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Neuromuscular Exercise Physiology > Midterm > Flashcards

Midterm Flashcards

1
Q

Muscle cells are made up of…

A

muscle fibers

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2
Q

muscle fibers are bound into bundles called…

A

fascicles

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3
Q

Fascicles are surrounded by heavy connective tissue layers called

A

perimysium

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4
Q

Whole muscle is surrounded by heavy CT layer called

A

epimysium

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5
Q

Each muscle fiber is surrounded by

A

sarcolemma

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6
Q

Surrounding the sarcolemma is the

A

endomysium (is a mesh work of loose connective tissue that surrounds each muscle fiber (endomysium also surrounds each muscle fiber)

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7
Q

muscle fibers are

A

multinucleated (b/c they are so long – need to be able to transmit messages)

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8
Q

Characteristics of muscle fibers (length, width, shape, etc)

A

Each muscle fiber has at least one capillary touching it
Fibers are long and thin
Fibers are 10-100 micrometer thick (1000 micrometer = 1 mm) – thickest muscle fiber is a thick as a human hair – very thin

A few mm to several cm long
1 micrometre of space b/w fibers
Polygonal shape allows greater packing density (fill in gaps so we have more efficient use of space
Shape isn’t circular if they were you have too many gaps and are wasting space – not very functional

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9
Q

What are myofibrils

A

Each muscle fiber is made up of myofibrils (make up ~85% of contents of fibre)
Myofibrils look stripy why we have straited/stripy muscle appearance
Most of the cell is made up of myofibrils – they are a lot thinner than the fibers
1-2 um in diameter (vs 10-100 um diameter for fiber)
A few hundred to several thousand myofibrils per fiber
Run whole length of muscle fiber
Made up of “thick” and “thin” myofilaments
Cause our muscle to produce tension, and to shorten our muscle

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10
Q

Thin myofilament

A

actin

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11
Q

thick myofilament

A

myosin

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12
Q

Myosin Filament Characteristics

A

has heads sticking off of it – stick out and cause attachment b/w 2 filaments, so they can pull against each other
Heads pointing in same direction on one half and on other half they are pointed in other direction for pulling

Each myosin filament is made up of myosin proteins (~100-400 myosin protein per filament)
The myosin protein
is made up of 2 myosin heavy chain – 2 individual proteins wound around each other and then they make up the tail and the head of the myosin protein (2 heads – made up of myosin light chain

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13
Q

Actin Filament and Actin protein characteristics (tropomyosin, troponin)

A

What the myosin heads tugs on
Actin filament are made up of a bunch of actin proteins
Actin Protein
These are globular shaped (circular)
Make up strands and these strands of actin protein’s wind around each other (see the red circles)
Also on top is tropomyosin a filament – thin and also wrap around the actin filament
Troponin globular protein attached to tropomyosin
Important for ensuring muscle contracting and allowing myosin to attach and pull = muscle contraction

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14
Q

Actin and myosin

A

together actin and myosin look like a bunch of people rowing in opposite direction– tugging and pulling – tug o war
Myosin heads like ores
Actually, pulling actin filaments together

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15
Q

How are sarcomeres unlike myofibrils and muscle fibers?

A

Unlike muscle fibres and myofibrils – run long lengths of portions of each muscle - Myofilaments only run a small portion of each myofibril and each section of the myofibril is called the sarcomere

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16
Q

Define Sarcomere

A

Each section of the myofibril that’s contained b/w the Z lines and they contain the actin and myosin myofilaments
And there’ll be a bunch of sarcomeres over on left and right and are in series to run length of myofibril
Within the one unit of then we have one sarcomere – within the sarcomere the myosin is about 1.5 um and the actin is about 1 um
sarcomere are about 2 um in length BUT this changes quite a bit they slide in and out depending on if muscle is relaxed or contracted so its about 2 um in length (sarcomere) but this varies depending on the time

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17
Q

Name the 5 important components of sarcomeres

A

Z line – marks start of one sarcomere and the end of the other. Under microscope look like dark thin line
A band – the thick dark band/stations in muscle fiber – what causes look of striation – contains mostly myosin and both actin – overlapped at this point
M line: middle line
H zone – lighter section than A band – only myosin thick filaments and none of actin
I band – straddle overtop of 2 different sarcomeres and it’s the light area

