scholarly journals Firing of antagonist small-diameter muscle afferents reduces voluntary activation and torque of elbow flexors

2013 ◽  
Vol 591 (14) ◽  
pp. 3591-3604 ◽  
Author(s):  
David S. Kennedy ◽  
Chris J. McNeil ◽  
Simon C. Gandevia ◽  
Janet L. Taylor
Keyword(s):  
Small Diameter ◽  
Muscle Afferents ◽  
Voluntary Activation ◽  
Elbow Flexors

Fatigue-related firing of distal muscle nociceptors reduces voluntary activation of proximal muscles of the same limb

2014 ◽  
Vol 116 (4) ◽  
pp. 385-394 ◽  
Author(s):  
David S. Kennedy ◽  
Chris J. McNeil ◽  
Simon C. Gandevia ◽  
Janet L. Taylor
Keyword(s):  
Magnetic Stimulation ◽  
Elbow Flexion ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
Voluntary Activation ◽  
Elbow Flexors ◽  
Group Iii ◽  
Distal Muscle ◽  
Fatiguing Exercise ◽  
Stimulation Of

With fatiguing exercise, firing of group III/IV muscle afferents reduces voluntary activation and force of the exercised muscles. These afferents can also act across agonist/antagonist pairs, reducing voluntary activation and force in nonfatigued muscles. We hypothesized that maintained firing of group III/IV muscle afferents after a fatiguing adductor pollicis (AP) contraction would decrease voluntary activation and force of AP and ipsilateral elbow flexors. In two experiments ( n = 10) we examined voluntary activation of AP and elbow flexors by measuring changes in superimposed twitches evoked by ulnar nerve stimulation and transcranial magnetic stimulation of the motor cortex, respectively. Inflation of a sphygmomanometer cuff after a 2-min AP maximal voluntary contraction (MVC) blocked circulation of the hand for 2 min and maintained firing of group III/IV muscle afferents. After a 2-min AP MVC, maximal AP voluntary activation was lower with than without ischemia (56.2 ± 17.7% vs. 76.3 ± 14.6%; mean ± SD; P < 0.05) as was force (40.3 ± 12.8% vs. 57.1 ± 13.8% peak MVC; P < 0.05). Likewise, after a 2-min AP MVC, elbow flexion voluntary activation was lower with than without ischemia (88.3 ± 7.5% vs. 93.6 ± 3.9%; P < 0.05) as was torque (80.2 ± 4.6% vs. 86.6 ± 1.0% peak MVC; P < 0.05). Pain during ischemia was reported as Moderate to Very Strong. Postfatigue firing of group III/IV muscle afferents from the hand decreased voluntary drive and force of AP. Moreover, this effect decreased voluntary drive and torque of proximal unfatigued muscles, the elbow flexors. Fatigue-sensitive group III/IV muscle nociceptors act to limit voluntary drive not only to fatigued muscles but also to unfatigued muscles within the same limb.

A comparison of central aspects of fatigue in submaximal and maximal voluntary contractions

2008 ◽  
Vol 104 (2) ◽  
pp. 542-550 ◽  
Author(s):  
Janet L. Taylor ◽  
Simon C. Gandevia
Keyword(s):  
Small Diameter ◽  
Force Production ◽  
Central Fatigue ◽  
Motor Units ◽  
Muscle Afferents ◽  
Voluntary Activation ◽  
Peripheral Fatigue ◽  
Force Output ◽  
Group Iii ◽  
Motor Cortical

Magnetic and electrical stimulation at different levels of the neuraxis show that supraspinal and spinal factors limit force production in maximal isometric efforts (“central fatigue”). In sustained maximal contractions, motoneurons become less responsive to synaptic input and descending drive becomes suboptimal. Exercise-induced activity in group III and IV muscle afferents acts supraspinally to limit motor cortical output but does not alter motor cortical responses to transcranial magnetic stimulation. “Central” and “peripheral” fatigue develop more slowly during submaximal exercise. In sustained submaximal contractions, central fatigue occurs in brief maximal efforts even with a weak ongoing contraction (<15% maximum). The presence of central fatigue when much of the available motor pathway is not engaged suggests that afferent inputs contribute to reduce voluntary activation. Small-diameter muscle afferents are likely to be activated by local activity even in sustained weak contractions. During such contractions, it is difficult to measure central fatigue, which is best demonstrated in maximal efforts. To show central fatigue in submaximal contractions, changes in motor unit firing and force output need to be characterized simultaneously. Increasing central drive recruits new motor units, but the way this occurs is likely to depend on properties of the motoneurons and the inputs they receive in the task. It is unclear whether such factors impair force production for a set level of descending drive and thus represent central fatigue. The best indication that central fatigue is important during submaximal tasks is the disproportionate increase in subjects' perceived effort when maintaining a low target force.

