Skeletal Muscle Physiology Flashcards
How big are muscle cells?
10-12 cm long
100 micron in diameter
What is the layer of surrounding tissue on muscle fibres called?
Endomysium
Layer of connective tissue coating individual muscle fibre
What are bundles of muscle fibres called?
Fascicles
Around the fascicles are structures called the perimysium
What is the layer around the muscle called?
Epimysium
Is skeletal muscle striated?
Yes, due to the organised structure of the contractile proteins.
Dark band = A band Anisotropic to light (Doesn’t allow polarised light through it)
Only find myosin filaments in the A band
M band is in the middle of the A band (myosin filaments are attached to one another)
Light band = I band
Isotropic to light
(Polarised light can pass through either direction)
Middle of the I band is the Z line
Sarcomere goes from one Z line to another (functional unit)
Thin filaments are attached at the Z line, also overlap the thick filaments but depends on how stretched the muscle is
Cardiac muscle is also striated.
What are myofilaments?
Protein complexes
What are thick filaments formed from?
From large numbers of myosin II molcules
Where is the enzyme activity regulated in myofilaments?
In the regulatory light chain
Which two light chains form a-helix?
Alkali light chain
Regulatory light chain
How are thin filaments formed?
From actin in the complex with troponin and tropomyosin
How is force generated in thin filaments?
By cross-bridges between myosin and actin
Conformational changes in the myosin head that generate force that causes the filaments to slide in opposite directions
Only works when the myosin binding sites are exposed
What does the troponin complex do?
It binds calcium
What is titin?
It is the third myofilaments
Its role is to stabilise the myosin filaments positions
What does titin do to sarcomere?
It extends the distance by half a sarcomere
Attaches at the M line and extends all the way to a Z line
Bound to the thick filament and then is in a free form to the Z line
How does titin resist muscles from being over-stretched?
It stops sarcomeres from being over extended
Amount of tension it develops depends on intracellular calcium levels. Increased levels = high titin levels compared to at rest
What happens at the motor neuron?
- Branching at the axon
- Synaptic terminals sitting on the end plate
What do the folds at the neuromuscular junction do?
The increase the surface area of the end plate membrane
What type of receptors are nicotinic ACh receptors?
They are inotropic receptors
What do T-tubules do?
They carry action potential into the depth of the muscle fibres
Speed up conduction and make fast twitching possible
What is the sarcoplasmic reticulum?
Its a specialised region of the endoplasmic reticulum
Intracellular store of calcium
What are end plate projections?
Electron density due to protein structures that extend to the t-tubules to the sarcoplasmic reticulum
How are triads formed?
Through three terminal cisternae bundling together
What are dihydropyridine receptors?
They are voltage gated channels that sense changes in membrane potential in the T-tubule during action potentials
What are ryanodine receptors?
They release calcium from SR into cytoplasm
Where does the calcium come from in skeletal muscle?
From the Sarcoplasmic reticulum from a process called voltage dependent calcium release
What happens at low or resting calcium levels?
Tropomyosin is inhibiting the binding of myosin to actin filaments
What happens when calcium levels rise and are at high levels?
It binds to tropoinin and moves the tropomyosin from the myosin binding site. Myosin binding site is exposed and cross bridge cycling can occur
What is the cross bridge cycle step 1?
- ATP binds to myosin head
What is the cross bridge cycle step 2?
- ATP is hydrolysed. Myosin head returns to resting position
What is the cross bridge cycle step 3?
- Cross-bridge forms at new position on actin
What is the cross bridge cycle step 4?
- P is released and conformational change results in power-stroke
Power stroke occurs when the phosphate is released from the complex
What is the cross bridge cycle step 5?
- ADP is released
What depends on the quickness of the cross-bridge cycling?
- The ATPase activity
- Different forms of myosin with different rates of ATPase activity
- Fast myosin ATP activity = quicker twitches
- Only occurs when ATP is in the cell and when calcium is elevated
What are the steps of excitation-contraction coupling?
1) End plate potential triggers AP in
muscle fibre
2) AP propagates along
sarcolemma and down T-tubules
3) Depolarisation of T-tubules is sensed by DHPRs that are mechanically coupled to RYR on SR causing them to open.
4) Ca2+ is released into the cytoplasm – initiates crossbridge
cycling and contraction
5) Ca2+ is pumped back into SR by SERCA (sarcoplasmic and endoplasmic reticulum calcium ATPase) and this terminates crossbridge cycling.