Dark stripes = myosin
Light = actin
Connective proteins make up z and m line

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18
Q

What is the structure of myofibrils

A

ndividual sarcomeres separated by z line also separated by sarcoplasmic reticulum and glycogen (black dots)
Stacked up end to end in series
Each myofibril has sarcomeres in series and in parallel

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19
Q

Why do we need stacking in series and in parallel

A

In series b/c a sarmoere can only shorten a few um in length so we need the additon of the ability to shorten a bunch in series to cause muscle measurably decrease in length
Also stacked up in parallel – side to side stacking (on top of each other)– within a myofibril and in muscle fibre
Side by side(parallel) and end to end (in series) stacked

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20
Q

What is the importance of the cytoskeleton and what are its components

A

Cystoskeleton Keeps Sarcomeres Aligned

Auxillary proteins are attached to myofibrils from M line to z line in order to connect them to the adjacent myofibirls
Nebulin and titin – important for the function of the sarcomere
Titin – attaches from end of myosin to z line
acts like a spring and allows sarcomere to snap back – allows them to return. The largest protein known in the body – M line to Z line 1um in lengt (30,000 AA
Nebulin – anchors to Z line and controls the length of actin (keep consistant)

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21
Q

Myofibril Structure

A

Actin and myosin filaments organize in a hexagonal array
rom a cross section then we can see that each myosin filament is surrounded by 6 different thin actin filaments
The cross bridges reach out to these filaments and they make this six-sided shape – hexagonal array
When you combine a bunch of actin and myosin filaments – myosin is sharing each of those actin filaments with 2 other myosin filaments. (don’t just get them to its own – efficient pattern)

Thick myosin filaments and thin actin filaments – looking at myosin we can see it surrounded by 6 actin and if we look at one actin we can see it surrounded by 3 myosin

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22
Q

What would happen if you took a cross-section of sarcomere

A

If you took a look at a random haphazardly cut muscle you wouldn’t get that perfect hexagonal view
You would have to make sure you are cross sectioning that muscle right where actin and myosin filaments both exist
Ex. Cross section like last slide – you hit it right where actin and myosin overlap
If you cut into, I band you’d only see actin filaments
If you cut right through M line you’d only see myosin, not myosin heads and you’d see axillary proteins

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23
Q

Working range of sarcomeres (lengths and calculation)

A

Muscle at optimal length = 2um
Flex bicep – you shorten sarcomeres and each Is getting shorter (filaments are overlapping
Extend elbow – sarcomeres in bicep get longer (3.5 um in length – pull apart filaments)
Not really a constant length of a sarcomere – Sarcomeres can vary in length
Working range of a sarcomere = 3.5-1.5(#sarcomeres) = 2.0 um - one sarcomere can change up to 2 um in length
See when they contract, they shorten by 2 um form longest to shortest length
To calculate many WR of sarcomeres = 3.5(# of sarcomeres) – 1.5(# of sarcomeres)

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24
Q

What is the working range of a muscle that contains 5000 um in series?

A

3.5(5000) – 1.5 (5000) = 10000 um or 10 mm (1000 um = 1 mm)
At optimal length this muscle fiber is 10000 um, 1cm, or 10 mm (2um x 5000)
At shortest length = 7500 um or 7.5 mm (1.5 x 5000
At longest length = 17500 um or 17.5 mm (3.5 x 5000)
17500 – 7500 = 10 000 um range

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25
Q

What is a power stroke?

A

Sarcomere shortening occurs via power strokes

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26
Q

How is a myosin cross-bridge formed?

