CH 8 Muscle Physiology Flashcards

1
Q

Where is smooth muscle found and what is its primary function?

A

it is found in the walls of hollow organs and tubes. Through the contraction of smooth muscle blood movement is controlled.

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2
Q

Where is cardiac muscle found and what is its primary purpose?

A

Found only in the walls of the heart, where the contraction pumps life sustaining blood throughout the body

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3
Q

What does the controlled contraction of muscles allow?

A

1) purposeful movement of the body (voluntary actions)
2) manipulation of external objects (picking up a chair, driving)
3) propulsion of contents through hollow organs (blood circulation)
4) emptying the contents of certain organs into the external environment (giving birth)

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4
Q

Describe a skeletal muscle cell, muscle fiber.

A

– Multi nucleated
– Large, elongated, and cylindrically shaped
– Fibers usually extend entire length of muscle

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5
Q

What is a myofibril?

A
  • A cylindrical intracellular structure extending the entire length of the muscle fiber, - specialized contractile element
  • Made of up thick/thin filaments
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6
Q

Thick filaments are composed of?

A

Myosin protein

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7
Q

Thin Filaments are composed of?

A

Actin protein

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8
Q

What is a sarcomere

A

– Functional unit of skeletal muscle = it is the smallest component of a muscle fiber that can contract
– Found between two Z lines (connects thin filaments of two adjoining sarcomeres)

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9
Q

How does a muscle increase in length?

A

By adding new sarcomeres on the ends of the myofibrils

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10
Q

Describe the shape of myosin

A

Protein molecule consisting of two identical subunits shaped somewhat like a golf club
– Tail ends are intertwined around each other (oriented toward the center of the fiber)
– Globular heads project out at one end
– Heads form cross bridges between thick and thin filaments

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11
Q

In myosin, there are 2 important sites on the head. What are they and what makes them important?

A

important sites critical to contractile process
– An actin-­‐binding site
– A myosin ATPase (ATP-­‐splitting) site

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12
Q

Describe the shape of Actin.

A

Spherical

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13
Q

What are the two proteins that make up actin?

A

Tropomyosin, troponin

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14
Q

Each actin molecule has special binding site for atachment. What does it attach to and what does it cause?

A

It attaches to myosin and this binding results in the contraction of the muscle fiber

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15
Q

Which proteins are regulatory proteins and which are considered contractile proteins?

A
Regulatory = troponin, tropomyosin
Contractile = actin, myosin
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16
Q

Which proteins are more abundant and highly organized in muscle cells?

A

Actin and myosin

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17
Q

What is the function of tropomyosin

A

It lays end to end alongside groove of an actin spiral which covers actin sites, blocking interaction that leads to muscle contraction

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18
Q

What is troponin made up of?

A

Made of three polypeptide units
• One binds to tropomyosin
• One binds to actin
• One can bind with Ca2+

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19
Q

What is the function of troponin when it is NOT bound with Ca2+

A

troponin stabilizes tropomyosin in blocking position over actin’s cross-bridge binding sites

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20
Q

What happens when Ca2+ binds to troponin?

A
  • tropomyosin moves away from blocking position
  • this allows actin and myosin to bind
  • interact at cross-bridges
  • contraction occurs
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21
Q

What happens during the sliding filament mechanism? (which is why cross-bridge interaction between actin and myosin occur)

A
  • Increase in Ca2+ starts filament sliding
  • Decrease in Ca2+ turns off sliding process
  • Thin filaments on each side of sarcomere slide inward over stationary thick filaments toward center of A band during contraction
  • As thin filaments slide inward, they pull Z lines closer together
  • Sarcomere shortens
  • All sarcomeres throughout muscle fiber’s length shorten simultaneously
  • Contraction is accomplished by thin filaments from opposite sides of each sarcomere sliding closer together between thick filaments
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22
Q

What is a twitch? What is it produced by?

A
  • a brief, weak contraction
  • It is produced from a single action potential
  • Too short and too weak to be useful
  • normally does not take place in the body
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22
Q

Describe the changes in the sarcomere during shortening

A
  1. Binding = Myosin cross-bridge binds to actin molecule
  2. Power stroke = Cross bridge bends, pulling thin myofilament inward
  3. Detachment = cross bridge detaches at the end of the power stroke and returns to original conformation
  4. Binding = cross bridge binds to more distal actin molecule; cycle repeats
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23
Q

What are two primary factors which can be adjusted to accomplish gradation of whole-muscle tension?

A
  • NUMBER of muscle fibers contracting within a muscle

- TENSION developed by each contracting fiber

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24
Q

What is a motor unit?

A

One motor neuron and the muscle fibers that it innervates

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25
Q

Then number of muscle fibers per motor neuron and number of motor neuron units per muscle vary widely. What type of muscles have more? Which have less?

