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Advanced A&P I > Exam 3 Skeletal and Smooth Muscle > Flashcards

Exam 3 Skeletal and Smooth Muscle Flashcards

1
Q

What percentage of the mass of a normal healthy adult comes from skeletal muscle?

A

40 %

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2
Q

What are some of the functions of skeletal muscle?

A
  • Movement
  • Expression
  • Communication
  • Body temperature regulation
  • Effectors of neurons
  • Store of ions, fluid, and proteins
  • Storage of glycogen
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3
Q

What is glycogen and where is it stored?

A
  • A long chain of glucose molecules
  • Skeletal muscle and liver
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4
Q

What is a bone-bone connection called?
What are some examples?

A
  • Ligament
  • ACL, MCL, Patellar
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5
Q

What are muscle-bone connections called?
What is an example?

A
  • Tendon
  • Achilles
    Exceptions: there are some intermediate tendons that connect muscle to muscle
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6
Q

What is a muscle cell called?

A

Muscle fiber

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7
Q

What is a group of muscle fibers called?

A

Fasiculous

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8
Q

What is a group of fasiculi?

A

Muscle Fiber

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9
Q

What are the internal cylinders of a muscle cell called?
What is contained within them?
How many are there per muscle cell?

A
  • Myofibril
  • Actin and myosin
  • Over 200
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10
Q

What determines how many myofibrils a muscle fiber has?

A

The function of the muscle
Muscles needed for lots of strength have more myofibrils
Muscles needed for fine motor have less myofibrils

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11
Q

What is the functional unit of a myofibril?
What’s important about this structure?

A

Sarcomere
Has overlap of thin and thick filaments

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12
Q

What is a motor unit?

A

A group of muscle fibers controlled by a single motor neuron

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13
Q

Describe activation and function of small and large motor units?

A
  • Typically small motor units are easier to excite and are activated first
  • If more muscles are needed, then the large motor units are also excited
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14
Q

What type of muscle is used for sustained contraction?
What do they contain lots of?

A
  • Type 1(slow)
  • Mitochondria and myoglobin
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15
Q

What is myoglobin and its function?
What does this do to the appearance of the muscle?

A
  • Very similar to hemoglobin and unloads oxygen from blood to muscles
  • Iron containing protein that makes the muscle appear red

Ex: duck breast

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16
Q

What type of muscle is used for “fast twitch”?
How are they different from “slow” muscles?

A
  • Type 2
  • Have very little myoglobin making them appear white
  • Have fewer mitochondria

Ex: chicken breast

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17
Q

Describe the differences in force of contraction over time for fast, intermediate, and slow muscles?
What are examples of each?

A
  • Slow muscles take longer to get to full force but can contract longer (soleus)
  • Fast muscles reach maximal force of contraction faster but contract for a short period (ocular)
  • Intermediate muscles are somewhere in between fast and slow (gastrocnemius)
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18
Q

What is the cell wall of a muscle called?

A

Sarcolemna

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19
Q

What are muscles called that have bands of alternating light and dark colors?
Where are these found?

A
  • Striated mucles
  • Skeletal and heart muscles
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20
Q

What are the thick and thin filaments called in a sarcomere?

A

Thick = myosin
Thin = actin

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21
Q

What creates the two ends of the sarcomere?
What is it comprised of?

A
  • Z disk
  • Bundle of actin wraped around each other
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22
Q

What is the area of the sarcomere where there is only thin filaments?
What is its appearance?

A

I band
Light colored
Extends across both sides of the Z disk

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23
Q

What are the areas of the sarcomere containing only thick filaments?
What is its appearance?

A

H zone or band
dark colored

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24
Q

What is the area called on the sarcomere where the thick and thin filaments overlap?

A

A band

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25
Q

What is the large elastic connective tissue that helps provide structure to the sarcomere?

A

Titin (protein)

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26
Q

How does contraction of a myofibril effect the structures of a sacrcomere?
What is this contraction called?

A

Sliding Filament Mechanism
* Z bands move closer together
* I bands shrink
* H bands disappear
* A band remains the same width

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27
Q

How do long neurons transport needed proteins to the end of the axon where the synapse is?