A

CB formed by myosin head
Cross bridge is connection b/w myosin head and actin filament
Once this attaches to actin the head ends up pulling actin towards it
Sarcomeres can only shorten by pulling towards each other (NOT LENGHTENED)
Only one of heads is involved in power stoke (one of the 2 myosin heads)

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27
Q

CB Power Stroke Step by Step

A

Cross bridge is detached – myosin head not attached to actin
Cross bridge attaches to actin; power stroke begins – myosin head attaches to point on actin filament and begins to do that power stoke
Z line starts to move towards myosin
Power stroke proceed; pulling actin and z-disk; goes to how far it can, pulling acti and z disk inwards – shortening the sarcomere (only 10% of the total time)
CB detaches and “springs” back; Once power stroke is completed – myosin head detaches and springs back into ready position
Myosin head attaches pulls and springs back

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28
Q

What is the Bare Zone?

A

There’s a section in middle called bare zone
Segemtn of myosin filament with no corss bridges (corresponds to H zone)
As sarcomere shortens bare zone becomes overlapped with actin filament

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29
Q

When power strokes occur what happens to the cytoskeleton bands?

A 
When muscle contracts the Z line moves toward each other when muscle contracts 
Some of the bands narrow and some don’t
A band (actin and myosin) – doesn’t actually get shorter b/c myosin filaments make up inside of a band and they don’t get shorter – A band stays constant 
I band gets shorter – area where there is no overlap of actin and myosin gets smaller 
Muscle contracts when there's more overlapping myosin and actin (muscle contracting = muscle shortening
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30
Q

Type of Muscle Contractions

A

Muscles always become shorter –
When muscle is contracting and this happens
Concentric = muscle shortening (muscle contracts and it gets shorter)
Eccentric = muscle lengthening (muscle is contracting and it’s lengthening – losing the battle, it’s trying to get shorter, but it’s getting longer
Static contraction = no change (same amount of contraction force upwards as downwards) – no change in muscle length while the muscle is contracting

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31
Q

Contraction Types in terms of a sarcomere

A

If you had a concentric contraction – the sarcomere gets shorter (pull together
Eccentric – the sarcomere is getting longer (even though its trying to get shorter) – actin and z line move apart
Static – equal shortening as lengthening

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32
Q

Cross Bridge Power Strokes and Types of contractions

A

Power strokes always want to cause sarcomere shortening
Always pulling in shortening direction even if they don’t succed
Whethere they succeed depends on the external laod imposed on the muscle and if cross-bridges are cycling (not enough force to shorten and external load is higher = eccentric
Tug of war – myosin pulls one way – muscle pulls another way – whatever one wins is the direction muscle

33
Q

Example of contraciton types: Pull Up

A

Muscles getting you up = Muscles letting you down
Same muscles for up, down and static
Pulling up – you are shortening elbow flexors and lats – concentric (sarcomeres overcoming force of gravity)
Down – lengthening contractions in elbow flexors and lats – force of contracting less – gravity overtakes
If you completely let go you just fall so you apply a little bit of force to slowly move down
Static – just hold steady/ stop half way – isometric – same amount of force to elbow flexors as gravity – neither lengthening or shortening – you aren’t using dif muscles on way up or down

34
Q

Are Cross bridge power strokes synchronized?

A

Cross bridges look like people are rowing – in rowing people are synchronized and each time balde is in the water it’s all at same time then they all let go and stoke again
Muscle cross bridges are Asynchronous – at any given time some cross bridges are attach and other arne’t – doing power stokes at different rate s
Muscle wouldn’t work well other wise

35
Q

Why are they not synched?

A

You’re climbing a rope – alternating with hands and feet – one hand holding on while other moved – if you tried to use both hands to grab up higher – you’d fall as you let go
Same idea with actin – if cross bridges were synched everytime a cross bridge let go all would let go and we have opposing forces that corss bridge would not be contracting and allowing actin to slip away – so during non-attached phases actin would slide away and amount of time cross bridge is attached is less than the time it is unattached – inefficient movement – asynchronously – at any given time always cross bridges attached so there’s no slipping of the muscle and allows for effective shortening

36
Q

How do we get energy for Power Stroke?

