Electrical stimulation (1-ms pulses, 100 Hz) produces more torque than expected from motor axon activation (extra contractions). This experiment investigates the most effective method of delivering this stimulation for neuromuscular electrical stimulation. Surface stimulation (1-ms pulses; 20 Hz for 2 s, 100 Hz for 2 s, 20 Hz for 3 s) was delivered to triceps surae and wrist flexors (muscle stimulation) and to median and tibial nerves (nerve stimulation) at two intensities. Contractions were evaluated for amplitude, consistency, and stability. Surface electromyograph was collected to assess how H-reflexes and M-waves contribute. In the triceps surae, muscle stimulation produced the largest absolute contractions (23% maximal voluntary contraction), evoked the largest extra contractions as torque increased by 412% after the 100-Hz stimulation, and was more consistent and stable compared with tibial nerve stimulation. Absolute and extra contraction amplitude, consistency, and stability of evoked wrist flexor torques were similar between stimulation types: torques reached 11% maximal voluntary contraction, and extra contractions increased torque by 161%. Extra contractions were 10 times larger in plantar flexors compared with wrist flexors with muscle stimulation but were similar with nerve stimulation. For triceps surae, H reflexes were 3.4 times larger than M waves during nerve stimulation, yet M waves were 15 times larger than H reflexes during muscle stimulation. M waves in the wrist flexors were larger than H reflexes during nerve (8.5 times) and muscle (18.5 times) stimulation. This is an initial step toward utilizing extra contractions for neuromuscular electrical stimulation and the first to demonstrate their presence in the wrist flexors.
The measurement of a variety of ambulatory activity parameters may aid clinicians and stroke survivors to determine whether exercise recommendations are being met with daily activity.
Tetanic neuromuscular stimulation evokes contractions by depolarizing motor axons beneath the stimulating electrodes. However, we have shown that extra torque can develop due to the discharge of spinal neurons recruited by the evoked sensory volley. The present experiments investigated whether extra torque in the ankle plantar- and dorsiflexors was associated with enhanced H-reflexes. The tibial and common peroneal nerves were stimulated using 7-s trains (20 Hz for 2 s, 100 Hz for 2 s, 20 Hz for 3 s). Extra torque was defined as significantly more torque during 20-Hz stimulation after the 100-Hz burst (time2) than before it (time1). In 9 of 11 subjects, extra plantarflexion torque developed during stimulation just above motor threshold. In these nine subjects, torque increased from 8 to 13% MVC (time1 to time2), the soleus H-reflex increased from 13 to 19% Mmax and the M-wave of approximately 2% Mmax did not change significantly. To evoke extra dorsiflexion torque, greater stimulation intensities were required. In 6 of 13 subjects, extra torque developed at intensities that evoked an M-wave of 5-20% Mmax at time1. In these six subjects, torque doubled from 2 to 4% MVC (time1 to time2), whereas tibialis anterior (TA) H-reflexes and M-waves did not change significantly (H-reflex from 0.8 to 2% Mmax; M-wave from 12 to 14% Mmax). In 7 of 13 subjects, extra torque developed at higher stimulation intensities (35-65% Mmax). In these seven subjects, torque increased from 13 to 20% MVC, whereas TA H-reflexes and M-waves were not significantly different (H-reflex from 0.7 to 1% Mmax; M-wave from 49 to 54% Mmax). Thus enhanced H-reflexes contributed to extra plantarflexion, however, other factors generated extra dorsiflexion.
. Corticospinal excitability is lower during rhythmic arm movement than during tonic contraction. J Neurophysiol 95: 914 -921, 2006. First published October 26, 2005 doi:10.1152/jn.00684.2005. Humans perform rhythmic, locomotor movements with the arms and legs every day. Studies using reflexes to probe the functional role of the CNS suggest that spinal circuits are an important part of the neural control system for rhythmic arm cycling and walking. Here, by studying motorevoked potentials (MEPs) in response to transcranial magnetic stimulation (TMS) of the motor cortex, and H-reflexes induced by electrical stimulation of peripheral nerves, we show a reduction in corticospinal excitability during rhythmic arm movement compared with tonic, voluntary contraction. Responses were compared between arm cycling and tonic contraction at four positions, while participants generated similar levels of muscle activity. Both H-reflexes and MEPs were significantly smaller during arm cycling than during tonic contraction at the midpoint of arm flexion (F ϭ 13.51, P ϭ 0.006; F ϭ 11.83, P ϭ 0.009). Subthreshold TMS significantly facilitated the FCR H-reflex during tonic contractions, but did not significantly modulate H-reflex amplitude during arm cycling. The data indicate a reduction in the responsiveness of cells constituting the fast, monosynaptic, corticospinal pathway during arm cycling and suggest that the motor cortex may contribute less to motor drive during rhythmic arm movement than during tonic, voluntary contraction. Our results are consistent with the idea that subcortical regions contribute to the control of rhythmic arm movements despite highly developed corticospinal projections to the human upper limb.
Changes in the reflex amplitude throughout the day have been observed in non-human mammals. The present experiment tested whether diurnal fluctuations also occur in humans. Hoffmann reflex (H-reflex) amplitude was measured in soleus and flexor carpi radialis (FCR) muscles from the data collected over a 12-h period between 7:00-9:00 a.m. and 7:00-9:00 p.m. At 4-h intervals, M/H recruitment curves were obtained, and two measures of H-reflex excitability were calculated. The maximal H-reflex (H (max)) was calculated as the average of the three largest H-reflexes. H-reflexes were also sampled from the ascending limb of the M/H recruitment curve (H (A), n=10), with a corresponding M-wave of 5% M (max). All values were normalized to the maximal M-wave (M (max)). Soleus H-reflex amplitude and plantar flexion maximal voluntary isometric contraction force (MVIC) were significantly smaller (p<0.05) in the morning (H (max)=57.2% M (max), H (A)=42.3%, M (max), MVIC=162.1 Nm) than in the evening (H (max)=69.1% M (max), a 20.1% increase, H (A)=54.1% M (max), a 27.4% increase and MVIC=195.8 Nm, a 20.8% increase). In contrast, FCR H-reflex amplitude and FCR MVIC were unchanged across all testing sessions. The data show that diurnal fluctuations are present in the amplitude of the human soleus but not in the FCR H-reflex. Diurnal fluctuation in the human soleus H-reflex amplitude must be considered when interpreting H-reflex data, especially when a repeated measures design spanning several days is utilized.
This combination of NMES and bilateral exercise may prove to be an effective component of a comprehensive shoulder rehabilitation program for patients with persistent trapezius muscle dysfunction as a result of SAN damage.
In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments. 1. To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave amplitude for ECR brevis. Stimuli were delivered during both isometric wrist flexions and radial deviation actions with an equivalent EMG amplitude in FCR (approximately 5% wrist flexion MVC). 2. To explore the homonymous Ia afferent pathway to FCR motoneurons, 50 stimuli were delivered to the median nerve at intensities ranging from below motor threshold to at least two times that which evoked a maximal M-wave during wrist flexion and radial deviation (matched FCR EMG at approximately 5% wrist flexion MVC). 3. EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) greater during MVCs in wrist flexion and extension (respectively) than radial deviation. ECR longus EMG was significantly greater during MVCs in radial deviation than extension. These results indicate that the gain of the Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex pathway to FCR is greater during wrist flexion than radial deviation. Transmission through both of these pathways probably contributes to the inability of individuals to maximally activate FCR during radial deviation MVCs.
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