A
  • Muscles that produce precise, delicate movements contain fewer fibers per motor unit.
  • Muscles performing powerful coarsely controlled movements have larger number of fibers per motor unit
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26
Q

What helps delay or prevent fatigue?

A

Asynchronous recruitment of motor units

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27
Q

What factors influence the extent to which tension can be developed?

A
  • Frequency of stimulation
  • Length of fiber at onset of contraction
  • Extent of fatigue
  • Thickness of fiber
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28
Q

What caused twitch summation?

A

It results from sustained elevation of cytosolic calcium

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29
Q

What is tetanus?

A
  • It occurs if muscle fiber is stimulated so rapidly that it does not have a chance to relax between stimuli
  • contraction is usually 3-4 times stronger than a twitch
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30
Q

Describe summation and tetanus

A
  • If a muscle fiber is restimulated after it has completely relaxed the second twitch is the same magnitude as the first twitch
  • if a muscle fiber is restimulated before is has completely relaxed, the second twitch is added on to the first twitch, resulting in summation
  • if a muscle fiber is stimulated so rapidly that it does not have an opportunity to relax at all between stimuli, a maximal sustained contraction known as tetanus occurs
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31
Q

What are the three major types of skeletal muscle fibers?

A
  1. Slow oxidative (type 1)
  2. Fast oxidative (type 2a)
  3. Fast glycoltic (type 2x)
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32
Q

Briefly describe the Cross-bridge cycle

A
  • Activated cross bridge bends toward center of thick filament, “rowing” in thin filament to which it is attached
  • Ca2+ is released into the sarcoplasm = the cytoplasm of the muscle cell
  • Myosin heads bind to actin
  • Myosin heads swivel toward the center of the sarcomere (power stroke)
  • ATP binds to myosin head and detached it from actin
  • Hydrolysis of ATP transfers energy to myosin head and reorients it
  • Contraction continues if ATP is available and Ca2+ level in sarcoplasm is high
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33
Q

What are Transverse Tubules?

A
  • They run perpendicularly from the surface of the muscle cell MEMBRANE into the central portions of the muscle FIBER
  • The action potential on the surface membrane spreads down into the T-tubule (this occurs because the membrane is contiguous with with surface membrane)
  • The spread of these action potentials down a T-tubule triggers the release of Ca2+ FROM the sarcoplasmic reticulum INTO the cytoplasm
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34
Q

What is the Sarcoplasmic Reticulum?

A
  • It is modified endoplasmic reticulum
  • It consists of a fine network of interconnected compartments that surround each myofibril
  • It is not continuous, but ENCIRCLES myofibril throughout its length
  • Segments are wrapped around each A and I band
    • the ends of these segments expand to form saclike regions - lateral sacs (terminal cisternae)
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35
Q

What is the relationship between the T-tubule and the Sarcoplasmic reticulum?

A
  • The T-tubule has voltage-gated receptors (dihydropyridine receptor)
  • The sarcoplasmic reticulum contains foot proteins that serve as Ca2+ release channels (ryanodine receptors)
    = meaning = The activation of dihydropyridine receptors by local APs in T tubule triggers opening of Ca2+ release channels in the sarcoplasmic reticulum
36
Q

What is the First step in Excitation-Contraction coupling?

A
  1. An action potential arriving at a terminal button of the neuromuscular junction stimulates release of acetylcholine
    • acetylcholine then diffuses across the cleft and triggers an AP in the muscle fiber
37
Q

What is the second step in Excitation- contraction coupling?

A

The AP moves across the surface membrane and into the muscle fiber’s interior through the T tubules. An AP in the T tubule triggers release of Ca2+ FROM the sarcoplasmic reticulum INTO the cytosol.

38
Q

What is the third step in Excitation- contraction coupling?

A

The Ca2+ binds to troponin on thin filaments

39
Q

What is the 4th step of Excitation-Contraction Coupling?

A

The Ca2+ binding to troponin causes tropomyosin to change shape, physically moving it away from its blocking position.
- This uncovers the binding sites on actin for the myosin Cross-bridges

40
Q

What is the 5th step in the Excitation-Contraction Coupling?

A

Myosin cross-bridges attach to actin on the exposed binding sites

41
Q

What is step 6 for the Excitation-Contraction Coupling?

A

The binding triggers the cross bridge to bend, pulling the thin filament over the thick filament toward the center of the sarcomere.
- This power stroke is powered by ATP

42
Q

What is the seventh step in Excitation-contraction Coupling?

A

After the power stroke, the cross bridge detaches from actin
- if Ca2+ is still present the cycle returns to step 5 = myosin cross bridges attach to actin at the exposed binding sites

43
Q

What is the eighth step of the excitation-contraction coupling?

