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Bio 273 > Unit 3: Muscles > Flashcards

Unit 3: Muscles Flashcards

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1
Q

What is myosin

A

A motor protein that consists of two coiled protein molecules (chains) that have two important parts: a head and a tail

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2
Q

What are the two regions of myosin joined by (heads and tails)

A

a flexible hinge

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3
Q

How do myosin arrange themselves (~250 in an arrangement)

A

heads facing outward and tails facing inward

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4
Q

What is actin

A

G-actin subunits that join to form F-actin chains
- two F-actin chains intertwine to form the basis of the filament

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5
Q

What regulatory proteins do the F-actin filaments interact with

A

troponin and tropomyosin

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6
Q

What do troponin and tropomyosin do

A

form the completed filament and regulate muscle contraction

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7
Q

Myosin _________ interact with actin filaments

A

heads

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8
Q

What are the interactions between myosin and actin called

A

crossbridges

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9
Q

What are the 5 areas that combine to create the striations on skeletal muscles (think about location names of various arrangements)

A
  • Z-line (disks)
  • I-band
  • A-band
  • H-zone
  • M-line
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10
Q

What is a Z-line

A

the site of attachment for thin filaments
- 1 sarcomere is made of 2 Z discs and the filament between them

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11
Q

What is the I-band

A

a region containing only thin filaments
- Z disc runs through an I-band (each 1/2 of the I-band is part of a different sarcomere)

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12
Q

What is the A-band

A

region containing thick and thin filaments
- thick and thin filaments overlap at the sides of the A-band
- middle of A-band is only thick filaments

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13
Q

What is the H-zone

A

part of the A band, containing ONLY thick filaments
- central region is lighter than the outer edges

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14
Q

What is the M-line

A

the site of attachment for thick filaments
- M line is the very centre of the sarcomere

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15
Q

What are other proteins (aside from troponin and tropomyosin) important for skeletal muscle function

A

titin and nebulin

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16
Q

What is muscle and what are the 3 types

A

tissue specialized to convert biochemical reactions into mechanical work
- cardiac, smooth, and skeletal

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17
Q

What makes up the majority of muscle cells

A

myofibrils

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18
Q

Muscle cells have lots of ____________

A

mitochondria

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19
Q

Where are nuclei found in muscle cells

A

on the surface, directly below the cytosol

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20
Q

What are the contractile elastic protein types in myofibrils

A

contractile, accessory, and regulatory muscles

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21
Q

Do muscles elongate or shorten when they contract

A

shorten

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22
Q

What was the early theory about muscle contraction

A

that muscles were made of molecules that shorten when activated and stretch at rest
- the molecule was thought to be myosin because it shortens when heated (think of grilling a steak)

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23
Q

Who observed that A band remains constant during muscle contraction

A

Sir Andrew Huxley and Rolf Niedeigerke

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24
Q

The A band is where the _________ is

A

myosin

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25
Q

How was the previous assumption of myosin being the contractile molecule in muscle tissues proven incorrect

A

myosin is found in the A band, and the A band remains constant, therefore it cannot be the contractile component of muscle tissue

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26
Q

What is the now understood reasoning of muscle contraction (and what are the components)

A

review figure 12.5 from course notes, this is important for midterm 2!*

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27
Q

What is the light band in muscle tissue

A

I band

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28
Q

What is the dark band in muscle tissue

A

A band

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29
Q

What is the area containing only thick bands called

A

H-zone

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30
Q

How is the H zone different from the Z disc

A

Z disc is all thin filaments, H zone is all thick filaments

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31
Q

How does sliding filament theory make sense?

A

the ends of thick and thin filaments overlap, allowing for the movement of filaments past one another during muscle contraction (figure 12.5)

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32
Q

What is sliding filament theory

A

the thin filaments (actin) slide along the thick filaments (myosin) towards the M line
- this brings Z discs closer together
- refer to figure 12.5 for a better understanding

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33
Q

How are thin filaments moved by the thick filaments

A

recall: thick filaments are made of myosin, and myosin is a motor protein
- therefore globular heads attach to the thin filaments and walk along them in a pulling motion

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34
Q

How does myosin move?

