Neuromuscular Fatigue

1
Neuromuscular Fatigue Definition of skeletal
muscle fatigue Central versus Peripheral
fatigue Evidence that voluntary activation is
submaximal in Maximal efforts Development of
Central fatigue Insights from stimulation at
supraspinal sites (output from motor
cortex) Other supraspinal factors and Central
fatigue
2
Definition of fatigue- - transient decrease in
performance of muscle when it has been active for
a certain time as demonstrated by a failure to
maintain or develop an expected tension or power
3

• Central fatigue proximal to the NMJ
• Reduced central neural drive to the muscle
• possible changes in ascending and descending
  control
• may be be psychological (lack of motivation)
• OR
• Neurophysiological (CNS inhibition)

4
Evidence that voluntary activation is submaximal
in maximal efforts Training for
strength Strength of a muscle is directly related
to the ACSA (or more correctly the PCSA).
Increased hypertrophy increased strength If
increase in muscle strengthACSA then improvement
must be attributable to changes in the
CNSlearning or altered patterns of muscle and
motor unit recruitment
5
Thus in the untrained state, voluntary activation
must have been insufficient to produce maximal
force any increase in force with training can be
split into peripheral and central adaptations
(neural training effect).
6
Scripture et al (1890s) trained grip strength of
right hand which increased over 2 weeks by 70
but also observed an increase of 40 with the
untrained left handearly phases of strength
training involve learning the right pattern of
muscle activation (can then be applied to
contralateral side)
7
Imagined training Yue Cole (J Neurophysiol 67
1114-1123,1992) Evaluated the effect of imagined
training on the MVC of abductor digiti minimi.
Voluntary strength increased by 22 in those
undertaking imagined training and 30 in those
undertaking real contractions (no increase in the
control group)
8
Unilateral and bilateral contractions Some
research suggests the MVC during bilateral
contractions is less than the sum of the forces
produced in unilateral MVCs thus voluntary
activation during the bilateral contractions is
deficient
9
Electromyography (EMG) can be used to determine
the extent of neural activation Electrical
stimulation - direct nerve - percutaneous
Twitch interpolation and voluntary
activation Tetanus interposed between voluntary
contractions
10
Central fatigue develops during sustained or
intermittent isometric MVCs A combination of
results from recordings of the discharge of
single motor units and the technique of twitch
interpolation reveals that the average motor unit
discharge usually declines too rapidly to
maintain maximal force.
11
Stimulation at supraspinal sites Stimulation of
the human cerebral cortex non-invasively is
achieved using high-voltage anodal stimulation
delivered through the scalp, or a rapidly
changing magnetic field evoked via a coil on the
scalp. Transcranial magnetic or electrical
stimulation over the primary motor cortex
produces excitatory EMG responses in most muscles
12
Central fatigue during isometric MVCs includes a
supraspinal component because transcranial
stimulation of the motor cortex can add
progressively more force to that generated
voluntarily.(focal changes in cortical
excitability and inhibitability) Feedback of
the force-generating capacity of the muscle and
its biochemical status may ultimately impair the
drive to the motor cortex, via effectively
supra motor cortical sites.
13
Central changes also occur at a spinal level due
to altered input from muscle spindle, tendon
organ, and group III IV afferents innervating
the fatigued muscle Thus there are spinal and
supraspinal factors in human muscle fatigue
Feedback
14
At a spinal level the declining performance and
deteriorating status of the muscle produces
competing excitatory and inhibitory influences on
the motoneuron poolmany of which may contribute
to the decline in motor unit firing rate observed
during MVCs
Such changes include altered input from muscle
spindle, tendon organ, and group III IV
afferents innervating the fatigued muscle. Thus
there are spinal and supraspinal factors in human
muscle fatigue
15
Task failure Eg Depending on the task performed,
the diaphragm can develop either a large degree
or no central fatigue.Twitch interpolation using
phrenic nerve stimulation indicates max voluntary
activation during max voluntary inspiratory and
expiratory efforts. However during endurance
efforts, the final sustainable force was
relatively lower for expulsive than inspiratory
efforts (less perfusion during the expulsive
task) Gandevia McKenzie 1985
16
Running and cycling exercise performance is
eventually limited when the velocity cannot be
maintained, yet no single metabolic factor is
tightly coupled with the decline in skeletal
muscle power in such activities. Neural control
factors may be important in such activities eg
the cycle cadence that minimises VO2cost,
presumed muscle fatigue and subjective effort and
breathlessness differs by up to 40
rev/min. Surface EMG has been reported to decline
during high intensity bursts during a 100K
cycling effort
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Note that when CHO loading is undertaken the
exercise time to fatigue is increased but the
remaining muscle glycogen content at this point
is higher than when a restricted CHO intake
precedes exercise and fatigue occurs
earlier. When such exercise is performed in hot
environmental conditions, the high muscle
temperatures are possibly just beyond the optimum
for tetanic force production. Recent research
suggests that each individual has a critical core
temperature, that once reached, signals a
hypothalamic offswitch.
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Some research suggests that a central disturbance
to amino acid metabolism is involved in central
fatigue during prolonged exercise Serotonin
(5-HT)central neurotransmitterprevents
perturbations within the neuronal networkplays a
neuromodulator role. Increased brain serotonin
activity may play a role in lethargy, loss of
drive and central fatigue.
19
Tryptophan (an essential amino acid) is important
for 5-HT synthesis Plasma FFA increase with ex
duration and may displace tryptophan from
albumentryptophan then available for transport
into the brain At the same time BCAA are taken up
by musclemetabolised Tryptophan and BCAA compete
for the same mechanism for transport across the
blood-brain barrier enhanced brain uptake of
tryptophan, serotonin synthesis and the
development of central fatigue
20
BCAA ingestion has had mixed results in
increasing performance a side effect of BCAA
ingestion is plasma and muscle ammonia
accumulation (potential fatigue factor) CHO
ingestion attenuates the increase in plasma FFA
and reduces the rise in ammonia.