4c

Question 1

Excitation-contraction coupling

Answer 1

Calcium initiates cross-bridge cycling after entering the cytoplasm.
How? = Excitation-contraction coupling
Key pathway: Transverse tubule or T-tubule => directly links the plasma membrane and the lateral sacs.
They run perpendicularly from the surface of the muscle cell membrane into the central portion of the
muscle fiber.

Question 2

Release of calcium from the sarcoplasmic reticulum

Answer 2

cytosolic calcium concentration is very low in a resting (relaxed) muscle!

Action potential => Rapid increase in cytosolic calcium concentration. The source of increased calcium
is the sarcoplasmic reticulum.
Very similar to the endoplasmic reticulum => Forms sleeve-like segments around each myofibril.
At the end of these segments = Lateral sacs => connected to each other via smaller tubular elements.
A single t-tubule and 2 lateral sacs on either side forms the triad – key for excitation-contraction coupling

Question 3

Activation

Answer 3

1. Action potential => T-tubule from the sarcoplasmic reticulum => Opening calcium channels.
2. Increase in cytosolic calcium concentration.
3. Calcium will bind to the subunit C (calcium) => Induces a change in the shape of the troponin.
4. Release of the inhibitory grip on tropomyosin.
5. Movement of tropomyosin making available myosin-binding sites.
6. Remove calcium from troponin => Reverses the process => Disconnects the cross bridge, relax
   muscle.

Question 4

DHPR

Answer 4

T-tubule membrane contains voltage-sensitive Dihydropyridine receptors (DHPR) – activate in
response to action potential travelling down t-tubule.

DHPR are coupled to sarcoplasmic reticulum proteins, the ryanodine receptor (Ca2+ release channels) –
activation leads to the release of calcium into the muscle cell

The extensive meshwork of sarcoplasmic reticulum assures calcium can readily diffuse to all of the troponin
sites.

Question 5

learn from lectyture process

Question 6

ATP-Powered cross-bridging cycling

Answer 6

How does this start?
Resting myofibre = low calcium concentration.
No interaction between actin and myosin.
Heads of myosin filament (M) are in an energized state
resulting from ATP hydrolysis. The hydrolysis products (ADP
and Pi) are both bound to the cross-bridge.
M + ATP => M-ADP-Pi
Calcium release => The myosin-binding site on actin
becomes available, so the energized myosin heads
bind and form a cross-bridge.
M + ATP => M-ADP-Pi => Able to interact with Actin (if tropomyosin removed)