A

We get energy from the breakdown from ATP to ADP and Pi and
How most energy is provided
ATP attaches to myosin head in the muscle

37
Q

Cross bridge cycle (atp roles)

A

Cross bridge has contracted sarcomere moves closer to itself and now it needs to detach
ATP binds to myosin head and causes detachment from actin
The ATP in the second step splits in half and released energy and causes myosin head to spring upright (adds energy to system -pull back arrow In archery – costs energy)
Inorganic phosphate is released and myosin can bind to actin
Once ADP is released (like letting go of bow) – causes energy to be released and causes cross bridge to go
2 ROLES of ATP
1. Provide energy to power stroke (– splitting of ATP) -PULLING BACK
2. Detachment of myosin from actin – attaches to myosin
Green circles are ATP – everytime atp attaches it allows myosin to detach and when atp splits it causes it to cock back and be ready to cause muscle contraction

38
Q

Regulatory Proteins of CB cycling (2)

A

Troponin
Circular protein
Made up of 3 complexes (3 parts)
Role: allows ca to bind to it, binds to tropomyosin, helps to inhibit binding b/w acting and myosin – inbits myosin head cross-bridge formation
Tropomyosin
Physically blocks binding site where myosin ahs to attach
Myosin head has to bind to a binding site which is hidden underneath tropomyosin, no corss bridge occurs when tropomyosin is covering the site
What happen is when ca is present then ca binds to troponin binding site – whne ca is bound to troponin it pulls aside the tropomyosin and expposes actin binding sites for myosin
Once they are exposed as long as theres eough atp ther we have myosin heads binds – ATP isn’t require for binding it’s requored for cross bridge cycle to occur
Need atp and Calcium for muscel contracting

39
Q

How is the binding of myosin to actin a calcium dependent process?

A

WE Need calcium and if it’s not there we don’t get state 3 of myosin binding to actin w/o Ca (you can have all ATP you want, still need Ca
Yellow balls are Calcium once they attach to troponin it moves the tropomyosin and exposes myosin-binding site s
IF NO CA is there?
Then tropomyosin slides back over actin-binding sites and myosin can’t bind and cross-bridge cycling stops and the muscle relaxes

40
Q

Organelle in muscle cell that is responsible for controlling Calcium concentration

A 
sarcoplasmic reticulum (wrap around myofibrils ) controls amount of Ca available to myofribrils 
Sarcoplasmic reticulum holds a lot of calclium the concetnraiton of Ca inside is very high
41
Q

3 main functions of sarcoplasmic reticulum

A

3 main functions:
Store Ca at trest
Releases ca Uptake when it wants to cause muscle concentration to occur (Ca leaves SR – binds to troponin moving tropomyosin and exposing binding sites)
Ca reuptake (removing ca from cytosol – remove availability to CB so no more cycling (requires ATP to pump it out of the cytosol

42
Q

What is Neuromuscular Transmission

A

How neuo system tells muscle to release or uptake that Calcium

43
Q

how do Motor Neuron Action Potentials work?

A

Neurons communicate via changes in the charges across membrane
CNS communicate with muscles via motor neurons
A resting membrane neuron: more negatively charged inside membrane than outside
When we have depolarization charge of neuron changes in on area and change spreads and moves down the axon and down the cell to communicate with other parts of body (to communicate with muscle fibers)
Looking at one small area of neuron – we’d see a change in charge that looks like graph (depolarization)

Action potential moves down the neuron (areas beside it and so on till it makes it to end and acts on axon terminal
Change in charge that moves down nerves and is used to communicate with CNS and rest of boy

44
Q

What is depolarization?

A

Depolarization (becoming more positive)
Occurs when cell depolarized to threshold (-55 mV)
Once at threshold it triggers depolarization and it happens automatically (once at -55) - Voltage gated Na+ channels open (charge becomes more positive) – sodium rushes in (positive charge moving inside = depolarization

45
Q

What is repolarization?

A

Repolarization (return to negative charge)
Voltage gated K+ channels open (charge becomes more negative again)
K+ allows K+ to rush out of cell (positive rushing out and it brings it back down to negative

46
Q

what is Hyperpolarization?

A

Hyperpolarization:
Overshoot, voltage gated K+ channels close
Sodium potassium pump return k+ AND Na+ to OG positions

47
Q

What is the neuromuscular junction?