Unilateral isometric muscle fatigue decreases force production and activation of contralateral knee extensors but not elbow flexors

2014 ◽  
Vol 39 (12) ◽  
pp. 1338-1344 ◽  
Author(s):  
Israel Halperin ◽  
David Copithorne ◽  
David G. Behm
Keyword(s):  
Muscle Fatigue ◽  
Force Production ◽  
Voluntary Activation ◽  
Knee Extensors ◽  
Elbow Flexors ◽  
Post Intervention ◽  
Nonlocal Effects ◽  
And Performance ◽  
Voluntary Contractions ◽  
Isometric Muscle

Nonlocal muscle fatigue occurs when fatiguing 1 muscle alters performance of another rested muscle. The purpose of the study was to investigate if fatiguing 2 separate muscles would affect the same rested muscle, and if fatiguing the same muscle would affect 2 separate muscles. Twenty-one trained males participated in 2 studies (n = 11; n = 10). Subjects performed 2 pre-test maximum voluntary contractions (MVCs) with the nondominant knee extensors. Thereafter they performed two 100-s MVCs with their dominant knee extensors, elbow flexors, or rested. Between and after the sets, a single MVC with the nondominant rested knee extensors was performed. Subsequently, 12 nondominant knee extensors repeated MVCs were completed. Force, quadriceps voluntary activation (VA), and electromyography (EMG) were measured. The same protocol was employed in study 2 except the nondominant elbow-flexors were tested. Study 1: Compared with control conditions, a significant decrease in nondominant knee extensors force, EMG, and VA was found under both fatiguing conditions (P ≤ 0.05; effect size (ES) = 0.91–1.15; 2%–8%). Additionally, decrements in all variables were found from the first post-intervention MVC to the last (P ≤ 0.05; ES = 0.82–2.40; 9%–20%). Study 2: No differences were found between conditions for all variables (P ≥ 0.33; ES ≤ 0.2; ≤3.0%). However, all variables decreased from the first post-intervention MVC to the last (P ≤ 0.05; ES = 0.4–3.0; 7.2%–19.7%). Whereas the rested knee extensors demonstrated nonlocal effects regardless of the muscle being fatigued, the elbow-flexors remained unaffected. This suggests that nonlocal effects are muscle specific, which may hold functional implications for training and performance.

Activation of Spinobulbar Lamina I Neurons by Static Muscle Contraction

2002 ◽  
Vol 87 (3) ◽  
pp. 1641-1645 ◽  
Author(s):  
L. B. Wilson ◽  
D. Andrew ◽  
A. D. Craig
Keyword(s):  
Muscle Contraction ◽  
Small Diameter ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Ventrolateral Medulla ◽  
Antidromic Activation ◽  
Lamina I ◽  
Arterial Blood ◽  
Autonomic Reflexes ◽  
Blood Pressure Responses

Spinal lamina I neurons are selectively activated by small-diameter somatic afferents, and they project to brain stem sites that are critical for homeostatic control. Because small-diameter afferent activity evoked by contraction of skeletal muscle reflexly elicits exercise-related cardiorespiratory activation, we tested whether spinobulbar lamina I cells respond to muscle contraction. Spinobulbar lamina I neurons were identified in chloralose-anesthetized cats by antidromic activation from the ipsilateral caudal ventrolateral medulla. Static contractions of the ipsilateral triceps surae muscle were evoked by tibial nerve stimulation using parameters that avoid afferent activation, and arterial blood pressure responses were recorded. Recordings were maintained from 13 of 17 L7 lamina I spinobulbar neurons during static muscle contraction, and 5 of these neurons were excited. Three were selectively activated only by muscle afferents and did not have a cutaneous receptive field. Spinobulbar lamina I neurons activated by muscle contraction provide an ascending link for the reflex cardiorespiratory adjustments that accompany muscular work. This study provides an important first step in elucidating an ascending afferent pathway for somato-autonomic reflexes.

scholarly journals NaV1.9 channels in muscle afferent neurons and axons

2018 ◽  
Vol 120 (3) ◽  
pp. 1032-1044 ◽  
Author(s):  
Tyler L. Marler ◽  
Andrew B. Wright ◽  
Kristina L. Elmslie ◽  
Ankeeta K. Heier ◽  
Ethan Remily ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Muscle Activity ◽  
Muscle Blood Flow ◽  
Small Diameter ◽  
Muscle Afferents ◽  
Inactivation Kinetics ◽  
Afferent Neurons ◽  
Internal Solution ◽  
Group Iii ◽  
Muscle Afferent

