Learner Resource 7 - How Skeletal Muscle
contracts
The neuromuscular junction is the place where the motor neuron forms a synapse with a muscle
cell.
A nerve impulse, in a motor neuron, arrives at the neuromuscular junction.
This causes the release of acetyl choline from the terminal of the motor neuron.
The acetyl choline diffuses across the synaptic cleft and binds to specific receptors in the muscle
cell membrane.
This initiates an action potential in the muscle cell membrane (sarcolemma).
The impulse spreads through the T tubule system in the muscle fibres.
Causing Ca2+ to be released from the sarcoplasmic reticulum.
Ca2+ binds to troponin which changes shape causing tropomyosin to move from the myosin binding
sites on the actin filaments.
Myosin filaments can now attach to actin forming cross bridges. Myosin is able to bind to actin due
to the removal of ADP from the myosin head.
Binding causes the myosin head to change shape – the ‘power stroke’, which pulls on the actin
filament.
ATP then attaches to the myosin head, breaking the cross bridge and returning the myosin head
back to its original shape.
ATP is hydrolysed again to form ADP, allowing another cross bridge to form, resulting in another
power stroke.
The process of cross bridges breaking and reforming continues as long as Ca2+ and ATP are
present.
As a result the actin and myosin filaments move past each other causing the muscle fibre to
contract.
When the nerve impulse to the muscle stops, Ca2+ is pumped back into the sarcoplasmic reticulum.
Actin reattaches to the troponin and tropomyosin covering the myosin binding sites.
No more cross bridges can form and the muscle relaxes.
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© OCR 2016
The neuromuscular junction is the
place where the motor neuron forms a
synapse with a muscle cell.
A nerve impulse, in a motor neuron,
arrives at the neuromuscular junction.
This causes the release of acetyl
choline from the terminal of the motor
neuron.
The acetyl choline diffuses across the
synaptic cleft and binds to specific
receptors in the muscle cell
membrane.
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Which initiates an action potential in
the muscle cell membrane
(sarcolemma).
The impulse spreads through the T
tubule system in the muscle fibres.
Causing Ca2+ to be released from the
sarcoplasmic reticulum.
Ca2+ binds to troponin which changes
shape causing tropomyosin to move
from the myosin binding sites on the
actin filaments.
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Myosin filaments can now attach to
actin forming cross bridges. Myosin
is able to bind to actin due to the
removal of ADP from the myosin
head.
Binding causes the myosin head to
change shape – the ‘power stroke’,
which pulls on the actin filament.
ATP then attaches to the myosin
head, breaking the cross bridge and
returning the myosin head back to its
original shape.
ATP is hydrolysed again to form ADP,
allowing another cross bridge to form,
resulting in another power stroke.
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The process of cross bridges
breaking and reforming continues as
long as Ca2+ and ATP are present.
As a result the actin and myosin
filaments move past each other causing
the muscle fibre to contract.
When the nerve impulse to the
muscle stops, Ca2+ is pumped back
into the sarcoplasmic reticulum.
No more cross bridges can form and
the muscle relaxes.
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