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Physiology 208 > 8. Chapter 12- Skeletal Muscle > Flashcards

8. Chapter 12- Skeletal Muscle Flashcards

1
Q

What is primary function of all muscle?

A

Generate force and movement in response to a physiological stimulus
Generation of force depends on conversion of chemical energy (ATP)

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2
Q

What are skeletal muscle, cardiac muscle, and smooth muscle?

A

Skeletal muscle- voluntary by somatic motor neurons
Multinucleated (largest cells in body)
Cardiac muscle- involuntary spontaneous electrical activity
Creates pressure gradient for flow of blood
Uninucleate
Smooth muscle- involuntary autonomic control spontaneous
Uninucleate
Mechanical control of tracts blood vessels and airways
Slides 4-6 oct 17

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3
Q

What are flexor and extensor skeletal muscles?

What attaches skeletal muscle to bone?

A 
Flexor- brings bones together (biceps)
Extensor- moves bones away (triceps)
Attached to bones by tendons
40% of total body weight
Slide 7 oct 17
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4
Q

What makes up muscle cells?

A

Myofibrils make up muscle cells

Study break down of muscle on slide 9-10 out 17

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5
Q

What are Z disks, I bands, A bands, H zones, and M lines of the sacromere?
How are these used in muscle contraction?

A

Z disk- zigzag protein that is attachment site for thin filaments
I bands- lightest band occupied by only thin filaments
A band- darkest band entire length of thick filament
H zone- central region of A band of thick filaments
M line- form attachment site for thick filaments
Equivalent to z disk for thin filaments
Slide 11 oct 17
Slide 16 oct 17
Sacromere shortens during contraction (H zone and so band both shorten while A band remains constant)

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6
Q

What is F-actin and Tropomyosin?

A

F-actin- back bone of thin filaments, double stranded alpha helical polymer of G-actin molecules (has binding site for thick filaments (myosin))
Tropomyosin- 2 identical alpha helicies that coil around each other and sit in the two grooves formed by actin strands
Prevents interaction between actin and myosin
Picture on slide 12 oct 17

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7
Q

What is the troponin complex?

A

Heterotrimer consisting of troponin T (binds to Tropomyosin), troponin C (Ca binding site), and troponin I (binds to actin in resting conditions

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8
Q

What are myosin molecules?

What are the two lights?

A

A bundle creates a thick filament (two intertwined heavy chains that contain two light chains)
Myosin head contains region for binding actin and binding and hydrolyzing ATP

Regulatory light regulates ATPase activity of myosin
Essential light chain stabilizes myosin head

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9
Q

What are the proteins titin and nebulin?

A

Titin- very large protein extending from M line to Z line
Stabilization and recoil behaviour of muscle

Nebulin- wraps around thin filament
Regulate length of thin filament

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10
Q

What are the important structures within a single muscle fibre?
(Picture slide 17 oct 17)

A

Sacroplasmic reticulum
Transverse tubules
Terminal cisternae
Mitochondrion

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11
Q

What is the neuromuscular junction and the excitation-contraction coupling in the initiation of skeletal muscle contraction?

A

Neuromuscular junction- point of synaptic contact between somatic motor neuron and individual muscle fibres
Excitation-contraction coupling- action potential initiated in skeletal muscle fibre results in increase in intracellular Ca2+

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12
Q

What are the regions that send muscle signal from brain to muscle?

A

Primary motor cortex (basal ganglia, thalamus, midbrain, cerebellum)
Corticospinal tract
Upper motor neuron synapses with (alpha) lower motor neuron that associates with desired muscle

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13
Q

What are motor units?

A

A single motor neuron and all the muscle fibres it innervates
Number of muscle fibres/motor units varies
<10 for precise work
>100 for powerful work
Slide 9 oct 19

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14
Q

What is myasthenia gravis?

A

Severe weakness of muscle
Disorder of neuromuscular transmission
Autoimmune
Impedes activation of AchR

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15
Q

Where to action potentials propagate from?

A

From the sarcolemma to the interior of muscle fibres along the transverse tubule network
Slide 20 Oct 19 picture

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16
Q

What is excitation contraction coupling?

A

Ultimate intracellular signal that triggers contraction in all muscle types is a rise in intracellular calcium
Ca2+ can enter sarcoplasm from extracellular space by voltage gated channels or intracellular Ca2+ storage reservoir
Increase in Ca2+ triggered by electrical excitation of surface membrane is excitation contraction coupling

17
Q

Where do T tubules (transverse tubules) penetrate muscle fibre and surround myobfibrils?

A

Two points in each sarcomere:
A band junction
I band junction
Picture on slide 6 oct 22

18
Q

What are the 4 steps in the initiation of a muscle action potential and excitation-contraction coupling?

A
  1. Somatic motor neuron releases ACh at neuromuscular junction
  2. Net entry of Na+ through ACh receptor-channel initiates a muscle action potential
  3. Action potential in t-tubule alters confirmation of DHP receptor
  4. DHP receptor opens RyR Ca release channels in sarcoplasmic reticulum, Ca enters cytoplasm
    Slides 7 and 8 oct 22
19
Q

How does an increase in Ca2+ trigger contraction?

A

Removes the inhibition of cross bridge cycling
Ca binds low affinity sites on troponin C which induced conformational change in troponin complex
Reveals myosin binding site on actin
Picture on slide 10 and 11 oct 22

20
Q

What are the steps to the power stroke?