The exercise pressor reflex (EPR) is activated by muscle contractions to increase heart rate and blood pressure during exercise. While this reflex is beneficial in healthy individuals, the reflex activity is exaggerated in patients with cardiovascular disease, which is associated with increased mortality. Group III and IV afferents mediate the EPR and have been shown to express both tetrodotoxin-sensitive (TTX-S, NaV1.6, and NaV1.7) and -resistant (TTX-R, NaV1.8, and NaV1.9) voltage-gated sodium (NaV) channels, but NaV1.9 current has not yet been demonstrated. Using a F−-containing internal solution, we found a NaV current in muscle afferent neurons that activates at around −70 mV with slow activation and inactivation kinetics, as expected from NaV1.9 current. However, this current ran down with time, which resulted, at least in part, from increased steady-state inactivation since it was slowed by both holding potential hyperpolarization and a depolarized shift of the gating properties. We further show that, following NaV1.9 current rundown (internal F−), application of the NaV1.8 channel blocker A803467 inhibited significantly more TTX-R current than we had previously observed (internal Cl−), which suggests that NaV1.9 current did not rundown with that internal solution. Using immunohistochemistry, we found that the majority of group IV somata and axons were NaV1.9 positive. The majority of small diameter myelinated afferent somata (putative group III) were also NaV1.9 positive, but myelinated muscle afferent axons were rarely labeled. The presence of NaV1.9 channels in muscle afferents supports a role for these channels in activation and maintenance of the EPR. NEW & NOTEWORTHY Small diameter muscle afferents signal pain and muscle activity levels. The muscle activity signals drive the cardiovascular system to increase muscle blood flow, but these signals can become exaggerated in cardiovascular disease to exacerbate cardiac damage. The voltage-dependent sodium channel NaV1.9 plays a unique role in controlling afferent excitability. We show that NaV1.9 channels are expressed in muscle afferents, which supports these channels as a target for drug development to control hyperactivity of these neurons.

Comparison of neuromuscular adjustments associated with sustained isometric contractions of four different muscle groups

2013 ◽  
Vol 114 (10) ◽  
pp. 1426-1434 ◽  
Author(s):  
Daria Neyroud ◽  
Jennifer Rüttimann ◽  
Anne F. Mannion ◽  
Guillaume Y. Millet ◽  
Nicola A. Maffiuletti ◽  
...  
Keyword(s):  
Muscle Fatigue ◽  
Upper Limb ◽  
Voluntary Contraction ◽  
Voluntary Activation ◽  
Knee Extensors ◽  
Elbow Flexors ◽  
Plantar Flexors ◽  
Task Failure ◽  
Before And After ◽  
Muscle Groups

The extent and characteristics of muscle fatigue of different muscle groups when subjected to a similar fatiguing task may differ. Thirteen healthy young men performed sustained contractions at 50% maximal voluntary contraction (MVC) force until task failure, with four different muscle groups, over two sessions. Per session, one upper limb and one lower limb muscle group were tested (knee extensors and thumb adductor, or plantar and elbow flexors). Changes in voluntary activation level and contractile properties were derived from doublet responses evoked during and after MVCs before and after exercise. Time to task failure differed ( P < 0.05) between muscle groups (220 ± 64 s for plantar flexors, 114 ± 27 s for thumb adductor, 77 ± 25 s for knee extensors, and 72 ± 14 s for elbow flexors). MVC force loss immediately after voluntary task failure was similar (−30 ± 11% for plantar flexors, −37 ± 13% for thumb adductor, −34 ± 15% for knee extensors, and −40 ± 12% for elbow flexors, P > 0.05). Voluntary activation was decreased for plantar flexors only (from 95 ± 5% to 82 ± 9%, P < 0.05). Potentiated evoked doublet amplitude was more depressed for upper limb muscles (−59.3 ± 14.7% for elbow flexors and −60.1 ± 24.1% for thumb adductor, P < 0.05) than for knee extensors (−28 ± 15%, P < 0.05); no reduction was found in plantar flexors (−7 ± 12%, P > 0.05). In conclusion, despite different times to task failure when sustaining an isometric contraction at 50% MVC force for as long as possible, diverse muscle groups present similar loss of MVC force after task failure. Thus the extent of muscle fatigue is not affected by time to task failure, whereas this latter determines the etiology of fatigue.

scholarly journals Increased Voluntary Activation of the Elbow Flexors Following a Single Session of Spinal Manipulation in a Subclinical Neck Pain Population

