping in humans with varying deficits of sensorimotor function after SCI.

Neuronal Actions of Transspinal Stimulation on Locomotor Networks and Reflex Excitability During Walking in Humans With and Without Spinal Cord Injury.

This study investigated the neuromodulatory effects of transspinal stimulation on soleus H-reflex excitability and electromyographic (EMG) activity during stepping in humans with and without spinal cord injury (SCI). Thirteen able-bodied adults and 5 individuals with SCI participated in the study. EMG activity from both legs was determined for steps without, during, and after a single-pulse or pulse train transspinal stimulation delivered during stepping randomly at different phases of the step cycle. The soleus H-reflex was recorded in both subject groups under control conditions and following single-pulse transspinal stimulation at an individualized exactly similar positive and negative conditioning-test interval. The EMG activity was decreased in both subject groups at the steps during transspinal stimulation, while intralimb and interlimb coordination were altered only in SCI subjects. At the steps immediately after transspinal stimulation, the physiological phase-dependent EMG modulation pattern remained unaffected in able-bodied subjects. The conditioned soleus H-reflex was depressed throughout the step cycle in both subject groups. Transspinal stimulation modulated depolarization of motoneurons over multiple segments, limb coordination, and soleus H-reflex excitability during assisted stepping. The soleus H-reflex depression may be the result of complex spinal inhibitory interneuronal circuits activated by transspinal stimulation and collision between orthodromic and antidromic volleys in the peripheral mixed nerve. The soleus H-reflex depression by transspinal stimulation suggests a potential application for normalization of spinal reflex excitability after SCI.

Plantar flexor muscle stretching depresses the soleus late response but not tendon tap reflexes.

The purpose of this study was to investigate changes in muscle spindle sensitivity with early and late soleus reflex responses via tendon taps and transcranial magnetic stimulation, respectively, after an acute bout of prolonged static plantar flexor muscle stretching. Seventeen healthy males were tested before and after 5 min (5 × 60-s stretches) of passive static stretching of the plantar flexor muscles. Maximal voluntary isometric torque and M wave-normalized triceps surae muscle surface electromyographic activity were recorded. Both soleus tendon reflexes, evoked by percussion of the Achilles tendon during rest and transcranial magnetic stimulation-evoked soleus late responses during submaximal isometric dorsiflexion were also quantified. Significant decreases in maximal voluntary isometric plantar flexion torque (-19.2 ± 13.6%, p = .002) and soleus electromyographic activity (-20.1 ± 11.4%, p < .001) were observed immediately after stretching, and these changes were highly correlated (r = 0.76, p < .001). No changes were observed in tendon reflex amplitude or latency or peak muscle twitch torque (p > .05). Significant reductions in soleus late response amplitudes (-46.9 ± 36.0%, p = .002) were detected, although these changes were not correlated with changes in maximal electromyographic activity, torque or tendon reflex amplitudes. No changes in soleus late response latency were detected. In conclusion, impaired neural drive was implicated in the stretch-induced force loss; however, no evidence was found that this loss was related to changes in muscle spindle sensitivity. We hypothesize that the decrease in soleus late response indicates a stretch-induced reduction in a polysynaptic postural reflex rather than spindle reflex sensitivity.

Rate of torque development and striatal shape in individuals with prodromal Huntington's disease.

The aim of the present study was to quantify explosive joint torque or the ability to develop joint torque rapidly, typically measured as the rate of torque development, in individuals with prodromal Huntington's disease and healthy controls and its associations with measures of disease burden and striatal pathology. Twenty prodromal Huntington's disease and 19 healthy control individuals volunteered for this study. Plantar flexor isometric rate of torque development values were evaluated using isokinetic dynamometry. Pathological changes in striatal shape were evaluated using magnetic resonance imaging. Disease burden was evaluated using the disease burden score and cytosine-adenine-guanine age product score. No statistical differences in the rate of torque development were observed between individuals with prodromal Huntington's disease and healthy controls. However, significant associations were observed between the rate of torque development values and measures of disease burden (r = -0.42 to -0.69) and striatal pathology (r = 0.71-0.60) in individuals with prodromal Huntington's disease. We found significant associations between lower rate of torque development values and greater striatal shape deflation and disease burden and striatal pathology in individuals with prodromal Huntington's disease. While no significant differences in the rate of torque development were found between prodromal Huntington's disease and healthy controls, the noted associations suggest that differences may emerge as the disease advances, which should be investigated longitudinally in future studies.