A

it is a motor protein capable to converting ATP into “walking” energy

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35
Q

What are the steps of filament movement

A
  1. Initially, myosin is tightly bound to actin. ATP binds to the globular head, and myosin releases from actin (this is called the rigor state)
  2. myosin hydrolyzes ATP to ADP (and Pi) which causes the myosin head to swing over and weakly bind to the new actin subunit (1-3 molecules away, TOWARDS the Z disc)
  3. The Pi is released, myosin head rotates on hinge, and swings back, pulling the actin along with it (this is called the power stroke)
  4. ADP is released, and the process returns to step 1

if this is unclear review figure 12.9 in course notes! its important for midterm 2!*

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36
Q

For each myosin head, there are ___ binding sites, one for ______ and one for _____________

A

2 sites
- actin subunit of thin filament site
- ATP site

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37
Q

What is the power stroke in muscle contraction?

A

The Pi (inorganic phosphate) is released, and the myosin head rotates on hinge, swings back, pulling the actin along with it

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38
Q

When is relaxed muscle found in relation to the step-by-step of muscle contraction

A

step 2!

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39
Q

During contraction, do the myosin heads this all at the same time together?

A

no, because then the contraction would never occur (there would be no attachment of actin and myosin without the crossbridges)

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40
Q

What would happen if all myosin cross bridges released at the same time?

A

thin filaments would slip back into their original positions & the contraction would not occur at all

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41
Q

What stops muscle from contracting whenever ATP is available

A

Recall that actin filament is associated with two regulatory proteins: troponin and tropomyosin (not just made up of actin subunits)

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42
Q

How does regulation of contraction work

A

tropomyosin coils around F-actin molecules and can cover or uncover each G-actin molecule in the strand
(when it covers the G-actin, the contraction mechanism is blocked)

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43
Q

What are the two possible positions of tropomyosin

A
  1. “off”: blocking binding site for myosin head
  2. “on”: allows free access to actin and allows binding for myosin head
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44
Q

What position is tropomyosin in at rest

A

“off” position (review figure 12.8)
- blocking ability for actin and myosin to interact

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45
Q

The position of tropomyosin is regulated by ___________

A

troponin

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46
Q

Troponin has 3 subunits, which is the most important one

A

troponin C: it is able to bind to calcium

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47
Q

What happens when calcium binds to troponin C

A

a conformational change; moves tropomyosin away from the actin (turning it into the “on” position)

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48
Q

What happens when calcium levels are HIGH

A

contraction

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49
Q

What happens when calcium levels are LOW

A

relaxation

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50
Q

What is excitation-contraction coupling

A

series of electrical and mechanical events in muscle which leads to muscle contraction

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51
Q

True or False:
Skeletal muscles ONLY contract when there is a signal from the nervous system

A

true!

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52
Q

What branch of the nervous system controls skeletal muscle

A

the somatic nervous system (review figure 11.10)

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53
Q

What is the motor end plate

A

the region of muscle membrane that contains high concentrations of ACh receptors

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54
Q

What type of receptor does ACh bind to on the skeletal muscle

A

nicotinic cholinergic receptors

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55
Q

What are the steps of the signalling to skeletal muscle

A
  1. action potential reaches the axon terminal
  2. calcium transfer
  3. vesicles bind to membrane and ACh neurotransmitters released into synapse at the neuromuscular junction
  4. ACh neurotransmitters bind to nicotinic cholinergic receptors on the neuromuscular junction
  5. signal is translated in the muscle
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56
Q

The post-synaptic membrane is modified into a _____ _____ _____ on skeletal muscle cells receiving signals

A

motor end plate

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57
Q

Explain how Na+/K+ channels act as receptors for skeletal muscle excitation

A

The receptors are Na+/K+channels
- The binding of ACh opens the channels: both Na+& K+move across the membrane
- ACh is removed by acetylcholinesterase
- Na+influx exceeds K+efflux; local depolarization occurs at the synapse (called an End Plate Potential – EPP)

