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Sliding Filament Thory, With Ref To Upper Arm

1419 words - 6 pages

Norah Carr
Co-ordination and movement
March 2012.

3:1 eplain the sliding filament theory of muscle contraction with reference to the antagonistic muscles of the upper arm.

3:2. Draw and label a diagram of a synovial joint, explaining the functions of each structure.

3:3. Distinguish between a hinge, pivot and a ball and socket joint with reference to named examples, shapes of bones and the ranges of movement possible.

To understand the sliding filament theory, one should first look at the muscles. All movement through the body is created and stopped by muscles. Muscles work in antagonistic pairs, that means that when one muscle relaxes, it antagonistic pair will ...view middle of the document...

(If the muscle is going to contract).
Once in the synaptic cleft, the ACH bind with receptors located on the membrane of the muscle fibre. (This area is where the receptors for neurotransmitter are located, and is found just beneath the synaptic end bulb, is called the motor end plate) Receptors for ACH on the motor end plate bind with ACH and cause a confirmation change and open chemically-gated Na+ channels. As a result Na+ enters the muscle fibre and a little bit of K+ leaves, causing a slight depolarization in the membrane potential (electrical activity) this depolarization spreads to areas adjacent to the motor end plate and when the depolarization (Na+ ions) reach this area, depending on how many Na+ ions are present (if we reach threshold or not) we then generate an action potential in the muscle fibre by opening up volt gated Na+ channels. Na+ then floods the cell and membrane potential quickly depolarizes.
Once the action potential has been created, it travels down the sarcolemma and down the T-Tubules of the muscle fibre. As it travels down the T-tubules it causes DHP receptors located on the membrane to change shape. When these receptors chain shape, they cause 'foot proteins' located on the Sarcoplasmic Reticulum to change shape also. And when the 'food proteins' move they allow Ca2+ into the muscle fibre.
Ca2+ is ESSENTIAL for muscle contraction. (In all muscle types) Ca2+ binds to the thin filament troponin and as a result troponin changes shape. When troponin changes shape, it causes the other thin filament tropomyosin to change shape also. And when tropomyosin changes shape, it exposes the binding site for the thick filament myosin, on the thin filament actin. As a result Actin and myosin quickly bind. Upon binding, myosin and actin undergo an isomerization (myosin rotates at the myosin-actin interface) extending an extensible region in the neck of the myosin head. Sliding occurs when the extensible region pulls the filaments across each other (like the shortening of a spring). Also called the "power stroke" Myosin remains attached to the actin. At the same time, ADP and inorganic phosphate (Pi) generated during the prior contraction cycle are released from the myosin head.
The binding of ATP allows myosin to detach from actin. While detached, ATP hydrolysis occurs "recharging" the myosin head, (Or resetting the myosin head) If the actin binding sites are still available, myosin can bind actin again.
The collective bending of numerous myosin heads (all in the same direction), combine to move the actin filament relative to the myosin filament. This results in muscle contraction in the upper arm.
In the presence of the biochemical adenosine triphosphate (ATP), the myosin and actin fibres would slide past each other, effectively shortening the muscle. (Huxley).

Scientists have come a long way in the research relating to muscle contraction. In the past several decades information has been added along the way...

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