Non-uniform adaptation of motor unit discharge rates during sustained static contraction of the upper trapezius muscle

2008 ◽  
Vol 191 (3) ◽  
pp. 363-370 ◽  
Author(s):  
D. Falla ◽  
D. Farina
2018 ◽  
Vol 120 (6) ◽  
pp. 3246-3256 ◽  
Author(s):  
Spencer A. Murphy ◽  
Francesco Negro ◽  
Dario Farina ◽  
Tanya Onushko ◽  
Matthew Durand ◽  
...  

Following stroke, hyperexcitable sensory pathways, such as the group III/IV afferents that are sensitive to ischemia, may inhibit paretic motor neurons during exercise. We quantified the effects of whole leg ischemia on paretic vastus lateralis motor unit firing rates during submaximal isometric contractions. Ten chronic stroke survivors (>1 yr poststroke) and 10 controls participated. During conditions of whole leg occlusion, the discharge timings of motor units were identified from decomposition of high-density surface electromyography signals during repeated submaximal knee extensor contractions. Quadriceps resting twitch responses and near-infrared spectroscopy measurements of oxygen saturation as an indirect measure of blood flow were made. There was a greater decrease in paretic motor unit discharge rates during the occlusion compared with the controls (average decrease for stroke and controls, 12.3 ± 10.0% and 0.1 ± 12.4%, respectively; P < 0.001). The motor unit recruitment thresholds did not change with the occlusion (stroke: without occlusion, 11.68 ± 5.83%MVC vs. with occlusion, 11.11 ± 5.26%MVC; control: 11.87 ± 5.63 vs. 11.28 ± 5.29%MVC). Resting twitch amplitudes declined similarly for both groups in response to whole leg occlusion (stroke: 29.16 ± 6.88 vs. 25.75 ± 6.78 Nm; control: 38.80 ± 13.23 vs 30.14 ± 9.64 Nm). Controls had a greater exponential decline (lower time constant) in oxygen saturation compared with the stroke group (stroke time constant, 22.90 ± 10.26 min vs. control time constant, 5.46 ± 4.09 min; P < 0.001). Ischemia of the muscle resulted in greater neural inhibition of paretic motor units compared with controls and may contribute to deficient muscle activation poststroke. NEW & NOTEWORTHY Hyperexcitable inhibitory sensory pathways sensitive to ischemia may play a role in deficient motor unit activation post stroke. Using high-density surface electromyography recordings to detect motor unit firing instances, we show that ischemia of the exercising muscle results in greater inhibition of paretic motor unit firing rates compared with controls. These findings are impactful to neurophysiologists and clinicians because they implicate a novel mechanism of force-generating impairment poststroke that likely exacerbates baseline weakness.


2016 ◽  
Vol 116 (2) ◽  
pp. 611-618 ◽  
Author(s):  
Jakob L. Dideriksen ◽  
Ales Holobar ◽  
Deborah Falla

Pain is associated with changes in the neural drive to muscles. For the upper trapezius muscle, surface electromyography (EMG) recordings have indicated that acute noxious stimulation in either the cranial or the caudal region of the muscle leads to a relative decrease in muscle activity in the cranial region. It is, however, not known if this adaption reflects different recruitment thresholds of the upper trapezius motor units in the cranial and caudal region or a nonuniform nociceptive input to the motor units of both regions. This study investigated these potential mechanisms by direct motor unit identification. Motor unit activity was investigated with high-density surface EMG signals recorded from the upper trapezius muscle of 12 healthy volunteers during baseline, control (intramuscular injection of isotonic saline), and painful (hypertonic saline) conditions. The EMG was decomposed into individual motor unit spike trains. Motor unit discharge rates decreased significantly from control to pain conditions by 4.0 ± 3.6 pulses/s (pps) in the cranial region but not in the caudal region (1.4 ± 2.8 pps; not significant). These changes were compatible with variations in the synaptic input to the motoneurons of the two regions. These adjustments were observed, irrespective of the location of noxious stimulation. These results strongly indicate that the nociceptive synaptic input is distributed in a nonuniform way across regions of the upper trapezius muscle.


