Skeletal muscle Flashcards

1
Q

What are the different roles of skeletal muscles?

A

Force generation for movement (of the skeleton)
Force generation for breathing (diaphragm)
Heat movement ( shivering- homeostasis)
Metabolism - a reservoir for amino acids
forms of glucose storage-glucose can be released upon demand

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2
Q

What are the types of muscles found in the human body

A

Cardiac
Smooth muscles
Skeletal

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3
Q

Describe the structure of skeletal muscle

A
Striated skeletal muscle 
Voluntary
Controlled by somatic nervous system
no branching 
MULTI NUCLEATED
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4
Q

Describe the structure of cardiac muscle

A
Striated cardiac muscle 
Involuntary
Controlled by autonomic nervous system
branching
cells joined by interrelated disk
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5
Q

Describe the structure of smooth muscle

A
Non-striated cardiac muscle
Involuntary 
Controlled by autonomic nervous system
single cells
spindle shaped
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6
Q

Describe some of the properties of skeletal muscles

A

Human muscles fibre= muscle cell

40-100 um in diameter and several cm long

Myonuclei located in the periphery - controls the COMMON cytoplasm- packed with myofibrils and mitochondria.

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7
Q

Describe the role of tendons in muscle contraction

A

Muscles attach to the skeleton via tendons- which transmits muscles force to the bone- these cause the skeleton to move at the joint.

Tendons are stiff and strong as they are made up of collagen

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8
Q

How do muscles work?

A

They work by pulling

they work in antagonistic pairs which allows for a range of movements- skeleton can return to original position

Flexor muscle- decreases the angle anteriorly-the muscle that bend the joint
Extensor muscle- increases the angle anteriorly- the muscle that extends the joint

Different movements possible depending on the type of joint and the muscle arrangement

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9
Q

What are the types of muscle contraction?

A

Isotonic- dynamic

Isometric

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10
Q

Concentric

A

the muscles shortens when it contracts

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11
Q

Eccentric

A

the muscle lengthens during force production eg slowly extending muscle after flexion

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12
Q

Isometric

A

the muscle exerts the force without changing the length

eg moving an immovable object

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13
Q

Prime mover

A

Agonist- muscle contraction is concentric (bicep)

eg Gravity

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14
Q

Antagonist-

A

It apposes the action of the prime mover (tricep)

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15
Q

Fixator-

A

steadies and holds position through isometric contraction

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16
Q

Synergist-

A

Compliments the action of the prime mover either with single movement by acting as a fixator or an intervening joints

17
Q

Describe the general structure of skeletal muscle and connective tissue

A

Epimysium- a piece of connective tissue (deep fascia) tough outermost layer surrounding the entire muscle
ensures that each muscle is separated and that there is a bit of fluid in that system- FRICTION FREE MOVEMENT- due to the lubrication

Perimysium -a piece of connective tissue which groups muscle fibres into fascicles. The space between fascicles allows for the vessels and nerves to supply muscle fibres

Endomysium- connective tissue seperating the muscle fibres- each one is electrically isolated as each one has a separate nerve supply- ensures that the structural integrity to remain

Blood vessels are embedded into the connective tissue

Tendons connect the bone to be continuous with muscle

18
Q

How does the number of branching of nerve supply affect the function of muscles

A

POWER- branches are greater than 2000

CONTROLLED- branches few than 16

19
Q

Describe the structure of the muscle fibres

A

Many myofibrils- Many contractile elements (sarcomeres)

Satellite cells

Sarcolemna-
Satellite cells are embedded into basal lamina
nuclei
T tubles-
terminal cisternae of sarcoplasmic reticulum- repeating series of networks around the myofibrils extending from one junction to another- meeting at terminal cisternae. Acts reservoirs for Ca 2+ and also contain many mitochondria

They contain voltage sensor proteins which activated when the membrane is depolarised- inducing sarcoplasmic reticulum to release Ca

20
Q

What are the advantages and disadvantages to having a longer muscle fibre

A

good because the longer fibres will result in greater contraction potential
But it does mean that it is not possible to move material up and down the cell
THIS IS WHY THE CELL IS MULTI NUCLEATED

21
Q

How are skeletal muscles formed

A

Myoblasts (single cell with single nuclei) encouraged to divide , expand and poliferate by responding to growth factor containing medium

To form muscle fibres, place in a medium of low growth factor which allows for differentiation

This will allow cells to fuse together to from a multinucleate myotube- immature muscle fibres

22
Q

What satellite cells?

A

Satellite cells are undifferentiated- specialised muscle stem cells
They are mitotically quiescent- normally
but they can be activated to enter the cell cycle into myoblast when applied the right trigger.
These can provide more myonucelei- existing or new

23
Q

What are the functions of satellite cells?