A

Once we make it to the end of that motor neuron we have a neuromuscular junction
Where neuron contacts muscle fibre and communicates AP from CNS to fibre to tell it to contract
A single motor neuron talks to multiple muscle fibres

48
Q

How does neurotransmitter release work?

A

Motor neuron to postsynaptic cell (muscle fiber)
Action potential depolarizing axon terminal
At axon terminal it activates voltage gated Ca channels – it opens Ca channel and calcium floods into the motor neuron and it acts on the vesicale (bubbles of neurotransmitter floating around axon terminal) – it causes them to move towards the edge of axon terminal and spew contents into neuromuscular junction – in this cause acetylcholine
Neurotransmitters move across junction and attach to receptor on muscle fiber – receptors are voltage gated Na channels (this causes Na into the cell =depolarization) – depolarization occurs in one area of cell and spreads across cell membrane

49
Q

How does a motor action potential lead to force output?

A

Neuromuscular junction and AP makes it ot cell membrane and spreads across outer membrane of muscle fiber
As Ap makes it way to muscle fiber to finds its way to these divots or holes which go into the muscle fiber/myofibrils – hole called transverse tubules –
action potential moves across sarcolemma of muscle fiber then down transverse tubules towards interior
change in charge is infiltrating inside of muscle fiber allowing AP to reach each f the myofibrils and inside the muscle fibre – w/o transverse tubules we’d only have myofibrils working right close to the edge and we’d never get AP in the middle
sarcolemma needs to extend into the centre of the muscle fiber

50
Q

How do you get transmission of an action potential

A

the myofibrils make up 85% of muscle fiber contents rest is sarcoplasmic reticulum and mitochondria
t tubules dive into muscle cell and reach/contact all myofibrils – make their way to myofibrils
on either side are large parts of sarcoplasmic reticulum called terminal cisternae of SR
junction b/w sarcoplasmic reticulum, the terminal cisternae and t-tubules is called a “triad”
2 triads per sarcomere in human skeletal muscle
The t -tubules which carry ap are right beside sarcoplasmic reticulum which carries the Caclicum

51
Q

Functions of Sarcoplasmic Reticulum

A 
Stores Ca (At rest) – sarcoplasmic reticulum is not permeable to Calcium at rest, calcium pump is active any axcess Ca cto be pumped back into SR. Ca is -10,000 times greater in SR (rigor mortis – calcium leaks out of Sr and XCa pump is not active – calcium cross bridges can attach but not enough atp so it stays in contracted condition 
Release Ca (in response to motor action potential) – as signal makes its way down t-tubules it open calcium channels (Calcium channels open, and the ca rushes out and into the myofibril space – CA binds to troponin and causes CB cycling to be able to occur b/c myosin binding site is active 
Re-uptake Ca after motor action potential is no longer there 
No more MAP no more depolarization – Ca channels close 
Ca pump work to pump Ca back  into SR nad once Ca returns then CB cycling stops – troponin is no longer bound to Ca and tropomyosin covers up binding site – ATP dependant process – used energy to cause muscle relaxation
52
Q

Summarize excitation coupling

A

Action potential causes synapse to release Ach
AP in the sarcolemma/membrane of muscle fiber
Ap moves down the muscle fibers and down t-tubules where it is paired with SR
Once it reaches SR it releases Ca into the myofibril space – in cytosol
Lots of CA IN cytosol we get Ca binding to troponin and exposes the binding site so myosin can bind
Cross bridge cycling (as long as binding site is exposed – CB keep cycling over and over – as long as ATP and CA available
Stop AP – Ca is removed -causes less ca to attach to troponin,
Tropomyosin blocks binding sites and muscle relax

53
Q

In vitro motility Assays: Studying Skeletal Muscle myosin

A

tick myosin on to plate
Put actin filaments on top of myosin heads in a fluid
As long as they get CA and ATP they keep contracting and actin moves around
Actin is fluorescent and you can see actin moving

record this and record velocity – faster more CB cycling is occurring
Add something to slow movement – impairs muscle filament
Say you added MORE Calcium and Atp = increase velocity, more Ca and ATP more binding sites available more CB cycling can occur. More ATP does the same thing = greater velocity, there is a point where all the binding sites available being used and are saturated with ATP there Is a maximum rate of contraction