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58
Q

What is end plate potential

A

local depolarization after flow of Na+ and K+ occurs to return the cell back to its original state

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59
Q

What are dihydropuradine receptors (DHP)

A

senses changes in membrane potential
- the DHP receptors change shape as action potential moves down the axon

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60
Q

What happens when signal reaches motor end plate and needs to be translated

A
  • signal binds to receptors on motor end plate
  • signal travels down T-tubule
  • binds to DHPs
  • changes RyR conformation which opens Ca2+ channels on the sarcoplasmic reticulum
  • Ca2+ leaves the sarcoplasmic reticulum
  • Ca2+ binds to troponin (which moves tropomyosin out of the way)
  • myosin completes power stroke
  • actin filaments slide towards M-line
    (review figure 12.10***)
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61
Q

When does relaxation of a contracted muscle occur

A

when Ca2+ moves back into the SR (through Ca2+ ATPase)

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62
Q

When is tropomyosin inactivated and placed back onto the binding site

A

decreasing Ca2+ concentration in cytosol causes Ca2+ and troponin to unbind
- tropomyosin is placed back onto binding site
- filaments are pulled back into their original positions

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63
Q

What does it mean when saying EEPs are always above threshold

A

they are ALWAYS excitory; results in contraction

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64
Q

What moves Ca2+ out of the cytosol

A

Ca2+ -ATPase

65
Q

What is the function of muscles

A

convert biochemical energy into mechanical work (contraction)

66
Q

What moves Na+/K+ into/out of the cell back to their original positions

A

Na+/K+ -ATPase

67
Q

What is the main energy currency of the cell

A

ATP

68
Q

Where is the energy transferred from to gain ATP

A

nutrients (aerobically and anaerobically)

69
Q

What systems produces ATP

A

glycolysis! (can be done with or without oxygen) (produces 2 ATP per mole of glucose used)
- also produces unwanted metabolites in the absence of oxygen; like lactic acid)

oxidative metabolism (requires oxygen)
- provides up to 15x more ATP per mole of glucose used
- does not produce toxic end products

70
Q

Which is more efficient/preferred; glycolysis or oxidative metabolism

A

oxidative metabolism
- produces more ATP and does not produce toxic end products

71
Q

What does oxidative metabolism require in order to happen

A

mitochondria (this is important**)

72
Q

What is phosphocreatine

A

a high-energy phosphate molecule (used for energy in addition to ATP)

73
Q

How is phosphocreatine useful in muscles

A
  • rapid source of energy
  • easily donates inorganic phosphate
  • provides a limited supply of ATP
74
Q

What catalyzes the reaction to produce ATP from phosphocreatine

A

creatine kinase (CK)

75
Q

Do muscles contain small or large amounts of CK

A

large amounts

76
Q

Where do resting muscles store energy

A

phosphocreatine

77
Q

What is phosphocreatine used for

A

buffer [ATP] over VERY short time scales (like seconds)
- consider reviewing figure 12.12

78
Q

What are the two important terms relating to muscle contraction

A

twitch and latent period

79
Q

What does twitch mean

A

single contraction-relaxation cycle (review figure 12.11)

80
Q

What does latent period mean

A

short delay between the action potential (in muscle fibre on motor end plate) and the beginning of muscle tension
- the delay is the time it takes for excitation-contraction to happen
(review figure 12.11)

81
Q

What are the three general types of muscle fibres

A

slow twitch fibres
fast-twitch oxidative-glycolytic fibres (type IIA)
fast-twitch glycolytic fibres (type IIX)

82
Q

What colour are oxidative muscle fibres and why

A

red; due to presence of myoglobin
- myoglobin is an oxygen-carrying haeme protein

83
Q

Oxidative muscle fibres are _________ than glycolytic, have numerous _________________, and are better ______________

A

smaller
have numerous mitochondria
are better vascularized (have more blood vessels)
(review figure 12.14)

84
Q

What does fast/slow mean in relation to muscle fibres

A

rate of myosin ATPase activity
- fast fibres split ATP more quickly and thus can contract faster
- slow fibres are the opposite and take longer

