Chapter 5 - Central Factors in Neuromuscular Fatigue Flashcards
Explain the difference between supramaximal and submaximal stimulation.
At supramaximal intensity, stimulation of the fatigue muscle via its motorneuron may or may not result in increased force.
On the contrary, at submaximal intensity when subjects are asked to generate a submaximal contraction until fatigue, muscle EMG increases gradually as additional motor units are recruited to maintain the force.
Explain what occurs to motoneuron excitability during late adaptation.
During late adaptation, motorneuron excitability firing frequency decreases gradually. This is due to decreased muscle activation that occurs with sustained or intermittent effort.
When considering central factors in neuromuscular fatigue what occurs in muscle spindle excitation and why?
In neuromuscular fatigue, muscle spindle excitation decreases due to its excitatory influence on motorneurons.
Gamma-motorneurons innervate intrafusal muscle fibers and cause contraction of their contractile components therefore the fusimotor neuron discharge constitutes an important component in the response of muscle spindle afferents during movement.
What is presynaptic inhibition?
Presynaptic inhibition is the depolarization of Ia afferent terminals to motorneurons via axoaxonal synapses, which reduces the size of the Ia excitatory postsynaptic potential.
Evidence shows that presynaptic inhibition, which usually decreases at the beginning of contraction, may also increase as the contraction continues, thus results in a gradual reduction in motorneuron excitation.
What happens to MVC as a result of presynaptic inhibition?
Some evidence shows that presynaptic inhibition, which decreases at the beginning of contraction, may increase as the contraction continues, which would involve a gradual reduction in motorneuron excitation.
Presynaptic inhibition system in maximal efforts to fatigue is supplied by the case of cocontraction, or Coactivation, of agonists and antagonists. During repeated isometric MVCs continued to fatigue, cocontraction of agonists and antagonists’ muscle increases, as evidence by a decrease in EMG of the agonist and no change in EMG of the antagonist.
One hypothesis states that supraspinal influence reduces the Ia presynaptic inhibition of afferents that convey reciprocal inhibition to antagonists during agonist fatigue, thus increasing Coactivation.
What is the “tug-of-war” between cortical inhibition and spinal excitation?
The “tug-of-war” term is used to describe the findings of an experiment that involves cortical inhibition and spinal excitation. The contraction lasted about 100 seconds and isometric force decreased about 25% of the original and it was reported that there was an increase in the duration of the silent period.
Authors concluded that either 1) there was no change in cortical excitability with fatigue or 2) there was change, but the changes in cortical and spinal excitability changed in equal and opposite directions.
They attributed the increase in cortical inhibitory influence to peripheral feedback from the fatiguing muscle. These two findings are how the “tug-of-war” came about as the authors can use any of the two findings to conclude their study.
The results from experiments using cortical and subcortical stimulation during a sustained MVC to fatigue were summarized. What are these six theories?
1) The level of cortical inhibition increases,
2) the level of cortical excitation increases,
3) the cortex appears to drive motorneurons at sufficient intensity to elicit maximal contractile responses in the control condition but perhaps not during fatigue,
4) this central fatigue is related to afferent information from the periphery,
5) decreases in corticospinal stimulation of motorneurons may also occur, and
6) since TMS results in a superimposed contractile response during fatigue, the locus of this central failure is somewhere in the sites driving the cortex.
What evidence is there pertaining to central fatigue during prolonged, low-force contractions?
Sogaard and colleagues and Smith and colleagues have used TMS to show that central fatigue occurs even with sustained low-force voluntary contractions of 15% and 5% of MVC, respectfully.
Their subjects held a submaximal isometric contraction of the biceps brachii for 43 minutes (15%) or 70 minutes (5%). In this study there’s evidence of muscle fatigue and central fatigue.
What is the difference in isometric versus anisometric tasks with regards to fatigue?
Most experiments in regard to fatigue use constant-load isometric contractions, this is due to intramuscular electrode stability during the contractions allowing unequivocal identification of the same motor unit over a prolonged duration.
Another study showed that motor unit discharge rates decreased when the triceps branchii performed contractions that were isometric but stimulated the torque changes that occur during an anisometric task involving elbow flexion.
This is due to the dynamic nature of this fatigue task, afferent information, blood flow, or both may be different, and the firing rate during fatigue may also be different.
What does the current evidence suggest about rotation of motor units during contractions maintained at very low intensities?
Current evidence suggests that at 10% of MVC, rotation amongst the synergist involved in plantar flexion, especially during the latter part of the task to fatigue.
At 50% of MVC, several motor units ceased being activated, only to be reactivated later in the session, while the whole-muscle activity and that of other units remained activated at a constant level.
PICs and activation and inactivation of ion currents that occur to various degrees among motorneurons during prolonged contractions plays a critical role on this phenomenon.
