Spinal and Supraspinal Factors in Human Muscle Fatigue

2001 ◽  
Vol 81 (4) ◽  
pp. 1725-1789 ◽  
Author(s):  
S. C. Gandevia
Keyword(s):  
Muscle Fatigue ◽  
Muscle Force ◽  
Cortical Excitability ◽  
Central Fatigue ◽  
Muscle Afferents ◽  
Human Muscle ◽  
Voluntary Activation ◽  
Group Iii ◽  
Exercise Induced ◽  
Human Muscle Fatigue

Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for “central” fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal changes in cortical excitability and inhibitability based on electromyographic (EMG) recordings, and a decline in supraspinal “drive” based on force recordings. Some of the changes in motor cortical behavior can be dissociated from the development of this “supraspinal” fatigue. Central changes also occur at a spinal level due to the altered input from muscle spindle, tendon organ, and group III and IV muscle afferents innervating the fatiguing muscle. Some intrinsic adaptive properties of the motoneurons help to minimize fatigue. A number of other central changes occur during fatigue and affect, for example, proprioception, tremor, and postural control. Human muscle fatigue does not simply reside in the muscle.

scholarly journals Changes in motor cortical excitability during human muscle fatigue.

1996 ◽  
Vol 490 (2) ◽  
pp. 519-528 ◽  
Author(s):  
J L Taylor ◽  
J E Butler ◽  
G M Allen ◽  
S C Gandevia
Keyword(s):  
Muscle Fatigue ◽  
Cortical Excitability ◽  
Human Muscle ◽  
Motor Cortical Excitability ◽  
Motor Cortical ◽  
Human Muscle Fatigue

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.

scholarly journals Is the notion of central fatigue based on a solid foundation?

2016 ◽  
Vol 115 (2) ◽  
pp. 967-977 ◽  
Author(s):  
Paola Contessa ◽  
Alessio Puleo ◽  
Carlo J. De Luca
Keyword(s):  
Muscle Fatigue ◽  
Muscle Force ◽  
Empirical Studies ◽  
Central Fatigue ◽  
Unit Force ◽  
The Central Nervous System ◽  
Solid Foundation ◽  
Exercise Induced ◽  
Voluntary Contractions ◽  
Central Factors

Exercise-induced muscle fatigue has been shown to be the consequence of peripheral factors that impair muscle fiber contractile mechanisms. Central factors arising within the central nervous system have also been hypothesized to induce muscle fatigue, but no direct empirical evidence that is causally associated to reduction of muscle force-generating capability has yet been reported. We developed a simulation model to investigate whether peripheral factors of muscle fatigue are sufficient to explain the muscle force behavior observed during empirical studies of fatiguing voluntary contractions, which is commonly attributed to central factors. Peripheral factors of muscle fatigue were included in the model as a time-dependent decrease in the amplitude of the motor unit force twitches. Our simulation study indicated that the force behavior commonly attributed to central fatigue could be explained solely by peripheral factors during simulated fatiguing submaximal voluntary contractions. It also revealed important flaws regarding the use of the interpolated twitch response from electrical stimulation of the muscle as a means for assessing central fatigue. Our analysis does not directly refute the concept of central fatigue. However, it raises important concerns about the manner in which it is measured and about the interpretation of the commonly accepted causes of central fatigue and questions the very need for the existence of central fatigue.

scholarly journals The physiological basis of neuromuscular fatigue during high intensity exercise

2017 ◽  
Vol 3 (2) ◽  
pp. 1-3
Author(s):  
Faryal Zahir ◽  
Radha Budhwar ◽  
Gabrielle Gonsalves ◽  
Lily Green ◽  
Aliza Barua
Keyword(s):  
Muscle Fatigue ◽  
Motor Unit ◽  
High Intensity ◽  
Muscle Fibers ◽  
Central Fatigue ◽  
Muscle Afferents ◽  
Neuromuscular Fatigue ◽  
High Intensity Exercise ◽  
Peripheral Fatigue ◽  
Group Iii

