Muscle contractile mechanisms Flashcards

1
Q

Overview of muscle function

what does it provide movement for? (2)

structure for? when?

2 different muscles?

what is needed for contraction?

A

Provides movement of skeleton, e.g. walking, running, playing sport
and
Provides movement of hollow organs, e.g. heart, blood vessels, GI tract

Provides structure to hollow organs when under pressure
e.g. chambers of the heart, blood circulation through vessels, bladder

Allows for voluntary and involuntary control of different muscle over different time scales

These different functions achieved by having two types of muscle

Striated - e.g. skeletal and cardiac muscle
Smooth - e.g. blood vessels, GI tract

Both types of muscle produce contraction by using
two contractile proteins – actin and myosin
and a regulatory protein called tropomyosin

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2
Q

striated vs non-striated

A

determined by the organisation of myosin + actin filaments

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3
Q

3 different muscle types

striated?
voluntaey?
controlled by?

A

skeletal -> striated, voluntary and controlled by motor nerves

Cardiac -> striated, involuntary, controlled by ANS
smooth -> not striated, involuntary, controlled by ANS

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4
Q

Why does smooth muscle not have striations?

how is it different?

A

there is no organisation hence the myosin and actin filaments are dis-organised

dense bodies (myosin randomly arranged) are linked up by thinner filaments which are actin hence there is a contraction around the whole cell

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5
Q

Organisation in striated muscle

z band?
I band? also known as?
A band? also known as?

A

Z band – attachment sites for actin
Light or I band – non-superimposed length of actin
Dark or A band – Entire length of myosin

Z line to Z line is a sarcomere which is 1 unit of contractile strength

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6
Q

What happens to sarcomere during contraction?

from where to where?
what is rowing motion?

A

Unit of striation: The sarcomere from Z line to Z line

rowing motion allow A + M to come together -> no change in actual length but row towards each other which is the sliding filament hypothesis

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7
Q

Actin

what is G actin? what does it have and what does it form?

what does it also contain? what does this do?

what is the tpoponin system? sub units?

A

G actin - Globular protein, binds ATP, contains ATPase activity -> can release energy and help globular protein form helical protein F-actin)

F actin - Helical protein, uses ATP to make filaments

Filaments contain active actin binding sites - allow interactions with myosin

Contains Tropomyosin
In striated not smooth muscle ‘covers’ active actin binding sites at rest – prevents myosin interactions

In striated muscle, actin also contains the Troponin system
TnI, TnC, TnT
Essential for modulating actin-myosin interactions

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8
Q

Myosin

what does it contain?
what forms head domain?
what else does it have?

A

Myosin II is found in muscle (thicker therefore denser)

Contains:
2 heavy chains – intertwined
Forms HEAD domain
ATP binding site, ATPase activity
Binds to active actin binding sites

4 light chains – 2 per head
Modulates myosin-actin interactions
Especially in Smooth muscle

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9
Q

How do actin and myosin interact to produce muscle contraction?

how do you increase affinity for actin?

what is the power stroke and how does it take place?

what causes detachment?

A

ATP bound to myosin heads which means no interactions between A + M (low affinity) therefore hydrolyse ATP as ADP has increased affinity for actin

Myosin heads bind to actin, forming crossbirdges. Myosin is 90 degrees cocked hence perpendicular to actin -> use energy of ADP binding + release of ADP to cause cocking motion of myosin head which will be 45 degrees now which causes a power stroke now (movement of myosin relative to actin) -> move side one another as they haven’t contracted -> ATP binds to myosin head therefore no M + A interaction as low affinity so detachment -> next time will bind to another area of the actin molecule + row further

Very fast process

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10
Q

Consequences of sliding filament hypothesis

3 sources of ATP?

what is rigor mortis?
when does it start? peak?
when does it stop?

A

Myosin heads need to be ‘primed’ with ATP ready for muscle contraction and movement

Hence we have lots of sources of ATP

1) Aerobic respiration – glycolysis (glucose metabolism) and oxidative phosphorylation in presence of O2
2) Anaerobic respiration – production of lactate into ATP in absence of O2
3) Phosphocreatine – source of ATP

Rigor mortis
Need ATP-myosin head interaction to enable detachment of myosin-action

Death - loss of ATP production causes stiffness of muscles – ‘rigor’
Starts 2-6 hours after death (anaerobic production of ATP stops it happening immediately), peaks after about 12 hours

Rigor stops after 24-48 hours due to decomposition of myosin/actin proteins

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11
Q

What initiates the sliding filament hypothesis?

how does this come about? (2)
effect of this?

A

Rise [Ca2+] in cytosol of muscle cells is CENTRAL of initiating muscle contraction

Rise [Ca2+] leads to removal of tropomyosin from active actin binding sites allowing myosin heads to interact with actin

Rise [Ca2+] produced by Ca2+ influx AND Ca2+ release from SR
Importantly, decrease in [Ca2+] initiates muscle relaxation

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