54
Q

Work of muscle shortening

A

concentric – trying to shorten and shortens
Eccentric
Isometric = force being applied is the same as the muscle is applying (by CB cycling – no movement
Isometric contraction doesn’t necessarily mean there;s no movement
Person is sitting in a chair and they are trying ot kick but they can’t move it (isometric)
You’d think no movement – in reality ther’s a lot of movement! No external work you are performing a lot of internal movement – due to the elasticity of the muscle
Difference b.e no movement around and joint and no movement within a muscle

55
Q

Impact on CB cycling: more frequent firing of motor action potential

A

More frequent acetylcholine release.
• More firing of action potentials along sarcolemma
• More frequent propagation of AP down T-tubules
• More Calcium released
• More open Calcium channels
• More calcium in the cytosol
• More calcium binding to troponin exposing more binding sites are available
• More cross bridge cycling
• Overall force of muscle contraction increases.

56
Q

Impact on CB cycling: loss of ATP producing ability (i.e. less mitochondria)

A

• Less likely to be a detachment from myosin
• Calcium can enter cytosol but less ATP to pump back into SR
Cross bridge cycle happens slower due to less ATP interaction
• Smaller force of contraction

57
Q

Impact on CB cycling: less myosin heads

A

Less myosin to bind
• Less binding, can cause slipping
• Fewer myosin and actin interactions = less cross bridge cycling
• Decrease force

58
Q

Impact on CB cycling: less calcium pumps (active) in SR

A

Muscle wouldn’t be able to relax, slower calcium reuptake into SR
• More calcium around in cytoplasm more exposed binding sites and this inhibits relaxation
• Impairs muscle function
• More contraction, probably more cross bridge cycling – force doesn’t increase, but lasts for
longer cause relaxation can’t occur – more time for cross bridges to cycle

59
Q

Impact on CB cycling: No motor endplate

A
  • No area of neuron where there can be contact between neuron and sarcolemma
  • No acetylcholine release
  • No muscle action potential (nothing passed down t-tubules)
  • Calcium stuck in SR - not able to expose binding sites
  • No contraction – muscle relaxed
60
Q

What is a motor unit?

A

an Alpha motor neuron (nerve from spinal cord and innervates muscle fibers) + innervated muscle fibers
Each motor neuron is going to innervate a bunch of muscle fibers
All the muscle fibers innervated by one neuron is called a motor unit
May see motor neuron from SC and axon splits and innervates b/w 10 and 2,000 muscel fibers
The eye innervates 10 msucel fibers ratio of 1 to 10
In gluteus amximus each mortor neuron innervates 2000 suchle fibers

61
Q

innervation ratio

A

number of fibers controlled by one neuron

62
Q

All or none principal

A

all muscle fibers fire with alpha-motorneruron action potential.
When an action potential goes down that motot neuron – all msucel fibers in that motor uit are going to contract – you can’t differentiate b/w differntnmuscle fibers within that mototr unit. If you’re activating that motot neuron than all the fibers are going to contrac t
In msucels where fine movemetns are rewuired each motor neuron only innervtates a few muscle fibers at the same time and the eye moves a little bit – this is good for fine movemetns
In the glute it doesn’t require fine movement – soyou can have a lot of movement with a little efforet form SC

63
Q

Effect of one motoneuron Action potential

A

Imagine this is one motor neuron and all muscle fibers it innervates
Motor neuron sends APP down and it splits off and innervates different fibre – once AP reaches motor end plate it reaches muscle fiber and spreads out sarcolemma (AP progate/spread along the fibers)
Causes muscle to contract and causes and increase in force
Amount of force over time – if just one AP is fired it is gonna cause blip in force that is increased than decreases (muscle twitch)
If you see it looks like two MAP being sent out (NOT TRUE) – just one MAP that spreads across muscle
Stone in pond – having waves spread across pond – like if you cause ap down a motor neuron – after it reaches end pa,te and reaches sarcolemma it spreads across sarcoleme like waves acoss a ponf (one AP spread, one wave)

