Skeletal Muscle Contraction Flashcards
Attachment to actin binding site causing a configuration change that releases phosphorous (Pi) from the head
Attach (Bind)
Head pulls and muscle contracts. ADP is released causing a configuration change that allows for an ATP to attach and the process starts over
Power Stroke (Flick)
ATP > ADP + Pi (stay in the myosin head)
Reposition/cock
ATP binds to myosin which causes release of the actin
No ATP = rigor mortis
Release
This gets in the way of binding sites on skeletal muscle - blocks actin binding sites?
Tropomyosin
Troponin has 3 parts:
1) This binds to calcium, causing the tropomyosin to move and exposes the binding site for myosin to bind
2) Inhibits the myosin from binding to actin
3) Binds to Tropomyson
- Troponin C
- Troponin I
- Troponin T
Two forces on the muscle?
What is the greater force?
- muscle’s total force of contraction
- passive resistance of the connective tissue around the muscle
*Passive resistance
Having action potential after action potential. Not allowing the muscle to relax by pumping out the calcium. Instead allowing more calcium to come into the cell, thus increasing the force of the contraction
*maximal possible contraction, not pathological just you trying to lift something heavy
Tetanization
This works by poisoning the sodium potassium atpase, can’t pump as much sodium out and as much potassium in. This drug has a very narrow therapeutic index, be careful when using it. If you use the right amount you decrease the sodium gradient into the cell.
Sodium gradient = Sodium usually high outside, low inside, sodium really wants to come back in. Use the energy stored up in that gradient to bring other things into or out of the cell. So if we want to pump calcium out of the cell we use the sodium gradient to do it. Sodium comes in, pumps the calcium out.
**What happens if we poison the pump just a little so the sodium gradient is not as strong - the rate at which we pump calcium out of cell will be slower. Which means there will be a little more calcium in that cell when the cardiomyocyte goes to contract the next time. Which means the force of contraction will be a little bit stronger.
(Increasing the calcium in the cell, increases the force of contraction. One way to increase it is to decrease the rate at which it is pumped out by decreasing the sodium gradient)
*This could go wrong by losing too much gradient or having too much calcium inside the cell
Digoxin
These have a lot of creatine phosphate stored up, very little ATP (use the phosphate to make ATP)?
Fast-twitch muscles (Type 2)
Enzyme that helps to catalyze the reaction of ADP to ATP using the phosphate from the creatine phosphate. Will see this enzyme in the blood if a cell that has it ruptures. We use this on lab tests.
Creatine (phopho) kinase (CPK)
Generic marker, can be elevated by any kind of damage to skeletal muscle.
*Helps catalyze the reaction of ADP to ATP using the phosphate from the CP)
Creatine Kinase (CK)
Exercising does not cause hyperplasia (increase in muscle cells) it causes _____.
_______ make copies of themselves and fuse with the muscle cell giving it more nuclei (so the nuclei can supply their area of muscle with the necessary proteins).
Hypertrophy (cell enlargement)
Satellite cells
3 Isozymes of CK:
1) if having cell damage in the heart, cardiomyocytes are dying?
2) if having cell damage in the skeletal muscles?
3) brain?
- CKMB
- CKMM
- CKBB