2010 ◽  
Vol 109 (5) ◽  
pp. 1455-1466 ◽  
Author(s):  
Carolina Vila-Chã ◽  
Deborah Falla ◽  
Dario Farina

The study investigated changes in motor output and motor unit behavior following 6 wk of either strength or endurance training programs commonly used in conditioning and rehabilitation. Twenty-seven sedentary healthy men (age, 26.1 ± 3.9 yr; mean ± SD) were randomly assigned to strength training (ST; n = 9), endurance training (ET; n = 10), or a control group (CT; n = 8). Maximum voluntary contraction (MVC), time to task failure (isometric contraction at 30% MVC), and rate of force development (RFD) of the quadriceps were measured before ( week 0), during ( week 3), and after a training program of 6 wk. In each experimental session, surface and intramuscular EMG signals were recorded from the vastus medialis obliquus and vastus lateralis muscles during isometric knee extension at 10 and 30% MVC. After 6 wk of training, MVC and RFD increased in the ST group (17.5 ± 7.5 and 33.3 ± 15.9%, respectively; P < 0.05), whereas time to task failure was prolonged in the ET group (29.7 ± 13.4%; P < 0.05). The surface EMG amplitude at 30% MVC force increased with training in both groups, but the training-induced changes in motor unit discharge rates differed between groups. After endurance training, the motor unit discharge rate at 30% MVC decreased from 11.3 ± 1.3 to 10.1 ± 1.1 pulses per second (pps; P < 0.05) in the vasti muscles, whereas after strength training it increased from 11.4 ± 1.2 to 12.7 ± 1.3 pps ( P < 0.05). Finally, motor unit conduction velocity during the contractions at 30% MVC increased for both the ST and ET groups, but only after 6 wk of training ( P < 0.05). In conclusion, these strength and endurance training programs elicit opposite adjustments in motor unit discharge rates but similar changes in muscle fiber conduction velocity.


2005 ◽  
Vol 30 (3) ◽  
pp. 341-351 ◽  
Author(s):  
Gary Kamen

Researchers have alluded to the existence of "neural factors" in the expression and development of muscular strength. Candidate neural factors including motor unit recruitment, rate coding, doublet firing, and motor unit synchronization are discussed in this review. Aging is generally accompanied by lower motor unit discharge rates. However, both young and older adults exhibit rapid changes in muscular strength with repeated strength testing. These strength changes occur with concomitant albeit transient increases in motor unit discharge rate. These and other neural factors may contribute to the initial increases in muscular strength observed during the early phases of resistance exercise training. Key words: firing rate, muscle, exercise


2005 ◽  
Vol 98 (3) ◽  
pp. 999-1005 ◽  
Author(s):  
Dario Farina ◽  
Lars Arendt-Nielsen ◽  
Thomas Graven-Nielsen

The aim of this human study was to investigate the effect of experimentally induced muscle pain on the modifications of motor unit discharge rate during sustained, constant-force contractions. Intramuscular and multichannel surface electromyographic (EMG) signals were collected from the right and left tibialis anterior muscle of 11 volunteers. The subjects performed two 4-min-long isometric contractions at 25% of the maximal dorsiflexion torque, separated by a 20-min rest. Before the beginning of the second contraction, hypertonic (painful; right leg) or isotonic (nonpainful; left leg) saline was injected into the tibialis anterior. Pain intensity scores did not change significantly in the first 150 s of the painful contraction. Exerted torque and its coefficient of variation were the same for the painful and nonpainful contractions. Motor unit discharge rate was higher in the beginning of the nonpainful contraction than the painful contraction on the right side [means ± SE, 11.3 ± 0.2 vs. 10.6 ± 0.2 pulses/s (pps); P < 0.01] whereas it was the same for the two contractions on the left side (11.6 ± 0.2 vs. 11.5 ± 0.2 pps). The decrease in discharge rate in 4 min was smaller for the painful (0.4 ± 0.1 pps) than for the control contractions (1.3 ± 0.1 pps). Initial value and decrease in motor unit conduction velocity were not different in the four contractions (right leg, 4.0 ± 0.1 m/s with decrease of 0.6 ± 0.1 m/s in 4 min; left leg, 4.1 ± 0.1 m/s with 0.7 ± 0.1 m/s decrease). In conclusion, stimulation of nociceptive afferents by injection of hypertonic saline did not alter motor unit conduction velocity but reduced the initial motor unit discharge rates and the difference between initial and final discharge rates during sustained contraction.


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