Introduction Neuromuscular fatigue refers to a reduction in maximal force generation capacity, and is categorized as central and peripheral. Central fatigue is defined as a reduction in the ability of the central nervous system to voluntarily activate muscles, and peripheral fatigue indicates a decrease in the contractile strength of muscle fibers. During high intensity exercise, motor neurons are involved in the recruitment of type IIB muscle fibers as they are fast-twitch, high glycolytic, and have low aerobic capacity. Furthermore, group III and IV muscle afferents detect the physiological circumstances in the body and convey signals to the brain that influence the onset of central and peripheral fatigue. Methods A PRISMA flow diagram was created to record relevant studies found from scholarly databases. Inclusion criteria required studies from 2005 to 2017, and subject grouping headings required key terms indicating that the presence of central and peripheral fatigue was analyzed on healthy adult subjects performing exercise. To ensure that high quality studies were analyzed, each article was independently rated using the National Institute of Health Quality Assessment Tool criteria. Discussion During low intensity exercise, asynchronous motor unit recruitment is involved in delaying the onset of muscle fatigue. However, this is not apparent in high intensity exercises, as maximal motor unit firing is required in order to sustain a maximal level of force output. Persistent firing of action potentials to maintain muscle contraction results in acetylcholine depletion at the motor end plate, initiating the process of central fatigue. Furthermore, due to prolonged metabolite accumulation in skeletal muscle fibers, group III and IV afferents convey signals to the motor cortex and cause a reduction in the action potential conduction velocities along the contracting muscle. This leads to the onset of peripheral fatigue. As high intensity exercise proceeds, electromyogram (EMG) measurements display this as an increase in amplitude to reflect heightened motor unit recruitment and a compressed power density spectrum alongside a decreased centre frequency. This is determined by the innervated muscle fiber’s conduction velocity and subsequent variations in the action potential waveform shape. Conclusion A record of current studies systematically display the overview of muscle fatigue and its underlying mechanisms during exercise. However, further research is yet to be conducted for a more comprehensive understanding regarding the onset and recovery of neuromuscular fatigue in varied population demographics and physiological circumstances. Likewise, the distinctive roles of group III and IV muscle afferents in supraspinal stimulation require further investigation in order to gain a holistic understanding of their involvement in central fatigue and resistance training. Additional research in this subject matter is currently being explored through technology involving imaging studies, as they have potential to elucidate motor cortex activity alongside other regions of the brain and portray neuromuscular muscle fatigue eminently.

Fatigue-related firing of muscle nociceptors reduces voluntary activation of ipsilateral but not contralateral lower limb muscles

2015 ◽  
Vol 118 (4) ◽  
pp. 408-418 ◽  
Author(s):  
David S. Kennedy ◽  
Siobhan C. Fitzpatrick ◽  
Simon C. Gandevia ◽  
Janet L. Taylor
Keyword(s):  
Lower Limb ◽  
Femoral Nerve ◽  
Central Fatigue ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
Lower Limbs ◽  
Voluntary Activation ◽  
Knee Extensors ◽  
Group Iii ◽  
Lower Limb Muscles

During fatiguing upper limb exercise, maintained firing of group III/IV muscle afferents can limit voluntary drive to muscles within the same limb. It is not known if this effect occurs in the lower limb. We investigated the effects of group III/IV muscle afferent firing from fatigued ipsilateral and contralateral extensor muscles and ipsilateral flexor muscles of the knee on voluntary activation of the knee extensors. In three experiments, we examined voluntary activation of the knee extensors by measuring changes in superimposed twitches evoked by femoral nerve stimulation. Subjects attended on 2 days for each experiment. On one day a sphygmomanometer cuff occluded blood flow of the fatigued muscles to maintain firing of group III/IV muscle afferents. After a 2-min extensor contraction ( experiment 1; n = 9), mean voluntary activation was lower with than without maintained ischemia (47 ± 19% vs. 87 ± 8%, respectively; P < 0.001). After a 2-min knee flexor maximal voluntary contraction (MVC) ( experiment 2; n = 8), mean voluntary activation was also lower with than without ischemia (59 ± 21% vs. 79 ± 9%; P < 0.01). After the contralateral (left) MVC ( experiment 3; n = 8), mean voluntary activation of the right leg was similar with or without ischemia (92 ± 6% vs. 93 ± 4%; P = 0.65). After fatiguing exercise, activity in group III/IV muscle afferents reduces voluntary activation of the fatigued muscle and nonfatigued antagonist muscles in the same leg. However, group III/IV muscle afferents from the fatigued left leg had no effect on the unfatigued right leg. This suggests that any “crossover” of central fatigue in the lower limbs is not mediated by group III/IV muscle afferents.

scholarly journals Human Muscle Fatigue Model in Dynamic Motions

2012 ◽  
pp. 349-356 ◽  
Author(s):  
Ruina Ma ◽  
Damien Chablat ◽  
Fouad Bennis ◽  
Liang Ma
Keyword(s):  
Muscle Fatigue ◽  
Human Muscle ◽  
Fatigue Model ◽  
Human Muscle Fatigue
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