  • this differential results in different isoforms of myosin*
    (review figure 12.14)
85
Q

How does the length of contraction very between fibres

A
  • fast fibres have shorter twitch
  • twitch duration is determined by the rate of removal of Ca2+ from cytosol
  • this sets the speed at which muscles relax
86
Q

What is short twitch useful for

A

used for rapid, small muscle contractions

87
Q

What is long twitch useful for

A

used for long sustained movements

88
Q

What type of muscle has the HIGHEST rate of Ca2+ removal from the cytosol

A

fast twitch (remember: duration of the twitch depends on the ability to remove the Ca2+ from the cytosol)

89
Q

What is the tension exerted in a single twitch influenced by

A
  1. muscle type
    - fast fibres can generate more force
  2. sarcomere length
    - degree of overlap between thick and thin filaments
90
Q

What happens when there is too little overlap of thick and thin filaments

A

few cross bridges and little force can be generated (review 12.15)

91
Q

What happens when there is too much overlap of thick and thin filaments

A

actin filaments interfere with one another and less force is generated (review 12.15)

92
Q

What happens when there is WAY too much overlap of thick and thin filaments

A

thick filaments collide with Z-disc and force rapidly decreases (review 12.15)

93
Q

A muscle twitch does NOT represent the maximum force that the muscle fibre can develop
- how can the force of a muscle fibre be increased

A

by increasing rate of action potentials that stimulates the fibre (summation)

94
Q

What is summation

A

increase in force generated by a muscle
- due to repeated stimulation of a muscle

95
Q

What is tetanus

A

term for state of a muscle when it reaches the maximum force of contraction

96
Q

What is incomplete (unfused) tetanus

A

slow stimulation rate; fibre relaxes slightly between stimuli
(on a graph - creates a ripple effect going up the graph)

97
Q

What is complete (fused) tetanus

A

fast stimulation; the fibre does not have time to relax
(on a graph - a smooth line going up the graph because it lacks relaxation periods like incomplete tetanus would have)

98
Q

Which of the following are energy sources for skeletal muscle contraction
a. oxidative metabolsim
b. glycolysis
c.
d. a & b
e. all of the above

*In class review question

A

all of the above

99
Q

What is the motor unit

A

the basic unit of contraction in an intact skeletal muscle

(review figure 12.18 to understand motor unit function)

100
Q

Does a muscle have one singular, or many motor units

A

many motor units

101
Q

What are the two components of a motor unit

A
  1. a group of muscle fibres (the # of fibres varies)
  2. one singular somatic neuron that controls them

(review figure on page 58 of course notes, adapted from figure 12.17 from the textbook)

102
Q

What are the two ways that contraction of muscles can vary

A
  1. changing the type of motor neuron activated
  2. changing the number of motor neurons that are active
103
Q

All muscle fibres in a motor unit are of _____ _____

A

one type

104
Q

Each motor unit contracts in an _____-___-____ fashion

A

all-or-none

105
Q

What is recruitment

A

increasing the force of attraction by using more motor units
- different fibres are recruited at different times
- slow oxidative fibres have a low threshold for stimulation
- fast glycolytic fibres have a high threshold for stimulation

106
Q

Which will have more muscle fibres per motor unit: those involved in fine movement or those involved in coarse movements?

*In class knowledge testing question

A

coarse movements
- large numbers of muscle fibres control the movement of larger muscles

107
Q

What is the role of the skeletal muscle in the body

A

move the body

108
Q

What are the two main types of muscle contraction

A

isotonic and isometric

109
Q

What is isotonic contraction

A

creates force/tension and moves a load
- the load is usually constant and the muscle length changes
(think about picking up a weight: the load stays constant, but to pick up the weight muscle contraction is required, and once it is set down, the muscle is relaxed)

110
Q

What is isometric contraction

A

creates force WITHOUT movement
- muscle length is constant
- the load is greater than the force that can be applied
(think about trying to pick up something too heavy: the muscle cannot reach the tension level required to lift it, therefore the muscle length remains the same and the load is not moved)

111
Q

How can an isometric contraction create force if there is no change in muscle length

A

even though the sarcomeres shorten, muscle length stays constant because these elastic elements stretch to take up force until fully stretched
(review figure 12.19*)

  • in isotonic contraction, the sarcomeres shorten but since the tension reaches the point of movement, the elastic elements stretch and allow the sarcomeres to overlap to a greater extent, contracting the muscle
112
Q

Where is smooth muscle found in the body?