Dual tasking impairments are associated with striatal pathology in Huntington's disease.

BACKGROUND: Recent findings suggest that individuals with Huntington's disease (HD) have an impaired capacity to execute cognitive and motor tasks simultaneously, or dual task, which gradually worsens as the disease advances. The onset and neuropathological changes mediating impairments in dual tasking in individuals with HD are unclear. The reliability of dual tasking assessments for individuals with HD is also unclear. OBJECTIVES: To evaluate differences in dual tasking performance between individuals with HD (presymptomatic and prodromal) and matched controls, to investigate associations between striatal volume and dual tasking performance, and to determine the reliability of dual tasking assessments. METHODS: Twenty individuals with HD (10 presymptomatic and 10 prodromal) and 20 healthy controls were recruited for the study. Individuals undertook four single and dual task assessments, comprising motor (postural stability or force steadiness) and cognitive (simple or complex mental arithmetic) components, with single and dual tasks performed three times each. Participants also undertook a magnetic resonance imaging assessment. RESULTS: Compared to healthy controls, individuals with presymptomatic and prodromal HD displayed significant deficits in dual tasking, particularly cognitive task performance when concurrently undertaking motor tasks (P < 0.05). The observed deficits in dual tasking were associated with reduced volume in caudate and putamen structures (P < 0.05),however, not with clinical measures of disease burden. An analysis of the reliability of dual tasking assessments revealed moderate to high test-retest reliability [ICC: 0.61-0.99] for individuals with presymptomatic and prodromal HD and healthy controls. CONCLUSIONS: Individuals with presymptomatic and prodromal HD have significant deficits in dual tasking that are associated with striatal degeneration. Findings also indicate that dual tasking assessments are reliable in individuals presymptomatic and prodromal HD and healthy controls.

Modulation of soleus H-reflex excitability following cervical transspinal conditioning stimulation in humans.

The aim of this study was to establish the effects of transcutaneous spinal cord (transspinal) stimulation over the cervical region on soleus H-reflex excitability in healthy subjects while at rest. Reflex effects were established at subthreshold and suprathreshold cervical transspinal conditioning stimulation intensities of the extensor carpi radialis transspinal evoked potential. Twenty soleus H-reflexes at 0.125 Hz were recorded randomly under control conditions and following transspinal conditioning stimulation at conditioning-test intervals that ranged from 0 to 55 ms and tested in increment of 5 ms steps and at 100 ms. Cervical transspinal stimulation at suprathreshold and not at subthreshold intensities produced short, medium, and long-latency soleus H-reflex facilitation. The observed facilitatory reflex effects are consistent with activation of excitatory components of long propriospinal neurons. We propose the use of cervical transspinal stimulation to potentiate excitatory neuronal interactions between arms and legs in neurological disorders.

Transspinal stimulation downregulates activity of flexor locomotor networks during walking in humans.

The objective of this study was to establish the effects of transspinal stimulation on short-latency tibialis anterior (TA) flexion reflex during walking in healthy humans. Single pulse transspinal stimulation was delivered at a conditioning-test (C-T) interval either after (~20 ms) or simultaneously with the last pulse of the pulse train (0 ms) delivered to the medial arch of the right foot. Transspinal stimulation was delivered at sub- and supra-threshold intensities of the spinally-mediated TA transspinal evoked potential. Stimulation was delivered randomly at different phases of the step cycle, based on the foot switch threshold signal, which was divided into 16 equal bins. The TA flexion reflex facilitation under control conditions occurred at heel contact and then progressively from late stance phase reaching its peak at early and late swing phases. Transspinal stimulation at a negative and suprathreshold 0 ms C-T interval depressed flexion reflex excitability at all phases of the step cycle. The short-latency TA flexion reflex depression was possibly mediated through spinal inhibitory interneurons acting at both pre- and post- motoneuronal sites or by transspinal stimulation affecting directly the activity of the flexor half spinal center. These results reveal direct actions of transspinal stimulation on human spinal locomotor networks.

