Excitation-Contraction Coupling

Question 1

What is the definition of excitation-contraction coupling?

Answer 1

electrical stimulus triggers the release of Ca by SR, initiating muscle contraction by sarcomere shortening

Question 2

What are subneural clefts?

Answer 2

receptors are located here (nAChRs) and they increase the surface area

Question 3

About how many vesicles are stored at each end plate of a pre-synaptic neuron and how many vesicles are released per AP?

Answer 3

about 300,000 vesicles, 125 of them are released per AP

Question 4

How does the binding of ACh to nAChRs propagate an action potential throughout the sarcolemma?

Answer 4

ACh binds to ligand gated nAChRs in the subneural crest, Na+ rushes in causing local AP
This will cause voltage gated Na+ channels (in deep subneural crest) to open and Na+ to come in, making full AP

Question 5

How does the AP release Ca2+ in order for the muscles to contract?

Answer 5

AP will travel to the T-tubule between 2 terminal cisternae, causing a conformational change in the DHP (dihydropyridine) receptor, which will pull RYR receptor (ryanodine) from the SR, releasing Ca2+

Question 6

What is calsequestrin and where is it located?

Answer 6

binds Ca allowing 40x more Ca to be stored, located in the sarcoplasmic reticulum

Question 7

What happens to the left over released Ca2+ once the AP resides?

Answer 7

The excess Ca is pumped back into the SR by CaATPase pumps, which are used due to the high concentration inside compared to outside

Question 8

Where are the 2 hinges on myosin and what do they do?

Answer 8

One located at neck, and make sure heads are extended away from eachother
one located at each head, so they are able to move independently

Question 9

What are the three components that make up the troponin complex and what does each have a strong affinity for?

Answer 9

Troponin I : strong affinity for actin, sits on myosin binding site
Troponin C: Strong affinity for Ca
Troponin T: Strong affinity for tropomyosin, holds it to it

Question 10

What are the steps in walk-along/ratchet theory for myosin binding to actin? (4ish)

Answer 10

1. ATP binds to mysoin, myosin detaches from actin
2. ATPase on myosin turns ATP into ADP and Pi, cocked state
3. Myosin binds to actin, releases Pi for energy to power stroke.
4. ATP comes in and released ADP, myosin head detaches from actin again

Question 11

What does the length-tension curve compare?

Answer 11

Relative tension of the sacromere vs. sacromere length

Question 12

How do you get the perfect, most amount of tension?

Answer 12

When actin and myosin heads are perfectly overlapped and all bound

Question 13

When they’re not fully overlapped, or too much overlapped (when sarcomere length is very large, to very short), what is the resulting tension?

Answer 13

When there is a major overlap or no overlap between myosin and actin, the tension will be low

Question 14

What is a motor unit?

Answer 14

all muscles innervated by a single nerve fiber

Question 15

What muscles, small or large, will have more nerves?

Answer 15

Small because there are more precise movements that require more nerve fibers (80-100 muscle fibers per motor unit usually)

Question 16

What is tetany or tetanization?

Answer 16

strength of /fully contracted muscle, which is cause by the summation of adding together the individual twitch contractions to increase intensity of overall muscle contraction

Question 17

What does summation of tetany result in?

Answer 17

Increase number of motor units contraction at once

Increase frequency of contraction

Question 18

What is rigor mortis, when does it happen, and why?

Answer 18

Rigor mortis is constant contracture after dying, lasting for about 15-20 hours. The body does this because it needs ATP to exchange ADP, but when deceased, there is no ATP to release myosin from actin = rigor mortis

Question 19

What are the four many sources of energy (ATP) for muscle contraction and how long does it last for? (4)

Answer 19

1. Stored ATP, 1-2s
2. Phosphocreatine (takes P adds to ADP = ATP) 8-10s
3. Glycogen (anaerobic 2ATP per) 1.3-1.6min
4. Oxidative Metabolism (Aerobic use O2) Unlimited amt

Question 20

What is unique to slow twitch type I muscle fibers?

Answer 20

They are red due to abundance mitochondria and myoglobin, they have more capillaries for nutrients and oxidative metabolism

Question 21

What is unique to fast twitch type II muscle fibers?

Answer 21

They are more white due to lack of mitochondria and myoglobin, 2x larger fibers, 2-3x more phosphocreatine and glycogen systems because no oxidative metabolism

Question 22

Examples of exercise with phosphagen system?

Answer 22

100M dash, weight lifting, football dash, Bball, tennis, hockey

Question 23

Examples of exercise that uses more glyocgen systems?

Answer 23

800Mdash, Boxing, 1-mile run, 400M swim

Question 24

Examples of exercises that use more aerobic system (oxidative metabolism)?

Answer 24

10,000M skate, marathon. jogging. cross country skiing

Question 25

What are strength and endurance determine by?

Answer 25

Strength by muscle size, endurance depends on glycogen store prior to exercise (high carbs)

Question 26

Hypertrophy increase diameter, not number of fibers in muscle, what are 4 ways they get bid?

Answer 26

1. Increased myofibirils
2. 120% increased mitochondria enzymes
3. 60-80% more componenets of phosphagen systems
4. 50% inc glycogen storage/75-100% more stored in fat