64
Q

Muscle Twitch

A

Contractile response to single nerve impulse/muscle action potential
Single twitiches are rare in normal function
Evoked (ST) artificially in research to study muscle function

65
Q

Femoral Nerve Stimulation

A

2 electods and send electrical impulse into femoral nerve (below) and it evoke muscle twitch – muscle contracts and use EMG – tell us about electrical acitivt of the msucel
EMG measue AP as they go across the msucel fibers
Muscle twitch is a small contraction and doesn’t cause much movement
Force applied by nuscle tiwthc may be 40 n.m at it’s peak and tis over short period of tiem – 220 md =0.22
Ca release/contraction par = 80ms
Ca reutpaek/relacxtaion = 140ms

66
Q

Twitch Summation: Low vs high frequency

A

Low=full relaxation b/w twitches
If you stimulate at low frequency and have full relaciton b/w twitches = twitches abck to back and they won’t affect each other

Summation:
High frequency of Ap, incomplete relaxation, stronger contraction
2 AP back to back – 3 back to back 6 back to back evokes each time there’s a seconds ap before other one fully relaxed it causes increase in a force and it compounds on itself

67
Q

Twitch Summation: Fused vs Unfused tetanus

A

Twitch Summation
Contractile response to a “train” of MAPs causing summation
5AP/sec (5HZ)
Contraction and a bit of relaxation(not full) before next AP comes
Jagged line =unfused tetanus
Unfused tetanus indicates that there jagged line and we haven’t fully allowed relactation before next AP
Ap very frequently (50 hz/50 times per sec) – don’t even time for relaxation to start! It causes smooth increase and plateau at top – no jagged force production its smooth – this is fused tetanus (bumps fused, completely fused
Strongest contraction you can initiate is via fused tetanus
Double frequency to 100 hz it won’t increase muscle contraction there is a plateau and that’s at fused tetanus – no relaxation in between it is at maximum contractile force
Summation causes tetanus to be stronger than twitch = more summation in fused teatmnsu than unf

68
Q

Twitch/Tetanus Ratio or Tetanus/twitch ratio

A

Muscle twitch evokes less force/increase in force than tetanus
Each muscle ahs different in Twitch/Tetanus Ratio or Tetanus/twitch ratio
This is the ratio b/w amount of force evoke by twitch and force produced by tetanus
Say 5 N of force in twitch and in tetanus you produce 50 N
5/50 = 0.1 10%
Or 50/5 = 10

69
Q

What is the series elastic component?

A

Muscles exert their force on the bones they are attached to
Say looking at bicep – it exerts force on bones it’s attahces to (inward force sent down msucel on tendon and orgin of muscle and insertions – forces pulled on bones its attached to
Inward force on origin and insertion
Muscle/tendon complex works like an elastic – when you pull on it it stretches a little bit and it tries to react by snapping abck together
Tendon and muscle are a bit elastic – once you shorten it doesn’t immediately occur b/c of elasticity it’s a bit delayed
Muscle itself acts like an elastic

70
Q

What makes up the SEC?

A

Tendon b/w the bone is elastic (the major elastic compoinent of the muscle
Connective tissue b/w the tendon and muscle
Titin – from z line t myosin head is elastic
Cross bridges themeseld
All contribute to series elastic compent: they are end ot end. Act in series ontop of each other

71
Q

2 types of Elastic components In Muscle

A

Series vs parallel
Contractile unit is a bit elastic and tension is elastic
Surrounding contractile unit/muscle fiber is sarcolemma which is also elastic – since it surrounds it has different elastic properties – elasticity in parallel (round contractile unit)
Series vs parallel – you’re trying to move a rock with a few elastic bands attached end to end (attached in series). Still very difficult to apply force of you pulling onto the rock b/c they stretch adding more end to end/in series just causes it to stretch a longer distance. Say you wanted to add force in parallel – attached elastic bands side by side . Attache them in other hand and more bands side by side then the force you apply will more be applied to the rock

