Neuromuscular electrical stimulation (NMES) generates contractions by depolarising axons beneath the stimulating electrodes. The depolarisation of motor axons produces contractions by signals travelling from the stimulation location to the muscle (peripheral pathway), with no involvement of the central nervous system (CNS). The concomitant depolarisation of sensory axons sends a large volley into the CNS and this can contribute to contractions by signals travelling through the spinal cord (central pathway) which may have advantages when NMES is used to restore movement or reduce muscle atrophy. In addition, the electrically evoked sensory volley increases activity in CNS circuits that control movement and this can also enhance neuromuscular function after CNS damage. The first part of this review provides an overview of how peripheral and central pathways contribute to contractions evoked by NMES and describes how differences in NMES parameters affect the balance between transmission along these two pathways. The second part of this review describes how NMES location (i.e. over the nerve trunk or muscle belly) affects transmission along peripheral and central pathways and describes some implications for motor unit recruitment during NMES. The third part of this review summarises some of the effects that the electrically evoked sensory volley has on CNS circuits, and highlights the need to identify optimal stimulation parameters for eliciting plasticity in the CNS. A goal of this work is to identify the best way to utilize the electrically evoked sensory volley generated during NMES to exploit mechanisms inherent to the neuromuscular system and enhance neuromuscular function for rehabilitation.
Neuromuscular electrical stimulation (NMES) can be delivered over a nerve trunk or muscle belly and can generate contractions by activating motor (peripheral pathway) and sensory (central pathway) axons. In the present experiments, we compared the peripheral and central contributions to plantar flexion contractions evoked by stimulation over the tibial nerve vs. the triceps surae muscles. Generating contractions through central pathways follows Henneman's size principle, whereby low-threshold motor units are activated first, and this may have advantages for rehabilitation. Statistical analyses were performed on data from trials in which NMES was delivered to evoke 10-30% maximum voluntary torque 2-3 s into the stimulation (Time(1)). Two patterns of stimulation were delivered: 1) 20 Hz for 8 s; and 2) 20-100-20 Hz for 3-2-3 s. Torque and soleus electromyography were quantified at the beginning (Time(1)) and end (Time(2); 6-7 s into the stimulation) of each stimulation train. H reflexes (central pathway) and M waves (peripheral pathway) were quantified. Motor unit activity that was not time-locked to each stimulation pulse as an M wave or H reflex ("asynchronous" activity) was also quantified as a second measure of central recruitment. Torque was not different for stimulation over the nerve or the muscle. In contrast, M waves were approximately five to six times smaller, and H reflexes were approximately two to three times larger during NMES over the nerve vs. the muscle. Asynchronous activity increased by 50% over time, regardless of the stimulation location or pattern, and was largest during NMES over the muscle belly. Compared with NMES over the triceps surae muscles, NMES over the tibial nerve produced contractions with a relatively greater central contribution, and this may help reduce muscle atrophy and fatigue when NMES is used for rehabilitation.
The afferent volley generated during neuromuscular electrical stimulation (NMES) can increase the excitability of human corticospinal (CS) pathways to muscles of the leg and hand. Over time, such increases can strengthen CS pathways damaged by injury or disease and result in enduring improvements in function. There is some evidence that NMES affects CS excitability differently for muscles of the leg and hand, although a direct comparison has not been conducted. Thus, the present experiments were designed to compare the strength and specificity of NMES-induced changes in CS excitability for muscles of the leg and hand. Two hypotheses were tested: (1) For muscles innervated by the stimulated nerve (target muscles), CS excitability will increase more for the hand than for the leg. (2) For muscles not innervated by the stimulated nerve (non-target muscles), CS excitability will increase for muscles of the leg but not muscles of the hand. NMES was delivered over the common peroneal (CP) nerve in the leg or the median nerve at the wrist using a 1-ms pulse width in a 20 s on, 20 s off cycle for 40 min. The intensity was set to evoke an M-wave that was ~15% of the maximal M-wave in the target muscle: tibialis anterior (TA) in the leg and abductor pollicis brevis (APB) in the hand. Ten motor-evoked potentials (MEPs) were recorded from the target muscles and from 2 non-target muscles of each limb using transcranial magnetic stimulation delivered over the "hotspot" for each muscle before and after the NMES. MEP amplitude increased significantly for TA (by 45 ± 6%) and for APB (56 ± 8%), but the amplitude of these increases was not different. In non-target muscles, MEPs increased significantly for muscles of the leg (42 ± 4%), but not the hand. Although NMES increased CS excitability for target muscles to the same extent in the leg and hand, the differences in the effect on non-target muscles suggest that NMES has a "global" effect on CS excitability for the leg and a "focused" effect for the hand. These differences may reflect differences in the specificity of afferent projections to the cortex. Global increases in CS excitability for the leg could be advantageous for rehabilitation as NMES applied to one muscle could strengthen CS pathways and enhance function for multiple muscles.
