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Sarcomere Question
Started by justadream
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@Cawolf
I'm trying to visualize how the muscle moves so much during contraction.
If each myosin can only bind to actin in the same exact place, isn't each contraction distance limited to to the length of movement of one myosin movement?
I'm trying to visualize how the muscle moves so much during contraction.
If each myosin can only bind to actin in the same exact place, isn't each contraction distance limited to to the length of movement of one myosin movement?
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@Cawolf
Wait so are you saying that the myosin head binds to different sites on the action molecule then?
Let's number the myosin-binding sites on actin from 1-10.
Like lets say one particular myosin head binds to actin site 5. After the power stroke, it will bind ATP, release action site 5.
So which actin site will it bind next? 4/6? or 5?
Wait so are you saying that the myosin head binds to different sites on the action molecule then?
Let's number the myosin-binding sites on actin from 1-10.
Like lets say one particular myosin head binds to actin site 5. After the power stroke, it will bind ATP, release action site 5.
So which actin site will it bind next? 4/6? or 5?
Broadly speaking, the thin filament is a long chain of actin molecules - each with a single active site.
The myosin head will move the actin filament and bind to the next closest site (on a different actin molecule on the same filament).
It might be easier if you looked up some good pictures.
I found this video that is decent.
The myosin head will move the actin filament and bind to the next closest site (on a different actin molecule on the same filament).
It might be easier if you looked up some good pictures.
I found this video that is decent.
@Cawolf
So what keeps the chains from sliding past each other forever?
So what keeps the chains from sliding past each other forever?
The acetylcholine released onto the muscle fiber (when a signal is sent through the motor neurons) results in the release of calcium from the SR - which starts the process as we said earlier.
Calcium binds to troponin which causes tropomyosin to move (revealing the active sites) and the power strokes begin.
Now for your question :
When the acetylcholine is broken down no more action potentials are propagated along the muscle fiber.
So now calcium is no longer released and it is taken back into the SR.
This causes the troponin/tropomyosin to undergo a change and block the active sites - ending contraction.
A note:
This is way too much detail for the MCAT IMO.
I think that knowing calcium plays the most important role in muscle contraction is a good idea, but other than that - likely too much detail.
Calcium binds to troponin which causes tropomyosin to move (revealing the active sites) and the power strokes begin.
Now for your question :
When the acetylcholine is broken down no more action potentials are propagated along the muscle fiber.
So now calcium is no longer released and it is taken back into the SR.
This causes the troponin/tropomyosin to undergo a change and block the active sites - ending contraction.
A note:
This is way too much detail for the MCAT IMO.
I think that knowing calcium plays the most important role in muscle contraction is a good idea, but other than that - likely too much detail.
It's more that there's a "resting" length, and when you contract, you are trying to make it not go back to its resting length. Think reverse rubber band. Or a stress ball that you squeeze.@Cawolf
So what keeps the chains from sliding past each other forever?
It's more that there's a "resting" length, and when you contract, you are trying to make it not go back to its resting length. Think reverse rubber band. Or a stress ball that you squeeze.
This is true - I guess I was answering, "what stops a muscle contraction?".
The acetylcholine released onto the muscle fiber (when a signal is sent through the motor neurons) results in the release of calcium from the SR - which starts the process as we said earlier.
Calcium binds to troponin which causes tropomyosin to move (revealing the active sites) and the power strokes begin.
Now for your question :
When the acetylcholine is broken down no more action potentials are propagated along the muscle fiber.
So now calcium is no longer released and it is taken back into the SR.
This causes the troponin/tropomyosin to undergo a change and block the active sites - ending contraction.
A note:
This is way too much detail for the MCAT IMO.
I think that knowing calcium plays the most important role in muscle contraction is a good idea, but other than that - likely too much detail.
I get all these steps but I'm unclear about when the sarcomere reaches the max contraction. Like, what keeps the myosin from continuing to pull the actin strands until there is no overlap?
An analogous situation would be like: pulling an anchor out of the water. If my hand is the myosin and the rope is the actin, my hand can keep pulling the rope. But at some point, it has to reach a point where you can't pull anymore.
Is it the bone that is limiting this?
I would imagine there is a limit at the end of the cell, but generally you hear more about the joints/tendons being limiting.
Think if you flex your elbow, the bicep is highly shortened, but you can still "tighten" it - so in this case it is limited by the ROM of the elbow.
There may be a more scientific answer, but I have never heard of anything along the lines of your anchor analogy.
Think if you flex your elbow, the bicep is highly shortened, but you can still "tighten" it - so in this case it is limited by the ROM of the elbow.
There may be a more scientific answer, but I have never heard of anything along the lines of your anchor analogy.