neuromuscular fatigue concepts Flashcards
where is the distinction between the CNS and PNS in terms of fatigue
peripheral = below motor end plate / NM junction
what is the response to sustained MVC
all muscle fibres recruited at the start of the MVC
- high amplitude of the EMG at beginning and decays
- gradually muscle fibres get tired and rely more on type 1 muscle fibres
what is the response to sustained sub max contraction
- slow fibres recruited first
- since type 1 will fatigue, more type 2 recuited to maintain force
- EMG amplitude increases as contraction continues because type 2 have higher amplitude on EMG
what is the source of central fatigue
group III/IV afferents send signals back to the brain, brain is inhibited and reduce central motor drive
what is the source of peripheral fatigue
from NMJ - anything that disrupts the activation of muscle is peripheral fatigue
what is neuromuscular fatigue
reduction in maximal force output
what is the process of ITT
stimulate the aMN of desired muscle
- stimulated on top of MVC to reach max activation
- stimulated after MVC to see the resting twitch
what is the superimposed twitch
extra force created by electrical stimulus
shows how much of the fatigue is the brain deficit
measures central fatigue
what can an increase in superimposed twitch mean
lower activation from brain on the whole MU
what can a decrease in amplitude of resting twitch mean
deficit in muscle’s ability to produce force
how is max voluntary activation measured
measured by having the participant perform an MVC
then stimulating the muscle on top of it to see the force produced when all muscle fibres produce force
what are the 5 mechanisms of peripheral fatigue
- NM junction
- sarcolemma
- excitation contraction coupling
- metabolic alterations
- slowing of relaxation
what is the role of NM junction in peripheral fatigue
- inhibition of presynaptic ending
- limited transmitter substance
- inability for post synaptic membrane to be excited
what is the role of sarcolemma in peripheral fatigue
- changes in the electrical property of the muscle surface membrane
- changes in the intra/extracellular Na+ and K+
what is the role of excitation contraction coupling in peripheral fatigue
- disruption in Ca2+ release or uptake
what is the role of metabolic alterations in peripheral fatigue
- ATP availability at the myosin head chain
- metabolites accumulation
- PCr, glucose, and glycogen concentrations
- accumulation of H+ ion, Pi, and ammonia
what is the role of slowing of relaxation in peripheral fatigue
- disruption in Ca2+ release or uptake
what are some factors that may modulate central motor output
music, sleep, prior experience, time deception, knowledge of end point, presence of competitors, etc
what is corollary discharge
internal copy of motor commands that is sent to the brain’s sensory system
- sensory can inhibit motor area if its too much sensory feedback
- allows the brain to predict the sensory consequences of the motor command
- helps distinguish between self generated sensations and external stimuli
what is the relation between corollary discharge and RPE
higher corollary discharge = higher RPE
exercising larger muscle groups = more signals sent = higher RPE
what is the sensory afferent feedback model
evidence for critical threshold of peripheral fatigue
- larger increase in peripheral fatigue (larger decrease in power output) in trial with no sensory feedback compared to when they could feel their legs
- shows that sensory feedback modulates muscle power output as signals to the CNS