Lack of cortical or Ia-afferent spinal pathway involvement in muscle force loss after passive static stretching.

This study investigated whether modulation of corticospinal-motoneuronal excitability and/or synaptic transmission of the Ia afferent spinal reflex contributes to decreases in voluntary activation and muscular force after an acute bout of prolonged static muscle stretching. Fifteen men performed five 60-s constant-torque stretches (15-s rest intervals; total duration 5 min) of the plantar flexors on an isokinetic dynamometer and a nonstretching control condition in random order on 2 separate days. Maximum isometric plantar flexor torque and triceps surae muscle electromyographic activity (normalized to M wave; EMG/M) were simultaneously recorded immediately before and after each condition. Motor-evoked potentials (using transcranial magnetic stimulation) and H-reflexes were recorded from soleus during EMG-controlled submaximal contractions (23.4 ± 6.9% EMG maximum). No changes were detected in the control condition. After stretching, however, peak torque (mean ± SD; -14.3 ± 7.0%) and soleus EMG/M (-17.8 ± 6.2%) decreased, and these changes were highly correlated (r = 0.83). No changes were observed after stretching in soleus MEP or H-reflex amplitudes measured during submaximal contractions, and interindividual variability of changes was not correlated with changes in EMG activity or maximum torque. During EMG-controlled submaximal contractions, torque production was significantly decreased after stretching (-22.7 ± 15.0%), indicating a compromised muscular output. These data provide support that changes in the excitability of the corticospinal-motoneuronal and Ia afferent spinal reflex pathways do not contribute to poststretch neural impairment.NEW & NOTEWORTHY This study is the first to specifically examine potential sites underlying the decreases in neural activation of muscle and force production after a bout of muscle stretching. However, no changes were found in either the H-reflex or motor-evoked potential amplitude during submaximal contractions.

Transspinal stimulation decreases corticospinal excitability and alters the function of spinal locomotor networks.

Locomotion requires the continuous integration of descending motor commands and sensory inputs from the legs by spinal central pattern generator circuits. Modulation of spinal neural circuits by transspinal stimulation is well documented, but how transspinal stimulation affects corticospinal excitability during walking in humans remains elusive. We measured the motor evoked potentials (MEPs) at multiple phases of the step cycle conditioned with transspinal stimulation delivered at sub- and suprathreshold intensities of the spinally mediated transspinal evoked potential (TEP). Transspinal stimulation was delivered before or after transcranial magnetic stimulation during which summation between MEP and TEP responses in the surface EMG was absent or present. Relationships between MEP amplitude and background EMG activity, silent period duration, and phase-dependent EMG amplitude modulation during and after stimulation were also determined. Ankle flexor and extensor MEPs were depressed by suprathreshold transspinal stimulation when descending volleys were timed to interact with transspinal stimulation-induced motoneuron depolarization at the spinal cord. MEP depression coincided with decreased MEP gain, unaltered MEP threshold, and unaltered silent period duration. Locomotor EMG activity of bilateral knee and ankle muscles was significantly depressed during the step at which transspinal stimulation was delivered but fully recovered at the subsequent step. The results support a model in which MEP depression by transspinal stimulation occurs via subcortical or spinal mechanisms. Transspinal stimulation disrupts the locomotor output of flexor and extensor motoneurons initially, but the intact nervous system has the ability to rapidly overcome this pronounced locomotor adaptation. In conclusion, transspinal stimulation directly affects spinal locomotor centers in healthy humans.NEW & NOTEWORTHY Lumbar transspinal stimulation decreases ankle flexor and extensor motor evoked potentials (MEPs) during walking. The MEP depression coincides with decreased MEP gain, unaltered MEP threshold changes, and unaltered silent period duration. These findings indicate that MEP depression is subcortical or spinal in origin. Healthy subjects could rapidly overcome the pronounced depression of muscle activity during the step at which transspinal stimulation was delivered. Thus, transspinal stimulation directly affects the function of spinal locomotor networks in healthy humans.