A

They have tracks along the length of the axon where proteins and other information can be sent down from the nucleus to the terminal end of the neuron.
Skeltal muscles cannot use this system because of the contents of the myofibrils.

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28
Q

How do muscle fibers obtain needed proteins and other information if they cant use the “track” system via neurons?

A

They are multinucleated and have many nuclei along the length of the myofibrils.

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29
Q

What makes up a myosin filament?
How many are there per filament?

A
  • Myosin molecules wrapped together
  • 200 myosin molecules per myosin filament
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30
Q

How many chains are there per myosin molecule?

A
  • 2 heavy chains in the tail
  • 4 light chains in the head (2 essential and 2 regulatory)
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31
Q

What are the 2 different heads in the myosin molecule and their function?

A
  • Regulatory light chains - regulate activity of essential light chains, used more in smooth muscle for phosphorylation
  • Essential light chains - possess ATPase activity, has high affinity for the active sites on F-actin
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32
Q

What is the structure of an actin filament?

A
  • F-actin strand: has active sites for binding myosin heads
  • Tropomyosin strand: Blocks the active sites on the f-actin strand when the muscle is at rest
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33
Q

What is the troponin complex?
How does it work?

A

Contains 3 protiens
* Troponin I: Binds to actin
* Troponin T: Binds to tropomysoin
* Troponin C: Binds to calcium with 4 binding sites
When troponin C is bound by calcium, the configuration changes, causing a twisting or unraveling of the filaments that exposes the actin active sites

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34
Q

Describe the “resting” or cocked state of the myosin head?

A

ATP binds to the myosin head and puts tension on the head, “cocking” it, making it ready to bind to myosin. This leaves an ADP and Pi group on the head.

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35
Q

Explain/draw cross bridge cycling?

A

Ca++ binds to tropomyosin C to reveal the active sites on actin during step 3

36
Q

What can happen in our muscles if we have an ATP deficency?

A

The myosin heads cannot unbind from the actin filaments resulting in stiffness
(rigor mortis)

37
Q

What would happen if our sarcomeres are overstretched and there is no overlap between the actin and myosin filaments?

A

There would not be any contraction
Although not so extreme, this is what happens overtime when our ventricles are stretched in heart failure leading to reduction in force of contraction

38
Q

What is the length of sarcomere that allows optimal force?

A

~2 micrometers

39
Q

What would be the effect if the sarcomeres were understretched?

A

There would not be much room to shorten leading to small amounts of contraction

40
Q

What keeps our skeletal muscles/sarcomeres at optimal length to provide good contractions?
What can affect this?

A

Our tendons keep the muscles at optimal length
Athletes with large muscles may need to stretch due to understretching while at rest
Repairs of tendons can cause dysfunction because the muscle length is not exactly the same as before

41
Q

What is the resting state of our heart sarcomeres?
Why is this necessary?

A

They are typically understretched
This is so that when more pressure or volume is added to the heart muscle, the sarcomeres can stretch to add more force of contraction (starling forces)

42
Q

Describe the difference in active and passive tension?

A

Active tension: the force of the muscle contraction as a result of an action potential
Passive tension: the outside force that causes stretch of the sarcomeres (tendons)

43
Q

How do you obtain total tension?

A

Total tension = passive + active tension

X = total tension, Y = active tension, Z = passive tension

44
Q

What tension is the weight providing?
How does the tension change during contraction?
How could we calculate the total force generated by contraction (active tension)?

A
  • Passive tension
  • Tension increases with contraction
  • Subtract the mass of the weight from the total tension measured
45
Q

Describe the load velocity relationship?
Where is the important?

A
  • The heavier the load, the slower the contraction speed
  • In the heart, when someones BP is high (high afterload) the slower the velocity of contraction (longer time to eject blood)
    -Can lead to problems with filling bc systole is taking longer
46
Q

Describe quantal summation?
What is this dependent on?

