Effects of aging and sex on voluntary activation and peak relaxation rate of human elbow flexors studied with motor cortical stimulation

Voluntary activation of muscle is commonly quantified by comparison of the extra force added by motor nerve stimulation during a contraction [superimposed twitch (SIT)] with that produced at rest by the same stimulus (resting twitch). An inability to achieve 100% voluntary activation implies that failure to produce maximal force output from the muscle must have occurred at a site at or above the level of the motoneurons. We have used cortical stimulation to quantify voluntary activation. Here, incomplete activation implies a failure at or above the level of motor cortical output. With cortical stimulation, it is inappropriate to compare extra force evoked during a contraction with the twitch evoked in resting muscle because motor cortical and spinal cord excitability both increase with activity. However, an appropriate “resting twitch” can be estimated. We previously estimated its amplitude by extrapolation of the linear relation between SIT amplitude and voluntary torque calculated from 35 contractions of >50% maximum (Todd G, Taylor JL, and Gandevia SC. J Physiol 551: 661–671, 2003). In this study, we improved the utility of this method to enable evaluation of voluntary activation when it may be changing over time, such as during the development of fatigue, or in patients who may be unable to perform large numbers of contractions. We have reduced the number of contractions required to only three. Estimation of the resting twitch from three contractions was reliable over time with low variability. Furthermore, its reliability and variability were similar to the resting twitch estimated from 30 contractions and to that evoked by conventional motor nerve stimulation.

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

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2014-0109 ◽

2014 ◽

Vol 39 (12) ◽

pp. 1338-1344 ◽

Cited By ~ 30

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.

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Motor Cortical Stimulation for Parkinsonism in Multiple System Atrophy

Archives of Neurology ◽

10.1001/archneur.60.11.1554 ◽

2003 ◽

Vol 60 (11) ◽

pp. 1554 ◽

Cited By ~ 35

Author(s):

Galit Kleiner-Fisman ◽

David N. Fisman ◽

Farooq I. Kahn ◽

Elspeth Sime ◽

Andres M. Lozano ◽

...

Keyword(s):

Multiple System Atrophy ◽

Cortical Stimulation ◽

Motor Cortical

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Motor Cortical Stimulation in Man

Biomagnetic Stimulation ◽

10.1007/978-1-4757-9507-3_4 ◽

1994 ◽

pp. 49-57 ◽

Cited By ~ 5

Author(s):

J. C. Rothwell

Keyword(s):

Cortical Stimulation ◽

Motor Cortical

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Effect of experimental muscle pain on maximal voluntary activation of human biceps brachii muscle

Journal of Applied Physiology ◽

10.1152/japplphysiol.00603.2011 ◽

2011 ◽

Vol 111 (3) ◽

pp. 743-750 ◽

Cited By ~ 18

Author(s):

Serajul I. Khan ◽

Chris J. McNeil ◽

Simon C. Gandevia ◽

Janet L. Taylor

Keyword(s):

Hypertonic Saline ◽

Muscle Pain ◽

Biceps Brachii ◽

Elbow Flexion ◽

Voluntary Activation ◽

Psychophysical Experiment ◽

Motor Point ◽

Experimental Muscle Pain ◽

Wide Range ◽

Motor Cortical

Muscle pain has widespread effects on motor performance, but the effect of pain on voluntary activation, which is the level of neural drive to contracting muscle, is not known. To determine whether induced muscle pain reduces voluntary activation during maximal voluntary contractions, voluntary activation of elbow flexors was assessed with both motor-point stimulation and transcranial magnetic stimulation over the motor cortex. In addition, we performed a psychophysical experiment to investigate the effect of induced muscle pain across a wide range of submaximal efforts (5–75% maximum). In all studies, elbow flexion torque was recorded before, during, and after experimental muscle pain by injection of 1 ml of 5% hypertonic saline into biceps. Injection of hypertonic saline evoked deep pain in the muscle (pain rating ∼5 on a scale from 0 to 10). Experimental muscle pain caused a small (∼5%) but significant reduction of maximal voluntary torque in the motor-point and motor cortical studies ( P < 0.001 and P = 0.045, respectively; n = 7). By contrast, experimental muscle pain had no significant effect on voluntary activation when assessed with motor-point and motor cortical stimulation although voluntary activation tested with motor-point stimulation was reduced by ∼2% in contractions after pain had resolved ( P = 0.003). Furthermore, induced muscle pain had no significant effect on torque output during submaximal efforts ( P > 0.05; n = 6), which suggests that muscle pain did not alter the relationship between the sense of effort and production of voluntary torque. Hence, the present study suggests that transient experimental muscle pain in biceps brachii has a limited effect on central motor pathways.

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.01166.2013 ◽

2014 ◽

Vol 116 (4) ◽

pp. 385-394 ◽

Cited By ~ 38

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.

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