Module 4 - Lecture 3 - Excitation-Contraction Coupling - Review Questions Flashcards
What is the general sequence of events that outline excitation-contraction coupling from the end plate potential to muscle fibre contraction?
1) Neuromuscular transmission 2) Action Potential generation @ postsynaptic Muscle fiber membrane 3) Action Potential spreads along muscle fiber membrane 4) Action Potential ‘penetrates muscle fiber via t-tubules 5) Ca2+ release from sarcoplasmic reticulum 6) excitation-contraction coupling 7) cross bridge shortening
Understand the steps of depolarization. How does an action potential propagates along a muscle?
Acetylcholine (Ach) opens the ion channels for Na and K, which allows the ions to enter (Na) or leave (K) the cell. This causes the depolarization, which is when the membrane potential becomes less negative.
The AP starts in the Alpha (lower) motor neuron, travels down the axon, across the neuromuscular junction (Ach released to access the K and Na channels to excite the muscle fibers and causes depolarization to occur, which causes an AP when it reached the muscle fiber) and to the muscle fiber.
What is the connection between t-tubules and the sarcoplasmic reticulum and the relevance of this?
The action potential can propagate into the T tubules and as it does so it will open up the special voltage gated calcium ion channels that ultimately allow for the release of calcium from the sarcoplasmic reticulum (where there is a high concentration of calcium) into the inside of the muscle fiber itself (cytosol of the muscle fiber). Sarcoplasmic Reticulum (SR): Lies within the cell close to the T-tubules. The AP in the t-tubules stimulates the ryanodine receptors in the SR to function as Ca2+ channels. The important thing to know is the depolarization of the T-tubules will result in the calcium ions via these ryanodine receptors to allow the calcium to exit the SR and enter the cytosol of the muscle fiber leading to the excitation-contraction coupling.
What is the role of calcium on muscle fibre contraction (where is it released from, what does it bind to)?
Ca2+ is released from the sarcoplasmic reticulum, it then binds to troponin to change shape and move tropomyosin to reveal binding sites for myosin heads. Muscle contraction begins and ends with calcium. No calcium, no contraction.
What is the state of actin and myosin when a muscle is resting and when it is excited?
Actin (Thin filament): At rest → binding sites are covered with Troponin and Tropomyosin.
Excited phase → binding sites clear for binding.
Myosin (Thick filament): At rest → head at rest.
Excited phase → Head cocked to prepare for binding to actin to complete a “power stroke”.
What are the steps of the sliding filament model and what filaments slide
Myosin pulls on actin by doing a “powerstroke”, which moves actin towards the centre of the sarcomere.
Sliding filament model steps: 1) myosin head in cocked position, 2) Ca2+ reveals binding site on actin, 3) Myosin head binds with actin (cross bridge), 4) ‘Powerstroke’ → myosin pulls actin towards the center of the sarcomere, ATP becomes present then 5) myosin dissociates from actin, myosin head is ‘re-cocked’ (to potential do another powerstroke), & myosin binds to active site, 6) cross bridge cycling (steps repeat until contraction is finished, which is when there is no more Ca2+ present).
What is the role of ATP and what step of the sliding filament model it is necessary for?
The role of ATP is to remove the myosin head from the actin binding site to allow myosin to prepare to bind to actin again. It is necessary for step 5 of the Sliding Filament model: “5) myosin dissociates from actin, myosin head is ‘re-cocked’ (to potentially do another powerstroke)”. Without ATP actin and myosin remain bonded (basically you have to be dead for this bond to remain because we always have ATP available in the body [rigor mortis]).
Explain the two mechanisms by which the tension of muscle fiber can change despite similar excitation.
What is the force-length relationship?
What is the tension-velocity relationship?
Force-Length relationship: The amount of tension that you are able to produce is dependent on the number of myosin heads bound to the actin. Because these sarcomeres are in theory bound to one another, they actually change as the length of the muscle changes.
Muscle into a long position = sarcomeres are further apart = less overlap between the myosin and the actin = less cross bridging formed
Muscle into an optimum length = as much myosin heads as there is actin binding sites.
Muscle into a shortened position = sarcomeres are closer together = actin sliding through regions where you don’t have myosin heads and potentially the actin overlapping one another.
Tension-Velocity relationship:
Tension varies with contraction velocity and direction.
Shortening = LESS TENSION FASTER = As you shorten a muscle, if you do it fast you may not produce as much force because cross bridge cycling takes a certain amount of time (its refractory period).
Lengthening = MORE TENSION FASTER The way that actin and myosin bind to each other and the configuration change that they undergo is designed to SHORTEN! So when you lengthen a muscle but it is excited the power stroke is not able to undergo the configuration change… the muscle cannot shorten.
***With INCREASING VELOCITY but now in a LENGTHENING position = producing more force
How are muscle contractions are terminated?
Muscle contractions are terminated by the removal of the AP (depolarization), which causes Ca2+ to not be released from the SR anymore, Ca2+ is actively [need ATP] pumped back into the SR where it is normally in high concentration, this triggers the actin binding sites to no longer be open for myosin to bind because troponin and tropomyosin return to their positions. As a result the muscle will now relax.