A
  • When APs stop, Ca2+ is taken up b the sarcoplasmic reticulum.
  • With no Ca2+ on troponin, tropomyosin moves back to its original position, blocking myosin cross bridge binding sites on actin
  • Contraction stops and the thin filaments passively slide back to their original relaxed positions
44
Q

What are the 4 steps that are involved to allow relaxation?

A
  • Reuptake of Ca2+ into the sarcoplasmic reticulum (through active transport with Ca2+ pump)
  • Aceytlcholinesterase breaks down ACh at neuromuscular junction
  • Muscle fiber AP stops
  • When local AP is no longer present, Ca2+ moves back into SR
45
Q

What is the Length-Tension Relationship?

A

Less that optimal length

  • bunching of thick filaments
  • thin filament overlap
  • Ca2+ influx reduced

Too stretched
- Less than optimal overlap

46
Q

Where is Smooth muscle found?

A

In the walls of hollow organs and tubes

47
Q

Describe the looks and shape of smooth muscle

A
  • Not striated
    • Filaments do not form myofibrils
    • Not arranged in sarcomere pattern found in skeletal muscle
  • Spindle shaped cells with a SINGLE nucleus
  • Cells arranged in sheets within the muscle
  • Have dense bodies containing same protein found in Z lines
48
Q

What are the three types of filaments of Smooth muscle?

A
  • Thick myosin filaments = longer than those in skeletal muscle
  • Thin actin filaments = contain tropomyosin but LACK troponin
  • Filaments of intermediate size
    • do not directly participate in contraction
    • form part of cytoskeletal framework that supports cell shape
49
Q

Compare the role of Calcium in bringing about contraction in smooth muscle and skeletal muscle

A

smooth muscle = muscle excitation –> rise in cytosolic Ca2+ (from extracellular fluid) –> series of biochemical events –> Phosporylation of myosin cross bridges in thick filament –> binding of actin and myosin at cross bridges –> contraction

skeletal muscle = muscle excitation –> rise in cytosolic ca2+ (from intracellular SR) –> Physical repositioning of troponin and tropomyosin –> uncovering of actin and myosin at cross bridges –> contraction

50
Q

What is different about a smooth muscle twitch as opposed to skeletal?

A

It is slower

  • Cross bridges slower
  • Ca2+ removal is slower
51
Q

what are the two major types of smooth muscle?

A
  • Multiunit smooth muscle

- single-unit smooth muscle

52
Q

Where are multiunit smooth muscle cells found?

A
  • walls of large blood vessels
  • small airways to lungs
  • muscle of eye that adjusts lens near or far vision
  • In iris of eye
  • At base of hair follicles
53
Q

Describe how the multiunit smooth muscle cells work

A
  • each cell receives input
  • There are very few gap junctions between cells
  • Each cell may contract independently of its neighbor Neurogenic (ANS)
  • Consists of discrete units that function independently of one another
  • units must be separately stimulated by nerves to contract
54
Q

How do single unit smooth cells function?

A
  • motor neuronal input to a few cells
  • MANY gap junctions for communication
  • cells contract as a GROUP
  • There is Functional syncytium = self excitable
    • Does NOT require nervous stimulation for contraction
  • AKA visceral smooth muscle
  • Fibers become excited and contract as a SINGLE UNIT
    • cells electrically linked by gap junctions
    • also be described as a functional syncytium
  • Contraction is slow and energy efficient
55
Q

What are single unit muscle cells suited for?

A

Forming walls of distensible, hollow organs (digestive, reproductive and urinary tracts)

56
Q

Is Cardiac muscle striated or unstriated? What are the cells connected by? Is this muscle voluntary or involuntary?

A
Cardiac muscle is
- striated
- connected by gap junctions
	intercalated disks
- innervated by the ANS
- Involuntary
57
Q

What is going on in the the skeletal muscle fibers when they are relaxed?

A
  • No excitation
  • No cross-bridge binding because cross-bridge binding site on actin is physically covered by tropin-tropyomyosin complex
  • muscle fiber is relaxed
58
Q

What is going on in the skeletal muscle when it is excited?

A
  • Muscle fiber is excited and Ca2+ is released
  • Released Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross-bridge binding site
  • Cross bridge binding occurs
  • Binding of actin and myosin cross bridge triggers power stroke that pulls thin filament inward during contraction
59
Q

What changes in banding pattern occur during the shortening/contraction of skeletal muscle?

A
  • Each sarcomere shortens as the thin filaments slide closer together between the thick filaments
  • The sliding of the thin filaments inward causes the Z lines to be pulled closer together
  • The width of the A bands do not change but the I and H zones become shorter
60
Q

What is the process of a single cross bridge cycle?

A
  1. Binding: Myosin cross bridge binds to actin molecule
  2. Power stroke: cross bridge bends, pulling thin myofilament inward.
  3. Detachment: Cross bridge detaches at end of power stroke and returns to original conformation
  4. Binding: Cross bridge binds to more distal actin molecule; cycle repeats
61
Q

All cross bridges stroke toward the center of the sarcomere. Why?