A
  • found in the walls of follow organs and tubes: not attached to the skeleton
  • fewer in terms of % body weight, but much more important
113
Q

What are some examples of important smooth muscle tissues

A
  • bladder sphincter
  • intestines
  • walls of blood vessels
114
Q

What are the two types of arrangements of smooth muscle tissues

A
  1. single unit
    - cells coupled by gap junctions
    - not necessary to electrically stimulate each individual fibre
    - found on walls of internal organs
    eg. blood vessels
  2. multi-unit
    - no gap junctions
    - each individual fibre is separately innervated
    eg. iris of the eye, parts of reproductive organs, etc.

(review figure 12.23)

115
Q

What are the bulges on the post-ganglionic autonomic neurons called

A

varicosities
(review figure 12.23*)

116
Q

What are varicosities

A

bulges on the autonomic neurons that contain neurotransmitters

117
Q

What are the 3 listed differences between smooth and skeletal muscle on a WHOLE MUSCLE level

A
  1. contraction of smooth muscle changes shape, not just the length
  2. smooth muscle develops force slowly
  3. smooth muscle can maintain contraction longer without fatiguing; important because some are contracted for most of the time
    eg. internal bladder sphincter
118
Q

What are the 6 listed differences between smooth and skeletal muscle on a CELLULAR level

A
  1. fibres are much smaller in smooth muscle (about the same diameter as a single myofibril in a skeletal muscle fibre)
  2. actin and myosin are NOT arranged in sarcomeres
  3. actin & myosin are arranged in bundles diagonally around the periphery of the cell
  4. actin anchored at cell membrane structures called dense bodies (not attached to the Z line like skeletal muscle)
  5. no T-tubules in sarcolemma, and not much sarcoplasmic reticulum (smooth muscle cells have special vesicles called caveolae that are invaginations of the sarcolemma that are specialized for cell signalling)
  6. the force of contraction is related to the amount of Ca2+ released
119
Q

What is the role of caveolae

A

holds onto calcium

120
Q

What is the effect of not having T-tubules

*In class knowledge testing question

A

no direct coupling of the action potential to release Ca2+ from the SR through DHP receptor-ryanodine receptor coupling (as in skeletal muscle)

  • instead, Ca2+ entering through the cell membrane causes Ca2+ release from SR
121
Q

What are the 5 listed differences between smooth and skeletal muscle on a MOLECULAR level

A
  1. less myosin per actin unit in smooth muscle
  2. actin and myosin filaments are longer and overlap more in smooth muscle
  3. myosin ATPase activity is much slower in smooth muscle
  4. myosin heads are located along the thick filaments, not just at the ends
  5. no troponin in smooth muscle
    (review figure 12.25)
122
Q

How do the molecular properties of myosin contribute to the characteristics of the smooth muscle as a whole?

*In class knowledge testing question

A

contract for longer periods of time (because of longer actin and myosin filaments) at a slower rate compared to skeletal muscle

123
Q

What would happen if the bladder was lined with muscles organized into sarcomeres?

*In class knowledge testing question

A

as the bladder gets larger, actin and myosin filaments would grow further away from one another, and would not be able to contract (would not be able to excrete)

124
Q

What is the major difference in the role of Ca2+ in smooth muscle contraction vs cardiac muscle contraction

A

the role of phosphorylation

125
Q

Describe the first step in the pathway of how Ca2+ plays a role in smooth muscle contraction

A

Signal to initiate contraction is increase in cytosolic Ca2+

Ca2+enters the extracellular fluid(ECF) through:
- Voltage-gated channels; open when cell depolarizes
- Stretch activated channels; open when membrane stretched
- Chemically gated channels; open in response to hormones