The loss of muscle force production after muscle stretching is not accompanied by altered corticospinal excitability.

PURPOSE: The aim of the present study was to determine whether depression of maximal muscular force and neural drive subsequent to prolonged ( ≥ 60 s) passive muscle stretching is associated with altered corticospinal excitability or intracortical (GABAB-mediated) inhibition. METHODS: Fourteen healthy adult males were tested before and after 5 min (5 × 60-s stretches) of intense, passive static stretching of the plantar flexor muscles. Two protocols (A and B) were conducted in a randomized order. Transcranial magnetic stimulation was delivered to the contralateral motor cortex at rest (Protocol A) and during maximal voluntary contractions (Protocol B). Changes in maximal voluntary isometric torque, voluntary surface electromyographic activity of triceps surae muscles (normalized to M-wave; EMG/M), motor-evoked potentials (MEP), and cortical silent period (cSP; Protocol B) in soleus elicited by transcranial magnetic stimulation were examined 10 min after stretch. RESULTS: In both protocols A and B, significant decreases were observed immediately after stretching in maximal voluntary plantar flexion torque ( - 20.1 ± 15.9%, P = 0.004; and - 17.2 ± 13.5%, P = 0.006) and EMG/M ( - 18.0 ± 18.2%, P = 0.023; and - 13.0 ± 9.3%, P = 0.003). Decreases in torque and EMG/M were highly correlated (r = 0.67-0.85, P < 0.05). However, no changes were observed in MEP amplitudes during rest ( + 29.3 ± 50.0%) or maximum voluntary contraction ( + 1.9 ± 16.8%), or in cSP ( + 2.1 ± 15.1%). CONCLUSIONS: Impaired neural drive contributed to the stretch-induced force loss; however, changes in corticospinal excitability and intracortical inhibition could not explain the phenomenon.

Neuromuscular Factors Contributing to Reductions in Muscle Force After Repeated, High-Intensity Muscular Efforts.

Multiple neuromuscular processes contribute to the loss of force production following repeated, high-intensity muscular efforts; however, the relative contribution of each process is unclear. In Experiment 1, 16 resistance trained men performed six sets of unilateral isometric plantar flexor contractions of the right leg (3 s contraction/2 s rest; 85% maximal voluntary contraction torque; 90-s inter-set rest) until failure with and without caffeine ingestion (3 mg kg-1) on two separate days. Corticospinal excitability and cortical silent period (cSP) were assessed before and immediately, 10 and 20 min after the exercise. In Experiment 2, electrically evoked tetanic force and persistent inward current (PIC)-mediated facilitation of the motor neuron pool (estimated using neuromuscular electrical stimulation with tendon vibration) were assessed before and after the same exercise intervention in 17 resistance trained men. Results showed decreases in peak plantar flexion torque (Experiment 1: -12.2%, Experiment 2: -16.9%), electrically evoked torque (20 Hz -15.3%, 80 Hz -15.3%, variable-frequency train -17.9%), and cSP (-3.8%; i.e., reduced inhibition) post-exercise which did not recover by 20 min. Electromyographic activity (EMG; -6%), corticospinal excitability (-9%), and PIC facilitation (-24.8%) were also reduced post-exercise but recovered by 10 min. Caffeine ingestion increased torque and EMG but did not notably affect corticospinal excitability, PIC amplification, or electrically evoked torque. The data indicate that a decrease in muscle function largely underpins the loss of force after repeated, high-intensity muscular efforts, but that the loss is exacerbated immediately after the exercise by simultaneous decreases in corticospinal excitability and PIC amplitudes at the motor neurons.

Effect of tendon vibration during wide-pulse neuromuscular electrical stimulation (NMES) on muscle force production in people with spinal cord injury (SCI).