A

So that all six of the surrounding thin filaments on each end of the sarcomere are pulled inward simultaneously

62
Q

What keeps the thin filaments from slipping back to their resting positions in between power stroke?

A

Asynchronous cycle = part of the cross bridges are attached to the thin filaments and are stroking, while others are returning to their original conformation in preparation for minding with another actin molecule

63
Q

What stimulates skeletal muscles to contract?

A

The release of acetylcholine at neuromuscular junctions between motor neuron terminal buttons and muscle fibers

64
Q

What does the binding of acetylcholine with the motor end plate of a muscle fiber bring about?

A

Permeability changes in t he muscle fiber which results in an AP that is conducted over the entire surface of the muscle cell membrane

65
Q

What two membranous structures within the muscle fiber play an important role in linking the excitation-contraction coupling?

A

Transverse tubules

sarcoplasmic reticulum

66
Q

The presence of a local AP in the T tubules leads to….?

A

permeability changes in the sarcoplasmic reticulum

67
Q

Where is insulin produced?

A

In the Pancreas

68
Q

What type of hormone is insulin

A

It is an anabolic hormone

69
Q

Insulin promotes the cellular uptake of what?

A

-Glucose
-Fatty acids
-AA
And enhances their conversion into glycogen, triglycerides and proeins

70
Q

When is prime secretion time for insulin?

A

It is increased during the absorptive state (post meal)

The primary stimulus for secretion being ithe increase in blood glucose concentration

71
Q

Describe the process of glucose stimulation that leads to insulin secretion

A
  1. Glucose enters beta cell by facilitated diffusion via the GLUT-2 receptor
  2. Glucose is phosphorylated to gluc-6-phos
  3. Oxidation of gluc-6-phos generates ATP
  4. ATP acts on ATP-sensitive K+ channel, closing it
  5. Reduced exit of K+ depolarizes membrane
  6. Depolarization opens voltage-gated Ca2+ channels
  7. Ca2+ enters the beta cell
  8. Ca2+ triggers exocytosis of insulin vesicles
  9. Insulin is secreted
72
Q

What is the most common of all endocrine disorders?

A

Diabetes Mellitus

73
Q

What is the most prominent feature of diabetes?

A

Elevated blood glucose levels

74
Q

What is the difference between Diabetes I and II?

A

Type I = characterized by lack of insulin secretion

Type II = characterized by normal or even increased secretion but reduced sensitivity of insulin’s target cells

75
Q

Where is glucogen produced?

A

in the pancreas

76
Q

In response to what, is glucagon secreted?

A

In response to a decrease in blood glucose on pancreatic alpha cells
It generally opposes actions of insulin

77
Q

What does glucagon do when secreted?

A

mobilizes energy-rich molecules from storage sites during postaborptive state

78
Q

What essential activities does Ca2+ play a vital role?

A
  • Excitation-contraction coupling in cardiac and smooth muscle
  • Stimulus-secretion coupling
  • Maintenance of tight junctions between cells
  • Clotting of blood
  • must be regulated to prevent changes in neuromuscular excitability
79
Q

What is hypercalcemia?

A

Reduces the excitability of calcium

80
Q

What is hypocalcemia? What can it cause?

A
  • brings about over-excitability of nerves and muscles
  • Severe over-excitability can cause fatal spastic contractions of respiratory muscles which can lead to asphyxiation and death
81
Q

What are the major functions of the skeleton?

A
  • support
  • protection of vital internal organs
  • assistance in body movement by giving attachment to muscles and providing leverage
  • Manufacture of blood cells (bone marrow)
  • sotorage depot for Ca2+ and PO4 3-, which can be exchanged with the plasma to maintain plasma concentrations of these electrolytes
82
Q

What three hormones regulate plasma concentration of Ca2+?

A
  • Parathyroid hormone (PTH)
  • Calcitonin
  • Vitamin D
83
Q

Which hormone is the primary regulator of Ca2+? How does it regulate it?

A

the parathyroid hormone is the primary regulator

it does so by raising free plasma calcium levels by its effect on bone, kidneys, and intestines

84
Q

Why it is essential? what other hormone does it affect?

A

it is essential for life because it prevents fatal consequences of hypocalcemia
it also facilitates the activation of vitamin D

85
Q

Where is calcitonin produced?

A

by the C cells of the thyroid gland

86
Q

What causes secretion of calcitonin?

A

It is secreted in response to increase in plasma calcium concentration in a negative-feedback fashion

87
Q

What is the job of calcitonin?

A

To lower plasma calcium levels by inhibiting activity of bone osteoclasts
It is unimportant except during hypercalcemia