A
They can self renew to maintain stem cell population:
Muscle growth after birth
Muscle Maintainance 
Muscle hypertrophy 
Muscle Repair and generation
24
Q

Describe the structure of the sacromere

A

2 major protein filaments-
thick filaments- myosin
thin filametns- actin

Titin molecule- holds the myosin filament from z- line to m line
In the relaxed form it curls up- providing the tension even though muscle is relaxed
In the contracted phase- titan molecule curls up even more

When one muscle contracts the other muscle on other side of the joint will stretch- muscle elongates- titin coils allowing myosin and actin to slide past with each other with minimal damage

Nebulin- extends from the z band along the length of one thin actin filament - TEMPLATE- ensures actin is regulated

25
Q

Describe the muscle innervation

A

a myofibril receives innervation from one motor neurone

Each motor neurone makes contact with multiple muscle fibres- ONE MOTOR UNIT.
The size of the motor unit dictates the degree of muscle control - small end plates in the muscle of hand and eye - finer degree of control. larger ones in the leg muscle

26
Q

Describe the innervation and initiation of contraction

A

1) ACH released from motor end plate to synaptical junction
These diffuse across and bind to voltage grated Na+ channels

2) The Na+ channels open and diffuse into the cell

3) This depolarises the plasma membrane spreading via the T tubule
(GIVEN THAT: depolarisation is sufficient enough to trigger AP)
4) This causes Ca 2+ to be released into the sarcoplasm

They bind to the troponin complex which causes tropomyosin to change shape- this allows myosin head to attach- contraction is initiated

27
Q

Describe the Contraction Cycle

A

1) Attachment- the myosin head is tightly bound to the actin molecule on the think filament
2) Release- ATP binds to the myosin head which induces the release of the myosin head from the actin filament- this relaxes the muscle

3) Bending- The ATP causes further changes to the myosin head allowing it to bend .
The bending initiates hydrolysis of ATP-ADP +Pi.
Both remain on the head

4) The myosin head binds to the new molecule and Pi is released.
This increases the binding affinity of the myosin for the actin

The myosin head creates a force to straighten up which forces the thin filament along the thick filament-
ADP released

5) This shortens the sarcomere because the z lines move closer together, the same amount at which h zone decreases in length
A band stays the same length

28
Q

Describe muscle relaxation

A

Ca 2+ removed from the cytosol
They are pumped back into the sarcoplasmic reticulum by ATP synthase

As [Ca 2+] decreases, Ca 2+ released from troponin, removes tropomyosin binding sites- cross bridged released- no filament sliding

29
Q

Comment on duration of action potential vs Twitch

A

AP time is much less than Twitch time

When a number of action potential occur before the initial is complete- they superimpose each other - the action potentials add up to reach the threshold

This is due to the fact that the frequency of twitch occurs at a faster rate than Ca 2+ is removed-continuing the AP

30
Q

Name the three types of Muscle fibres

A

Slow Twitch oxidative Type 1
Fast Twitch Oxidative glycolytic Type 2A
Fast Twitch Glycolytic Type 2B

31
Q

Slow Twitch oxidative Type 1

A

sustained contraction
slow speed of development of max tension and myosin ATP activity
small diameter of fibre
oxidative:aerobic
High capillary density and many mitochondria
fatigue resistant
Supplied by myoglobin

32
Q

Fast twitch oxidative Type 2A

A

phasic movements- walking
intermediate speed of development of max tension fast myosin ATP activity
medium diameter of fibre
glycolytic but can become more oxidative:aerobic with training
Medium capillary density and moderate number of mitochondria
fatigue resistant

33
Q

Fast twitch oxidative Type 2B

A

phasic movements- explosive
fastest speed of development of max tension fast myosin ATP activity
large diameter of fibre
glycolytic- anaerobic
Low capillary density and Low number of mitochondria
fatigued easily

34
Q

Describe the pathway of activating groups

A

the greater the load- the more groups are activated over time- max Type II B

when one group fatigues another group takes over

35
Q

What is Duchenne Muscular Dystrophy

A

Symptomatic- less than 1 year to 5 years
Leads to death between 20-30- due to respiratory and cardiac causes

This is due to dystrophin function- x chromosome- it helps link contractile apparatus to the ECM
Stabilises sarcolemma, transmitting forces laterally across sarcolemma to ECM

People with dystrophy- the re[air for torn muscle fibres is constant- necrosis and fibrosis of muscle tissue occurs not by alike tissue.
ie. non contractile

36
Q

How is muscle formed embryonically

A

All the trunk/limbs derived from embryonic structures called somites- turn into progenitors of skeletal and muscle cells- when they go into certain environments- the myoblasts differentiate accordingly dependant on the environment due to cell signalling

37
Q

Describe the length tension relationship

A

Tension in a muscle can generate related to the number of the cross bridges formed between thick and thin filaments
In elongated fibres there will be few cross bridges - therefore little power generated
As sarcomere shortens- increase in number of cross bridges- the force increases until fully overlapped- hence the tension decreases rapidly since there are no new binding sites