3.6.3 Skeletal muscles are stimulated to contract effectors

Question 1

how muscle act with skeleton

Answer 1

muscles act in antagonistic pairs against an incompressible skeleton

Question 2

gross structure of skeletal muscle

Answer 2

muscle
muscle bundle
muscle fibre
myofibril
Sarcomere (functional unit)

Question 3

Term describing muscle fibre are made of individual cells that have merged together.

Answer 3

Muscle fibres are multinucleate

Question 4

two types of protein filaments in skeleton muscle

Answer 4

Actin (thinner)

Myosin (thicker with head projections

Question 5

structure of sacromere

Answer 5

myosin
actin
z line

H zone
A band
I band

Question 6

How do muscle contract ?
How does this show in sacromere microscopic image?

Answer 6

sliding filament mechanism (visually shorten muscle)

I band gets narrower
H zone gets narrower
A band remains the same width - myosin does not get shorter
Z lines get closer together - more overlap between actin and myosin

Question 7

two type of muscle fibre

Answer 7

fast twitch
slow twitch

Question 8

fast vs slow

slow vs fast twitch muscle

Answer 8

anaerobic vs aerobic
low myoglobin concentration vs high myoglobin concentration (o2)
pale in color vs red in color
low blood supply vs high blood supply
fatigue rapidly vs fatigue slowly
low number of cappillary vs large number of cappilary
low number of mitochondria vs large number of mitochondria
more force short duration vs less force long duration

glucose/ glycogen vs glucose (pyruvate), fatty acid (acetyl coenyzme A)

fast twitch rely on phosphocreatine

slow ATP generation vs fast
more ATP generate (36-38) vs less ATP generate (2)
more mitochondria (in slow twitch) vs less
by oxidative phosphorylation (oxygen storage : myoglobin in muscle release O2) vs from glucose
lactic acid cause fatigue

Question 9

rapid procrosses in producing ATP in fast twitch fibres

role of the substance in this process

Answer 9

phosphate creatine + ADP (at rest) <—> creatine + ATP (muscle contraction)

provide phosphate to form ATP

Question 10

Neuro musclar junction muscle contraction precoess

Answer 10

• ACh release and bind to complementary receptor on cell surface membrane od muscle (sacromere)
• open Na+ channel, Na+ diffuse in
• depolarisation
• AP over cell

1. Calcium ions (released and) diffuse into myofibrils (cytoplasm) from the sarcoplasmic reticulum;
2. Calcium ions cause movement of tropomyosin on actin;
3. This movement causes exposure of the binding sites on the actin;
4. Myosin heads attach to binding sites on actin; (actinomyosin bridge formed)
5. Hydrolysis of ATP on myosin heads to ADP & Pi causes myosin heads to bend (ATPase on myosin head is activated by calcium ions);
   [ADP + Pi release]
6. Energy stored in the ‘cocked’ myosin head is then released to pull actin past it; (power stroke)
7. Attachment of a new ATP molecule to each myosin head breaks the actinomyosin bridges, causing myosin heads to detach from actin sites. (recock) (recovery stroke)

Question 11

Muscle relaxation

Answer 11

Calcium ions are actively transported into the sarcoplasmic reticulum (using energy from ATP hydrolysis)
This stops the myosin head forming actinomyosin bridges

Question 12

role of ATP in muscle contraction

Answer 12

Breaking actino- myosin bridges
Calcium reuptake into the SR

Question 13

what is rigor mortis and how is it form

Answer 13

After death, muscles become stiff

No respiration
ATP levels in the muscle fibres decrease
so actinomyosin bridges can’t be broken

Calcium leaks out of the sarcoplasmic reticulum (no longer actively transported in), so this exposes the myosin binding site on the actin thin filaments.