A
  • Recruiting more and more motor units to increase the amount of force generated
  • Requires a strong enough voltage to stimulate all of the motor neurons
47
Q

Describe temporal summation?

A

By increasing the rate of simulation of the neuron, there is an additive effect that increases the strength of muscle contraction until ~40Hz (tetany). This additive affect is due to calcium not having enough time to be removed from the sarcoplasm between stimuli, increasing the force of contraction. After ~40Hz the calcium receptors become saturated, and the muscle cannot contract more.

48
Q

What happens to skeletal muscles with atrophy?

A
  • Lose myofibrils
  • If not used for a long time muscle fibers can disappear
  • Muscle fibers can’t regenerate at this point
49
Q

What happens to skeletal muscles with hypertrophy?

A
  • Increased use will increase the amount of myofibrils and cell size
  • Will have a lot of the mass of the muscle due to increased vascularization
50
Q

What happens to skeletal muscles with hyperplasia?

A
  • Excercising a lot for a long period of time can cause a very slow regeneration of muscle cells
  • This happens in the heart, again very slowly (post MI)
51
Q

How much of our body weight is our smooth muscle?

A

~10 % of body mass

52
Q

Where is smooth muscle found?

A

All over the body: intestines, blood vessels, lungs, heart.
Specialized for different organs

53
Q

Why are smooth muscles more efficient than skeletal muscle?

A

They have slower cross-bridge cycling that results in slower myosin head release from actin. This allows for longer maintainence of force and less ATP use.

54
Q

What muscle is stronger per gram?

A

Smooth muscle

55
Q

Describe the “latch” mechanism in smooth muscle?

A

Very slow cross-bridge cycling that allows the muscle to maintain contraction for a long time with the use of very little energy.

Ex: Boaconstrictor

56
Q

How are the amounts of actin and myosin different in skeletal and smooth muscle?

A
  • Skeletal muscle: 2 actin/myosin
  • Smooth muscle: 10-20 actin/myosin
57
Q

What is the equivalent structure of the z disk in smooth muscles?

A

Dense bodies
Anchor neighboring cells, comprised of wound actin filaments

58
Q

Describe the SR in smooth muscle and how the cells operate differently than skeletal muscle because of this?

A
  • The SR is not as well developed in smooth muscle
  • Smooth muscle is dependent on outside calcium for muscle contraction via Ca++ leak channels, VG-Ca++ channels, and ligand gated Ca++ channels.
59
Q

How does severe hypocalcemia affect blood pressure?

A

Causes hypotension primarily because the vascular smooth muscle doesn’t have enough Ca++ to maintain tone
And secondly, the heart cannot contract as strongly in low calcium states

60
Q

Describe the set up of visceral smooth muscle?
What is the other name for it?
Where are these found?

A
  • Also called unitary, makes up the vast majority of smooth muscle
  • Smooth muscles cells are attached by gap junctions that allows for the cells to contract as a unit
  • Found in the intestinal smooth muscle
61
Q

Describe the set up of mutli-unit smooth muscle?
Where are these used?

A
  • The cells are not connected by gap junctions, they require neurotransmitters to be activated
  • This allows for delicate control of the muscles
  • Found in the cilliary muscle and iris
62
Q

What type of muscle is found in the esophagus?

A

Hybrid of skeletal and visceral smooth muscle
Only hybrid muscle structure

63
Q

What is indicated by 1? What is its function? What is the other name for this layer?

A
  • Adventitia
  • Structural support connective tissue of vascular smooth muscle
  • Tunica externa
64
Q

What is number 2? Where is it found? What is the other name for this layer?

A
  • Endothelium
  • Found in all of our vascular smooth muscle
  • Tunica intima
65
Q

What vessels are only endothelial cells and have no smooth muscle?

A

Capillaries

66
Q

What is the tunica media?

A

The smooth muscle layer of the vascular system

67
Q

What is the difference in the set up of myosin heads in smooth muscle compared to skeletal muscle?
What does this allow?

A
  • The myosin heads are aligned on one actin molecule without a gap (M line).
  • This allows for much greater shortening of the muscle which can produce a strong contraction
68
Q

What is ACh effect of mACh-R in blood vessels and in the small intestine?