A
  1. ATP binds to myosin (myosin releases actin)
  2. Myosin hydrolyzes ATP (energy from ATP rotates myosin head to cocked position, myosin binds weakly to actin)
  3. Power stroke begins when Pi is released
  4. Myosin releases ADP at the end of power stroke
    As long as light chain is phosphorylated this cycle can occur
    Slide 13 and 14 oct 22
21
Q

What is the sliding filament theory (shortening of sarcomere and contraction)?

A

As contraction takes place, action and myosin slide by eachother while the H zone and I band both shorten
Slide 15 oct 22

22
Q

How is contraction terminated?

A

Once AP has subsided Ca must be removed so myosin binding site on actin can be covered by Tropomyosin
Ca can be removed to extracellular space by Na-Ca exchanger or by Ca pump by ATp
High Ca in sarcoplamsic reticulum inhibits pump
Picture on slide 18 oct 22

23
Q

What is rigor mortis?

A

Development if rigid muscle several hours after death

Ca leaks into sarcoplasm and binds troponin

24
Q

What happens when ATP production stops in muscles?

A

Ca cannot be removed since SERCA pump needs ATP
ATP needed to release myosin head from actin
Remains in latched cross bridge formation until muscles begin to deteriorate

25
Q

How are motor neuron potentials and muscle fiber potentials times differently?

A

Slight delay between motor neuron AP and muscle fiber AP
Day between muscle fiber AP and contraction (latent period) time when Ca is being released and binding troponin
Graphs on slide 20 oct 22

26
Q

What are two sources of ATP for muscles?

A
  1. Free intracellular ATP (few seconds)
  2. ATP stored as phosphocreatine (10 sec)
    Phosphocreatine on slide 21 oct 22
27
Q

What are the two determinants of muscle force/tension?

A

Force/muscle cell
-initial resting length and frequency of activation (degree of overlap between actin and myosin filaments)
Slide 7 oct 26

Number of muscle cells activated

28
Q

What are single twitches and summation in muscles?

A

Single AP results in an individual muscle twitch
Single twitches- muscle relaxes completely between stimuli
Summation- stimuli closer together do not allow muscle to relax fully
Increases force developed by muscle fiber

29
Q

What is unfused tetanus and fused tetanus?

A

Unfused tetanus- reaches steady state of contraction but stimuli are far apart so muscle fiber slightly relaxes between stimuli
Fused tetanus- stimulation rate is fast enough that the fiber does not relax, it reaches maximum tension and remains there
One way to increase tension is to increase rate of AP in muscle fiber
Slide 10-11 oct 26

30
Q

What is muscle fatigue, central fatigue, and peripheral fatigue?

A

Muscle fatigue- decrease in muscle tension resulted by previous contractile activity that is reversible with rest
Central fatigue- feeling of tiredness and a desire to cease activity
Peripheral fatigue- ACh synthesis can’t keep up with neuron firing rate
Failed excitation contraction coupling
Decrease neurotransmitter release->decrease AChR activation->muscle finals to reach threshold for firing AP

31
Q

What are the two ways to classify skeletal muscle?

A
  1. Velocity of shortening depends on ability to hydrolyze ATP
    Slow fibres contain myosin with slow ATPase (TYPE I)
    Fast fibers myosin with more rapid ATPase (TYPE II)
  2. Type of enzymatic machinery available for synthesizing ATP
    Fibers containing lots mitochondria can aerobic oxidative metabolism and are called oxidative fibers with few mitochondria store gylcogen are called glycolytic fibers
    Picture on slide 13 oct 24
32
Q

What are motor units and motor neuron pools?

A

Motor units- single motor neuron and all the muscle fibres it innervates, 1 motor neuron innervates 1 fibre type
Small motor neurons innervate least number of muscle fibres
Large motor neurons innervate large number of muscle fibres
Motor neuron pool- group of all motor neurons innervating a single muscle
Slide 12-15 oct 26

33
Q

What is isotonic contraction (Concentric and eccentric) and isometric contraction?

A

Isotonic- muscle contracts, shortens, and has enough force to move the load
Concentric- muscle shortens
Eccentric- muscle lengthens (slide 18)
Isometric- muscle contracts, but does not shorten, force created cannot move load
Slide 17 oct 26 pic

34
Q

How do sarcomeres shorten during isometric contraction without the muscle changing length?

A

Elastic elements in tendons, elastic and connective tissue in and around muscle fibres
Picture on slide 19 oct 26

35
Q

What are the two mechanism by which muscle mass can be increased?

A

Hypertrophy- increase diameter of muscle fibres, increase size number of contractile proteins, increase # of sarcomeres, and increase sarcoplasmic storage (slide 22 oct 26)
Hyperplasia (no evidence in humans)- muscle fibres can split if they become too large

Muscle fibre number does not change
Slide 21 oct 26

36
Q

Which type of muscle fibre results in greater rate of myofiber hypertrophy, type I or type II?

A

Type II

37
Q

What is skeletal muscle atrophy?

A

Immobilization, bed rest or unloading
Decrease in muscle size (protein degradation>protein synthesis)
Myonuclear loss, decrease in myofibrillar proteins, decrease in myofiber CSA
Slide 24-25 oct 26

38
Q

What is cachexia?

A

Weakness and/or wasting due to chronic disease
Cancer is associated with loss of weight or weakness of muscles
Slide 26 oct 26

Physiology 208 (22 decks)

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