Ca2+entry from the ECF results in the release of SR Ca2+and Ca2+from caveolae

126
Q

Describe the second step in the pathway of how Ca2+ plays a role in smooth muscle contraction

A

Ca2+ binds to calmodulin in the cytosol
(review figure 12.26)

127
Q

Describe the third step in the pathway of how Ca2+ plays a role in smooth muscle contraction

A

Ca2+/CaM activates the enzyme myosin light chain kinase (MLCK)
(review figure 12.26)

128
Q

Describe the fourth step in the pathway of how Ca2+ plays a role in smooth muscle contraction

A

MLCK activates myosin by phosphorylating the light chain of the myosin molecule in the head using energy and Pi from ATP: this ATP is used to activate the myosin through phosphorylation (not for cross-bridge cycling)
- When myosin is not phosphorylated, ATPase activity is blocked
- When myosin is phosphorylated, ATPase is active
(review figure 12.26)

129
Q

Describe the fifth step in the pathway of how Ca2+ plays a role in smooth muscle contraction

A

The phosphorylated myosin (active) can now interact with actin and go through cross-bridge cycling (see pg 51 in notes) and allow contraction to occur in the smooth muscle cell; remember, additional ATP is needed for each cross-bridge cycle – MLCK uses the Pi from ATP to activate myosin (turn it “on”), but ADDITIONAL ATP is needed to go through cross-bridge cycling for contraction to occur.
(review figures 12.26 and 12.9)

130
Q

Draw the 5-step process in which Ca2+ plays a role in smooth muscle contraction

A

(review figure 12.26 and compare)

131
Q

In smooth muscle the ___________ is regulated by _________________ of myosin
In skeletal muscle the ________ is regulated by ___________/_____________ interaction with actin

*this is the KEY POINT in how contraction is regulated between the two types and how to differentiate; know this!

A

smooth muscle: myosin regulated by phosphorylation of myosin
skeletal muscle: actin regulated by troponin/tropomyosin interaction with actin

132
Q

What would happen to the contraction of smooth muscles if placed in a Ca2+ free saline solution

*In class knowledge testing question

A

there would be no contraction at all

133
Q

Describe the first step in how smooth muscles relax

A

Ca2+is removed from the cytosol
- Pumped back into the SR using ATP to the extra-cellular environment through: Ca2+-Na anti-port, Ca2+ -ATPase

134
Q

Describe the second step in how smooth muscles relax

A

A decrease in Ca2+levels in the cytosol causes Ca2+ to unbind from calmodulin
(review figure 12.26)

135
Q

Describe the third step in how smooth muscles relax

A

Myosin light chains are dephosphorylated by myosin light chain phosphatase (MLCP)
(review figure 12.26)

136
Q

Does the dephosphorylation of myosin light chains automatically relax the muscle?

A

no!
- this allows smooth muscle to enter the latch phase (not well understood)
- tension is maintained, but with minimal ATP consumption

137
Q

Draw the 3 step relaxation process of smooth muscle

A

review figure 12.26 and compare

138
Q

What is the latch state

A

dephosphorylation of myosin does not automatically relax the muscle
- this allows smooth muscle to enter the latch state
- the tension is maintained (myosin remains bound to actin) but with minimal ATP consumption

139
Q

What is cardiac muscle, what are its cells called, and what are its characteristics

A

myocardial cells (specialized to the heart)
- shares features with both skeletal and smooth muscle
- most myocardial cells are striated muscle (contractile fibres organized into sarcomeres like skeletal muscle)

140
Q

How does cardiac muscle differ from skeletal

A
  • cardiac muscle cells are much smaller with a single nucleus
  • about 1/3 of the cell volume is occupied by mitochondria (think about the need for oxygen supply to the cardiac cells)
  • T-tubules are much larger and branched
  • SR is smaller
  • adjacent cells joined by intercalated discs with desmosomes
141
Q

Which of the following directly phosphorylates myosin in smooth muscle
a. MLCK
b. MLCP
c. Ca2+ - CaM
d. troponin
e. none of the above

