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.

Recruitment and repetitive firing of spinal motoneurons depend on the activation of persistent inward calcium and sodium currents (PICs) that are in turn facilitated by serotonin and norepinephrine that arise primarily from the brain stem. Considering that in rats motoneuron PICs are greatly facilitated by increasing the presynaptic release of norepinephrine with amphetamine, we sought similar evidence for the modulation of PICs in human motoneurons. Pairs of motor units were recorded during a gradually increasing and then decreasing voluntary contraction. The firing frequency (F) of the lower-threshold (control) motor unit was used as an estimate of the synaptic input to the higher-threshold (test) motor unit. Generally, PICs are initiated during the recruitment of a motoneuron and subsequently provide a fixed depolarizing current that helps the synaptic input maintain firing until derecruitment. Thus the amplitude of the PIC in the test motor unit was estimated from the difference in synaptic input (DeltaF) needed to maintain minimal firing once the PIC was fully activated (measured at the time of test unit derecruitment) compared with the larger synaptic input required to initiate firing prior to full PIC activation (measured at the time of test unit recruitment; DeltaF = F(recruit) - F(derecruit)). Moreover, the activation time of the PIC was estimated as the minimal contraction duration needed to produce a maximal PIC (DeltaF). In five subjects, oral administration of amphetamine, but not placebo, increased the DeltaF by 62% [from 3.7 +/- 0.6 to 6.0 +/- 0.8 (SD) imp/s, P = 0.001] and decreased the time needed to activate a maximal DeltaF from approximately 2 to 0.5 s. Both findings suggest that the endogenous facilitation of PICs from brain stem derived norepinephrine plays an important role in modulating human motoneuron excitability, readying motoneurons for rapid and sustained activity during periods of high arousal such as stress or fear.

Neuromuscular electrical stimulation (NMES) can be delivered over a nerve trunk or muscle belly and both can generate contractions through peripheral and central pathways. Generating contractions through peripheral pathways is associated with a nonphysiological motor unit recruitment order, which may limit the efficacy of NMES rehabilitation. Presently, we compared recruitment through peripheral and central pathways for contractions of the knee extensors evoked by NMES applied over the femoral nerve vs. the quadriceps muscle. NMES was delivered to evoke 10 and 20% of maximum voluntary isometric contraction torque 2–3 s into the NMES (time1) in two patterns: 1) constant frequency (15 Hz for 8 s); and 2) step frequency (15–100-15 Hz and 25–100-25 Hz for 3–2-3 s, respectively). Torque and electromyographic activity recorded from vastus lateralis and medialis were quantified at the beginning (time1) and end (time2; 6–7 s into the NMES) of each pattern. M-waves (peripheral pathway), H-reflexes, and asynchronous activity (central pathways) during NMES were quantified. Torque did not differ regardless of NMES location, pattern, or time. For both muscles, M-waves were ∼7–10 times smaller and H-reflexes ∼8–9 times larger during NMES over the nerve compared with over the muscle. However, unlike muscles studied previously, neither torque nor activity through central pathways were augmented following 100 Hz NMES, nor was any asynchronous activity evoked during NMES at either location. The coefficient of variation was also quantified at time2to determine the consistency of each dependent measure between three consecutive contractions. Torque, M-waves, and H-reflexes were most variable during NMES over the nerve. In summary, NMES over the nerve produced contractions with the greatest recruitment through central pathways; however, considering some of the limitations of NMES over the femoral nerve, it may be considered a good complement to, as opposed to a replacement for, NMES over the quadriceps muscle for maintaining muscle quality and reducing contraction fatigue during NMES rehabilitation.

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