How quickly force is developed depends on?
- Myosin ATPase and how quickly cross bridge cycling can occur
- Efficiency of SR, how organised it is and how quickly calcium is released
What is a motor unit?
A single alpha motor neuron and the fibres that it innovates
What are the muscle fibre types?
- Type I (slow) Make up 50% of fibres in an average muscle - Type II (fast) Type IIa (fatigue resistant) 25% Type IIx (fast fatigue) 25%
What are the differences between type I and type II?
Speed - Fast myosin ATPase = fast contraction cycling
Slower myosin ATPase = slower contraction cycle
Sarcoplasmic reticulum - Type II fibres have more developed SR, Fast calcium release
Motor units -
Type I motor unit: smaller neuron, less than 300 fibres
Type II motor unit: larger neuron, more than 300 fibres
What happens if you increase the action potential firing frequency?
You will get summation of force
Total amount of force is increased till you cant see the individual twitches
How long in weeks do we see an increase of muscle fibre size?
8-10 weeks of training that you start to see muscle hypertrophy. Cant get muscle hypertrophy without neural adaptations
What are short term strengths due to?
Neural adaptations
What happens if you scream loudly before exercise?
Stimulation of the sympathetic nervous system (rush of adrenaline)
How does hypnotism (told they would not get injured) provide for the best strength training method?
It stimulates the CNS in influencing strength and power output
How does strength gain occur?
Through neural adaptations via plasticity
Synchronous recruitment –> Strength gains
Strength gain may also result from greater motor unit recruitment, neural drive will increase and frequency of neural discharge will increase
How else can strength gains occur?
By decreasing inhibitory inputs to the muscles
Inhibition of firing to the muscle occurs, like a negative feedback loop
Prevents damage to bones and tendons
More force can be occurred
Reduced coactivation may lead to strength gain. Normally antagonists oppose agonist force
What is transient muscle hypertrophy?
Swelling of the muscles after exercise
Due to adema, fluid leaking into the interstitial spaces, plasma leaving the blood vessels, causes swelling
What is chronic muscle hypertrophy?
Increases strength
Increases in the size of individual muscle fibres
Maximised by high velocity eccentric training
Disrupts sarcomere Z-lines
How much % larger is weightlifters fibres in cross sectional area?
45% larger
What happens when myonuclei numbers are increased?
Muscle fibre cross-sectional area increases
How many weeks after traning do the myonuclei numbers increase?
5-6 weeks
What are the source of the nuclei?
Myogenic stem (satellite cells) that fuse with muscle fibre
What happens if you stop training?
The number of myonuclei are retained in the cell for long periods after training even after the muscle have atrophied.
Myonuclei may be source of muscle memory - along with neural adaptations
Retraining - muscle can be built back faster than if you didn’t train at all
What happens to synthesis and degradation during and after exercise?
During exercise: synthesis decreases, degradation increases
After exercise: synthesis increases, degradation decreases
What is the mechanisms that relies on the dramatic increase of protein synthesis?
Activation of mTOR (mechanistic target of rapamycin)
It regulates all sorts of cellular processes that are involved in energy utilisation and metabolism
Receives inputs, coordinates the inputs and regulates the protein synthesis that occurs
Inactive form moves to the lysosome and becomes activated
LEADS TO PROTEIN SYNTHESIS
All of this is synergistic, need exercise, amino acids and insulin to activate mTOR
How much protein do you need to increase muscle mass per day?
1.6-1.7 grams of protein per kg body weight per day
What is hyperplasia?
Increase of muscle size per increase of muscle number
Increase of muscle number cells
Intense strength training = fibres splitting
NOT CLEAR IF ITS HAPPENING IN HUMANS
Satellite cells are involved in skeletal muscle regeneration
What are myogenic stem cells important in?
- Hypertrophy
- Hyperplasia
- Injury
Are fibre type alterations possible?
No, exercise unlikely to completely change fibre type in short to medium term
What are the adaptations with aerobic training?
- Change of cardiovascular and repiratory system to influence increase of VO2 max
- Increases muscle hypertrophy of type I fibres
- Increased number of capillaries supplying each fibre (angiogenesis)
- Increased myoglobin content by 75 to 80% (increased oxidative capacity)
What do mitochondria do during aerobic training?
Increased size and number of mitochondria
Utilises oxygen to generate ATP
Exercises increases good healthy number of mitochondria
Old mitochondria gets removed via mitophagy through exercise
