Wk7: Neuromuscular responses to acute exercise Flashcards
What is the definition of muscular fatigue?
the decline in muscle tension or force capacity with repeated stimulation or during a given time period.
What are the 4 main components voluntary muscle actions exhibit?
- CNS
- PNS
- Neuromuscular junction
- Muscle Fiber
Is muscle weakness reversible?
No
Is muscle fatigue temporary?
Yes
What is the relationship between fatigue and motor units?
- Fatigue is highly dependent on the motor unit
- Fast isoforms are type 2a and type 2s and type 2b
- Initially recruit slow twitch muscle fibres and then progress to fast.
- Slow to fast the structure and metabolic properties change
- Slow – higher capillarisation, mitochondrial densitive, oxidative capacities, fatigue resistant, can’t generate high muscle contractions, much slower shortening velocity.
- Fast – increased fibril cross sections (motor neurone neuromuscular junction has an increased density), causes large amounts of fatigue, generate high muscle contractions, fast shortening velocity.
- Nutrition and hydration status as a large influence on fatigue
Outline the neuromuscular transmission pathway?
- Motor cortex originates impulse and travels down spinal cord
- Motor neurone sends an action potential to the neuromuscular junction
- Muscle action potential initiated
- Releasing calcium into the cytoplasm
- neuromuscular transmission pathway: centrally or peripherally located
What is loci of failure?
- central is originated from the motivational drive, principally motor cortex down to the motor neuron. Travels down the peripheral nerve and downstream
- you can electively stimulate the muscle to see the sights that cause muscle fatigue.
Define central fatigue
when the force goes back to what it was
Define peripheral fatigue
when the force doesn’t go back to where it was
What is the role of central fatigue?
to prevent peripheral muscle injury
What is neuromuscular junction failure?
Failure of nerve impulse to elicit normal muscle action potential, which may occur at pre- or post-synaptic terminal
What causes neuromuscular junction failure?
neuro fatigue
what is implied sarcolemma/t-tubule function?
A reduced sarcolemmal action potential can block t-tubule transmission that could inhibit Ca2+ release to impair force output.
reduced sarcolemma AP may be due to changes in Na+/K+, increased K+ or impaired Na+/K+ pump during repeated contracts, which may lead to cell depolarisation.
What is impaired Ca2+ handling?
- impairments to Ca2+
handling:
1) Rrelease of calcium from the sarcoplasm into the cytosol
2) Binding (to troponin c) of calcium
3) Reuptake - slowing the pump of calcium into the sarcoplasmic reticulum can impair muscle fatigue.
How does central fatigue occur?
if the failure to contract muscles occurs in the CNS or the motor neurone
How does peripheral fatigue occur?
if the failure to contract muscles occurs in the PNS or in the Ca2+/cross bridge cycle
what would happen if the failure to contract a muscle occurred in the nervous system?
no AP’s would form
What leads to a decreased force of contraction?
- electrical properties of the muscle fibre
- excitation-contraction coupling failure
- impaired cross-bridge function changes in the metabolite levels
what happens if the concentration of potassium becomes too high?
what happens if the concentration of potassium becomes too high?
it leaks into the T tubules which affects the DHPR
this affects Ca2+ into the cell
what happens if Ca2+ release from the SR fails?
Ca2+ can’t enter the cell which affects the cross bridge cycle
what can cause a decrease in Ca2+ release?
RYR1 failure
what does a decrease in Ca2+ responsiveness cause?
increase in H+ which decreases Ca2+ troponin binding
what does a decrease in Ca2+ sensitivity cause?
for any given concentration of Ca2+ there is less force of contraction compared to normal
what is a slowed reaction caused by?
a decrease in SR Ca2+ uptake and ATPase activity
what does impaired cross bridge cycling cause?
decrease in velocity of shortening and slowed relaxation
what can NMR be used for?
to assess the levels of metabolites present during contraction
what changes can be seen in metabolite levels during contraction?
PC levels fall as it binds to ADP to form ATP
Pi levels increases as ATP is broken down to produce energy
ATP levels stay constant
what does the release of Pi cause?
increases the concentration which inhibits further Pi release as there is no gradient for it to travel down
the cross bridge cycle can’t occur so there is a decrease in force
when an action potential occurs how does the concentration of potassium in the t tubule change?
it goes from 4mM to 9mM
what effect does a high potassium concentration have on action potentials?
it changes the shape of the action potential, there isn’t as large an amplitude, the duration of the action potential is longer
What are reactive oxygen species?
are highly reactive oxygen-derived molecules (e.g., H2O2) that are elevated during fatiguing contractions
What is the effect of acute increases in reactive oxygen species?
damage myofibrillar proteins and reduce Ca2+ sensitivity