H-reflexes are progressively depressed, relative to the first response, at stimulation frequencies above 0.1 Hz (postactivation depression; PAD). Presently, we investigated whether H-reflexes "recover" from this depression throughout 10-s trains of stimulation delivered at physiologically relevant frequencies (5-20 Hz) during functionally relevant tasks (sitting and standing) and contraction amplitudes [relaxed to 20% maximum voluntary contraction (MVC)]. When participants held a 10% MVC, reflex amplitudes did not change during 5-Hz stimulation. During stimulation at 10 Hz, reflexes were initially depressed by 43% but recovered completely by the end of the stimulation period. During 20-Hz stimulation, reflexes were depressed to 10% and recovered to 36% of the first response, respectively. This "postactivation depression and recovery" (PAD&R) of reflex amplitude was not different between sitting and standing. In contrast, PAD&R were strongly influenced by contraction amplitude. Reflexes were depressed to 10% of the first response during the relaxed condition (10-Hz stimulation) and showed no depression during a 20% MVC contraction. A partial recovery of reflex amplitude occurred when participants were relaxed and during contractions of 1-5% MVC. Surprisingly, reflexes could recover completely by the third pulse within a stimulation train when participants held a contraction between 5 and 10% MVC during stimulation at 10 Hz, a finding that challenges classical ideas regarding PAD mechanisms. Our results support the idea that there is an ongoing interplay between depression and facilitation when motoneurons receive trains of afferent input. This interplay depends strongly on the frequency of the afferent input and the magnitude of the background contraction but is relatively insensitive to changes in task.
Reflex pathways connect all four limbs in humans. Presently, we tested the hypothesis that reflexes also link sensory receptors in the lower leg with muscles of the lower back (erector spinae; ES). Taps were applied to the right Achilles' tendon and electromyographic activity was recorded from the right soleus and bilaterally from ES. Reflexes were compared between sitting and standing and between standing with the eyes open versus closed. Reflexes were evoked bilaterally in ES and consisted of an early latency excitation, a medium latency inhibition, and a longer latency excitation. During sitting but not standing, the early excitation was larger in the ES muscle ipsilateral to the stimulation (iES) than in the contralateral ES (cES). During standing but not sitting, the longer latency excitation in cES was larger than in iES. This response in cES was also larger during standing compared to sitting. Responses were not significantly different between the eyes open and eyes closed conditions. Taps applied to the lateral calcaneus (heel taps) evoked responses in ES that were not significantly different in amplitude or latency than those evoked by tendon taps, despite a 75-94% reduction in the amplitude of the soleus stretch reflex evoked by the heel taps. Electrical stimulation of the sural nerve, a purely cutaneous nerve at the ankle, evoked ES reflexes that were not significantly different in amplitude but had significantly longer latencies than those evoked by the tendon and heel taps. These results support the hypothesis that reflex pathways connect receptors in the lower leg with muscles of the lower back and show that that the amplitude of these reflexes is modulated by task. Responses evoked by stimulation of the sural nerve establish that reflex pathways connect the ES muscles with cutaneous receptors of the foot. In contrast, the large volley in muscle spindle afferents induced by the tendon taps compared to the heel taps did not alter the ES responses, suggesting that the reflex connection between triceps surae muscle spindles and the ES muscles may be relatively weak. These heteronymous reflexes may play a role in stabilizing the trunk for maintaining posture and balance.
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