A
  • Blood vessels: smooth muscle relaxation
  • Intestine: smooth muscle contraction
69
Q

What is the difference between activation of actin in smooth muscle and skeletal muscle?
Be able to describe the pathway.

A

In skeletal muscle the active sites on actin are hidden by the tropomyosin complex and are revealed to bind with myosin when ca++ binds to Troponin C.
In smooth muscle the active sites are always visible and require phosphorylation of the regulatory light chain in order to cause muscle contraction.

70
Q

How is MLCK activated?

A

It is activated by the Ca++-calmodulin complex

71
Q

Where does Ca+ come from to activate calmodulin?

A

SR and L-type, leak, and VG- Ca++ channels

72
Q

How is contraction ended in smooth muscle?

A
  • Calcium removed from sarcoplasm by SERCA, PMCA (plasma membrane calcium ATPase), and NCX
  • Phosphate group removed from MLC by myosin phosphatase
  • Phosphate group eventually will fall off on their own
73
Q

Describe how nitrates affects vascular smooth muscle cells?

A
  • Nitrates increase the release of NO
  • NO increases the activity of guanylyl cyclase
  • This increases cGMP
  • cGMP increases PKG which adds phosphate groups to MLCK and Ca+ entry channels to prevent contraction
74
Q

Describe how NO is produced in the endothelium and its affect of vascular smooth muscle cells?

A
  • NT like ACh and bradykinin bind to mACh-R on endothelium
  • Causes release of Ca from SR that binds to calmodulin
  • Ca-calmodulin increases the activity of eNOS
  • eNOS converts L-arginine to NO
75
Q

What does phosphodiesterase do?
What would inhibition of phosphodiasterase cause?
What drug does this?
What disease is this used for?

A
  • Phosphodiesterase normally breaks down cGMP to GMP
  • Increase in the life of cGMP which increases PKG leading to VSMC relaxation
  • Sildenafil
  • Pulmonary hypertension
76
Q

Describe activation of alpha1 receptors in VSMC?
What can activate this pathway?

A

NE and 5-HT

77
Q

What is the only neurotransmitter that can constrict brain blood vessels?
Drugs that act on this pathway and what they are treating?

A
  • 5-HT
  • SSRI can reduce headaches in some cases
78
Q

Do all smooth muscles require an AP to be activated?

A

No, they can be activated just by calcium entry and any other compound that can activate that system as well as generate their own AP (pacemaker activity)

79
Q

What is this graph showing? Where is it found?

A
  • Pacemaker activity of smooth muscle action potentials
  • Happens in the intestine (muscle cramps; come in waves)
80
Q

How does calcium get released from the SR in the heart?

A

There must be entry of Ca through the cell wall via L-type calcium channels and T-type calcium channels (faster to open and close)
Called “trigger” calcium

81
Q

How much of calcium during cardiac contraction is from the SR and ECF?

A

80% from the SR
20% from the ECF

82
Q

Where is a large source of Ca+ that is involved in “trigger” calcium?

A

T-tubules

83
Q

How is Ca++ removed from the cardiac smooth muscle?

A

Primarily via the NCX, then the Ca ATPase

84
Q

What is calsequestrin and its role?

A
  • A protien in the SR of all smooth muscle
  • Sequesters Ca++ for storage
  • Helps the SERCA pump function by removing Ca++ from the SR solution
85
Q

What is phospholamban?
What would happen if it was inhibited?

A
  • Inhibitor of SERCA pump only in cardiac muscle
    -Allows Ca++ to stay in sarcoplasm longer to provide for longer/stronger contractions
  • Increase activity of SERCA causing shorter length of contraction allowing the cell the reset faster and increasing HR
86
Q

Describe cholinergic and adrenergic activation in the heart?

A
  • Beta increases Adenylyl cyclase which increases cAMP - increases PKA - increases contraction and HR
  • mACh-R inhibits Adenylyl cyclase - decreases cAMP - and decreases PKA (this is different than mACh at the nodes that are tied to potassium channels)

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