BACKGROUND: Neuromuscular electrical stimulation (NMES) is commonly used in skeletal muscles in people with spinal cord injury (SCI) with the aim of increasing muscle recruitment and thus muscle force production. NMES has been conventionally used in clinical practice as functional electrical stimulation (FES), using low levels of evoked force that cannot optimally stimulate muscular strength and mass improvements, and thus trigger musculoskeletal changes in paralysed muscles. The use of high intensity intermittent NMES training using wide-pulse width and moderate-intensity as a strength training tool could be a promising method to increase muscle force production in people with SCI. However, this type of protocol has not been clinically adopted because it may generate rapid muscle fatigue and thus prevent the performance of repeated high-intensity muscular contractions in paralysed muscles. Moreover, superimposing patellar tendon vibration onto the wide-pulse width NMES has been shown to elicit further increases in impulse or, at least, reduce the rate of fatigue in repeated contractions in able-bodied populations, but there is a lack of evidence to support this argument in people with SCI. METHODS: Nine people with SCI received two NMES protocols with and without superimposing patellar tendon vibration on different days (i.e. STIM and STIM+vib), which consisted of repeated 30 Hz trains of 58 wide-pulse width (1000 µs) symmetric biphasic pulses (0.033-s inter-pulse interval; 2 s stimulation train; 2-s inter-train interval) being delivered to the dominant quadriceps femoris. Starting torque was 20% of maximal doublet-twitch torque and stimulations continued until torque declined to 50% of the starting torque. Total knee extensor impulse was calculated as the primary outcome variable. RESULTS: Total knee extensor impulse increased in four subjects when patellar tendon vibration was imposed (59.2 ± 15.8%) but decreased in five subjects (- 31.3 ± 25.7%). However, there were no statistically significant differences between these sub-groups or between conditions when the data were pooled. CONCLUSIONS: Based on the present results there is insufficient evidence to conclude that patellar tendon vibration provides a clear benefit to muscle force production or delays muscle fatigue during wide-pulse width, moderate-intensity NMES in people with SCI. TRIAL REGISTRATION: ACTRN12618000022268 . Date: 11/01/2018. Retrospectively registered.

Effect of tendon vibration during wide-pulse neuromuscular electrical stimulation (NMES) on the decline and recovery of muscle force.

BACKGROUND: Neuromuscular electrical stimulation (NMES) is commonly used to activate skeletal muscles and reverse muscle atrophy in clinical populations. Clinical recommendations for NMES suggest the use of short pulse widths (100-200 µs) and low-to-moderate pulse frequencies (30-50 Hz). However, this type of NMES causes rapid muscle fatigue due to the (non-physiological) high stimulation intensities and non-orderly recruitment of motor units. The use of both wide pulse widths (1000 µs) and tendon vibration might optimize motor unit activation through spinal reflex pathways and thus delay the onset of muscle fatigue, increasing muscle force and mass. Thus, the objective of this study was to examine the acute effects of patellar tendon vibration superimposed onto wide-pulse width (1000 µs) knee extensor electrical stimulation (NMES, 30 Hz) on peak muscle force, total impulse before "muscle fatigue", and the post-exercise recovery of muscle function. METHODS: Tendon vibration (Vib), NMES (STIM) or NMES superimposed onto vibration (STIM + Vib) were applied in separate sessions to 16 healthy adults. Total torque-time integral (TTI), maximal voluntary contraction torque (MVIC) and indirect measures of muscle damage were tested before, immediately after, 1 h and 48 h after each stimulus. RESULTS: TTI increased (145.0 ± 127.7%) in STIM only for "positive responders" to the tendon vibration (8/16 subjects), but decreased in "negative responders" (-43.5 ± 25.7%). MVIC (-8.7%) and rectus femoris electromyography (RF EMG) (-16.7%) decreased after STIM (group effect) for at least 1 h, but not after STIM + Vib. No changes were detected in indirect markers of muscle damage in any condition. CONCLUSIONS: Tendon vibration superimposed onto wide-pulse width NMES increased TTI only in 8 of 16 subjects, but reduced voluntary force loss (fatigue) ubiquitously. Negative responders to tendon vibration may derive greater benefit from wide-pulse width NMES alone.