In: Anatomy and Physiology
A discussion of microscopic muscle contraction should include all activities, chemicals and structures involved in muscle contraction. So a discussion of the depolarization of the sarcolemma, the role of the ACH receptor, sodium and potassium in generating an action potential as well as the role of calcium, T tubules, the sarcoplasmic reticulum and tropomycin is expected. You should describe the myofilaments and the process of the sliding filaments. A discussion of the contraction of a whole muscle should include the macroscopic structures of a muscle and the motor end plates, connective tissue covering and the relationships between these structures.
The skeletal muscle contract only when stimulated by somatic
motor unit.This can cause muscle fibre to contract. One somatic
motor neurone can innervate 3-1000 muscle Fibres.
The unit of nerve fibre and muscle fibre is called a motor
unit.
The muscle contain many muscle fibre units called fascicles.
Within a motor unit that assist the contraction of muscle, there is
axon terminal of motor neurone. The end bulb of axon of the motor
neurone have some vesicles. These vesicles contain neurotransmitter
called acetylcholine. The muscle fibre contain many myofibrils.
Within the muscle fibre there is mitochondria which can provide
ATP.There are many nucleus around the muscle fibre, because the
muscle fibre is multinucleated. The muscle fibre has a membrane
called sarcolemma which contains many receptors and Ion channels.
Myofibrils contain thin and thick filaments. The portion between
one z line and adjacent z line is called a sarcomere. The are
T-tubules that run around the myofibril. Surrounding the T-tubule,
there are sarcoplasmic reticulum. These sarcoplasmic reticulum
contain calcium ions.
T-tubules essentially connect with the outer membrane and wrap around the myofibril. T tubules contain special Ion channels for calcium ions. Surrounding the T tubules we have sarcoplasmic reticulum which contain calcium ions, specifically called terminal cisternae. The terminal cisternae contain calcium ions. But these ions cannot enter into T-tubules because the calcium channels are blocked.
Within the myofibrils there are thin and thick filaments. Thin filaments require calcium in order to initiate muscle contraction.
Action potential is arrived at the neurone terminal.This action potential causes the vesicles containing acetylcholine to release the acetyl choline into the synapse. The acetyl choline bind to the receptors on the sarcolemma.
Outside the sarcolemma in the extracellular fluid, there is high
concentration of sodium ions. Inside the sarcolemma, there is high
concentration of potassium ions. When the vesicle containing
acetylcholine release the acetylcholine out, it will bind to the
receptors causing the receptors to open. When the receptors open,
the sodium ions come inside, which will open the voltage gated Ion
channels and causes action potential. This action potential travels
through the sarcolemma and comes down to T-tubules. This causes the
calcium channels in the T-tubules which are close ld ; to to open
up.this is because the change in the voltage of the T-tubule which
cause open the channels. The calcium move out from the terminal
cisternae into the T-tubules. Calcium ions travel down and bind to
the thin filaments.Calcium and ATP initiate the muscle contraction
through sliding filament theory at a molecular level.
The muscle contractions are controlled by the actions of calcium.
The thin actin filaments are associated with the regulatory
proteins called troponin and trop. When a muscle is relaxed,
tropomyosin blocks the crossbridges binding sites on actin. When
calcium ion levels are high enough and ATP is present calcium ions
bind to the troponin which displaces tropomyosin exposing the
myosin binding sites on actin. This allows myosin to attached to a
binding site on actin forming a cross bridge.
The contraction begins when a bound ATP is hydrolyzed to ADP and
inorganic phosphate. This causes of the myosin head to extend and
can attach to a binding site on actin forming a cross bridge.an
action called the power stroke is triggered allowing myosin to pull
the actin filament towards the M line thereby shortening the
sarcomere. ADP and inorganic phosphate are released during the
power stroke. The myosin remains attached to actin until a new
molecule of ATP binds freeing the myosin to either go through
another cycle of binding and more contraction or remains unattached
to allow the muscle to relax.
The muscle contract when thick and thin filaments slide past each
other. The thick filaments are myosin which are anchored at the
centre of sarcomere called the M line. The thin filaments are
composed of the protein
in actin which are anchored to the z line on the outer edges of the
sarcomere. Sarcomere shortens from both sides when actin filaments
slide along the myosin filaments. Although the action between the
filaments is described as sliding the myosin filament actually
pulls the actin along its length.The cross bridges of the myosin
filaments attached to the actin filaments and exert force on them
to move. This action is known as the sliding filament mechanism of
muscle. In this the sarcomere contracts without shortening the
length of thick and thin filaments. Is cause of the muscle to
contract.