72
Q

SEC: Potential Cross bridge force versus force applied to the bone

A

the SEC means that less force is applied to the bone initially
once the SEC is taken up:
CB force=force applied to bone

73
Q

Internal vs external force applied to the bone during a muscle twitch

A

External force- rise much smaller and is a bit higher than internal force during relation – reason is b/c SEC
Analogy – person holding a spring – muscle twitch s one quick step out (starting to stretch Elastic component of muscle – only going to apply a bit of force ot bone – block only feels a bit og forfc e
Once you relax not more steps – elasticity has some potential force and it’s trying to pull you back towards blaokc – elasticity tries to add to the force inot more contacted position – even though CB aren’t minimally contracting Elastic component tries to apply that force
You provide energy and it comes back somehow by bringing muscle to a more contracited potion

74
Q

Tetanus: Potential cross bridge force

A

THE FORCE is being applied by the CB every single time there’s a cross bridge there’s a max force apply internally
External force takes a bit of time to reach potential amount of internal force
Person holding a spring 1 AP = 1 sig step
Cb keeps shorting more AP – taking up more spring – spring gets stiffer and pulls block a bit more
Once you’ve been stretching/pulling for extended period it’ll be full extended – like pulling on metal wire no elasticity and put force you’re using to run/pull into the block and then
At this point , The external force = to internal force no more elastic stretch occurs and all force from CB is being applied to bone
Once sec of a muscle is fully stretch there’s no force lost to elasticity

75
Q

Timing Factor

A

Rising phase of twitch lasts only ~50-100ms (short) not enough time for CB to shorten enough to take up SEC
A tetanus can lasts seconds (logner) sufficient time to take up elastic component easily and apply CB force directly to bone

76
Q

Force Ca Relationship

A

Force – Ca concentration Relationship
if we graph Ca that’s available in the cytosol to amount of force being applied by muscle we can see that there’s an increase in force applied to muscle with more ca
Little Ca (like with low frequency AP) = little force applied
Saturating Ca (high frequency) = large force applied
Certain point we reach saturating Ca = interaction b/w ca and troponin all the troponin have ca bound to them and all sites available – adding more Ca won’t free up any more sites b/c they are all available = most amount of force possible – not more increase in force with more added ca

77
Q

Force-Frequency Relationship

A

experimental setting – apply electoral impulse to femoral nerve
1 impulse = muscle twitch
Apply electrical signals at low rate 10 x per sec = unfused tetanus – not as strong as fused tetanus
Impulse at 50 times per sec = fused tetanus – more frequent MAP more frequent release of Ca from SR
More Ap that reach SR per sec more Ca release and we will reach suturing ca rate = fused tetanus
Unfused gap b/w each AP and ca taken up
Fused Ca – no time for Ca to be taken up and always lots Ca available and cause max contraction
Higher frequency MAP
more Ca release from SR
more force produced

78
Q

Force frequency and Ca

A

More ca = more force
Take forec ca relationship and overly oaver frwuency ca relations
And increasing frwuency of AP (twitch = lowest AP frwuncy)
Increasing frwuncy AP = more CA released = more force applied
10 hz (10AP/sec) vs 50HZ = max force
Diminishing returns diff b/w 1AP/sec to 10 hz increase foec from 5 – 50%
Diff b/e 10hz to 50hx increases forec gives you an increase of force from 50 – 100 %
So more ap per sec the elss each ap contributes to an increase in force

79
Q

Why tetanus is stronger than a twitch (force v time graph):

A

1 AP/SEC and 50 AP/SEC
In tetanus 1AP intiate little blip and this is internl force vs many AP cause large internal force (potential force)
However at external force (applied to bone) – not as much applied ot bone during tiwthc and suring tetanus the extrenal force lags behind due to SEC
External force vs internal during a twitch due to SEC
During tetanus external force lags behind because of SEC, delay in equalizing external and internal force during tetanus is due to SEC (being taken up ) takes time for ti to be taken up and twich doesn’t case enough time for shortening
Tetanus more ap and more ca relase = more mysin to actin and cause more CB cyucling and more force generated

Neuromuscular Exercise Physiology (1 decks)

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