2019 ◽  
Vol 9 (6) ◽  
pp. 136 ◽  
Author(s):  
Mat Kingett ◽  
Kelly Holt ◽  
Imran Khan Niazi ◽  
Rasmus Wiberg Nedergaard ◽  
Michael Lee ◽  
...  
Keyword(s):  
Neck Pain ◽  
Repeated Measures ◽  
Spinal Manipulation ◽  
Maximum Voluntary Contraction ◽  
Elbow Flexion ◽  
Voluntary Contraction ◽  
Voluntary Activation ◽  
Elbow Flexors ◽  
Single Session ◽  
Post Intervention

To investigate the effects of a single session of spinal manipulation (SM) on voluntary activation of the elbow flexors in participants with subclinical neck pain using an interpolated twitch technique with transcranial magnetic stimulation (TMS), eighteen volunteers with subclinical neck pain participated in this randomized crossover trial. TMS was delivered during elbow flexion contractions at 50%, 75% and 100% of maximum voluntary contraction (MVC) before and after SM or control intervention. The amplitude of the superimposed twitches evoked during voluntary contractions was recorded and voluntary activation was calculated using a regression analysis. Dependent variables were analyzed with two-way (intervention × time) repeated measures ANOVAs. Significant intervention effects for SM compared to passive movement control were observed for elbow flexion MVC (p = 0.04), the amplitude of superimposed twitch (p = 0.04), and voluntary activation of elbow flexors (p =0.03). Significant within-group post-intervention changes were observed for the superimposed twitch (mean group decrease of 20.9%, p < 0.01) and voluntary activation (mean group increase of 3.0%, p < 0.01) following SM. No other significant within-group changes were observed. Voluntary activation of the elbow flexors increased immediately after one session of spinal manipulation in participants with subclinical neck pain. A decrease in the amplitude of superimposed twitch during elbow flexion MVC following spinal manipulation suggests a facilitation of motor cortical output.

Arm-cycling sprints induce neuromuscular fatigue of the elbow flexors and alter corticospinal excitability of the biceps brachii

2016 ◽  
Vol 41 (2) ◽  
pp. 199-209 ◽  
Author(s):  
Gregory E.P. Pearcey ◽  
David J. Bradbury-Squires ◽  
Michael Monks ◽  
Devin Philpott ◽  
Kevin E. Power ◽  
...  
Keyword(s):  
Evoked Potentials ◽  
Biceps Brachii ◽  
Motor Evoked Potentials ◽  
Neuromuscular Fatigue ◽  
Corticospinal Excitability ◽  
Voluntary Activation ◽  
Elbow Flexors ◽  
Mean Power ◽  
Arm Cycling ◽  
Spinal Excitability

We examined the effects of arm-cycling sprints on maximal voluntary elbow flexion and corticospinal excitability of the biceps brachii. Recreationally trained athletes performed ten 10-s arm-cycling sprints interspersed with 150 s of rest in 2 separate experiments. In experiment A (n = 12), maximal voluntary contraction (MVC) force of the elbow flexors was measured at pre-sprint 1, post-sprint 5, and post-sprint 10. Participants received electrical motor point stimulation during and following the elbow flexor MVCs to estimate voluntary activation (VA). In experiment B (n = 7 participants from experiment A), supraspinal and spinal excitability of the biceps brachii were measured via transcranial magnetic and transmastoid electrical stimulation that produced motor evoked potentials (MEPs) and cervicomedullary motor evoked potentials (CMEPs), respectively, during a 5% isometric MVC at pre-sprint 1, post-sprint 1, post-sprint 5, and post-sprint 10. In experiment A, mean power output, MVC force, potentiated twitch force, and VA decreased 13.1% (p < 0.001), 8.7% (p = 0.036), 27.6% (p = 0.003), and 5.6% (p = 0.037), respectively, from pre-sprint 1 to post-sprint 10. In experiment B, (i) MEPs decreased 42.1% (p = 0.002) from pre-sprint 1 to post-sprint 5 and increased 40.1% (p = 0.038) from post-sprint 5 to post-sprint 10 and (ii) CMEPs increased 28.5% (p = 0.045) from post-sprint 1 to post-sprint 10. Overall, arm-cycling sprints caused neuromuscular fatigue of the elbow flexors, which corresponded with decreased supraspinal and increased spinal excitability of the biceps brachii. The different post-sprint effects on supraspinal and spinal excitability may illustrate an inhibitory effect on supraspinal drive that reduces motor output and, therefore, decreases arm-cycling sprint performance.

Sign in / Sign up

Export Citation Format

Share Document