*In class review question

A

a. MLCK

142
Q

What percentage of cardiac muscle is not involved in contraction

A

about 1% - called autorhythmic/pacemaker cells
- these muscles are used for electrical excitation of the heart (known as the electrical conduction system)

143
Q

What is the electrical conduction system

A

the autorhythmic/pacemaker cells that conduct electrical excitation in the heart
- they initiate heart beat and allow the electrical excitation to spread rapidly throughout the heart

144
Q

What connects autorhythmic/pacemaker cells to other cardiac cells

A

gap junctions

145
Q

Contraction of cardiac muscle is similar to skeletal muscle, except for what three exceptions

A
  1. Ca2+enters through Ca2+channels on the cell membrane as well as the SR
    - First: calcium enters through external Ca2+channels
    - Next: calcium-induced calcium release; release of stored Ca2+from SR
    - SR calcium provides about 90% of that needed for contraction
  2. Cardiac cells have a Na+/Ca2+ antiport (in addition to Ca2+-ATPase)
    - Removes Ca2+from cytosol and pumps it into the extracellular space
  3. Exhibit GRADED, not “all-or-none” contraction; the force generated is proportional to the number of active crossbridges
    - Number of active crossbridges is proportional to cytosolic [Ca2+]
    - Therefore, the force generated is proportional to cytosolic [Ca2+]

(review figure 14.10)

146
Q

What 2 factors influence cardiac muscle contraction force

A
  1. changes in [Ca2+] in the cytosol
  2. sarcomere length
147
Q

How do changes occur in [Ca2+] in the cytosol to affect force of cardiac muscle contraction

A
  • regulated by epinephrine and norepinephrine; bind to B1 adrenergic receptors
  • this binding activates cAMP second messenger signalling pathway, which leads to both phosphorylation of Ca2+ channels (which increases probability of channels opening and therefore increases probability of Ca2+ release) and phosphorylation of phospholamban (leads to increased SR Ca2+-ATPase activity, increasing Ca2+ in the SR)
  • overall results in a more forceful contraction AND a shorter duration of contraction*
148
Q

How do changes occur in sarcomere length to affect force of cardiac muscle contraction

A
  • tension generated is proportional to the length of the muscle fibre
  • due to the overlap between actin and myosin; there is an optimal amount of overlap
    *note: stretching of the myocardial muscle cell may also allow for more Ca2+ to enter through the cell membrane via the channels. This contributes to a stronger, more forceful next contraction
149
Q

Is cardiac muscle an excitable tissue? What does this mean for cardiac muscle?

A

yes, it can generate action potentials

150
Q

What is the major sequence of events for action potentials of cardiac muscles

A

phase 4: resting membrane potential
phase 0: depolarization
phase 1: initial repolarization
phase 2: the plateau
phase 3: rapid depolarization

(review figure 14.10)

151
Q

What happens in phase 4 of cardiac muscle excitation

A

sitting at resting membrane potential

152
Q

What happens in phase 0 of cardiac muscle excitation

A

depolarization: action potential opens the Na+ channels, causing rapid Na+ permeability (close again)

153
Q

What happens in phase 1 of cardiac muscle excitation

A

initial repolarization: opening of K+ channels

154
Q

What happens in phase 2 of cardiac muscle excitation

A

the plateau: initial depolarization triggered voltage-gated Ca2+channels to slowly open, causing an increase in Ca2+permeability and the fast K+channels close

155
Q

What happens in phase 3 of cardiac muscle excitation

A

the Ca2+channels close and the slow voltage-gated K+channels open (initial depolarization was the trigger), and the resting stage ion permeability is restored (phase 4)

156
Q

What causes the sustained depolarization in cardiac muscle excitation

A

due to the slow opening of Ca2+ channels

157
Q

What is the result of sustained depolarization in cardiac muscle excitation

A

typical action potential in neuron or skeletal muscle cells = 1-5 msec
typical action potential in cardiac muscle = >200 msec

158
Q

Why don’t cardiac muscle cells undergo summation and tetanus

*in class knowledge testing question

A

because of the longer refractory period: means that the cell has finished contracting before the next action potential

Bio 273 (8 decks)

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