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BIOL 273 Physiology > Unit 3 - Muscle > Flashcards

Unit 3 - Muscle Flashcards

1
Q

what is a muscle

A

tissue specialized to convert biochemical reactions into mechanical work

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2
Q

2 main functions of muscle

A

motion
force

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3
Q

muscles can only ____ and they cannot _____

A

contract
expand (except when physically pulled by antagonistic muscle groups)

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4
Q

muscles can also generate _____

A

heat
contribute to body temp homeostasis

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5
Q

muscles can also generate _____

A

heat
contribute to body temp homeostasis

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6
Q

muscle types (3)

A

skeletal
cardiac
smooth

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7
Q

skeletal muscle

A
  • attached to bones of the skeleton -> control body movement
  • contract in response to signal from somatic motor neuron -> can NOT initiate contractions on its own or be influenced by hormones
  • multiple nuclei in one cell
  • striations
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8
Q

cardiac muscle

A
  • found only in heart -> pump to move blood around body
  • striations
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9
Q

smooth muscle

A
  • primarily muscle of internal organs & tubes (e.g. stomach, blood vessels, urinary bladder)
  • influences movement of materials through body
  • no striations
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10
Q

skeletal muscle characteristics

A
  • responsible for positioning and movement of skeleton (skeletal muscles ~40% body weight)
  • attached to bones via tendons
  • tendons are composed of dense regular connective tissue -> collagen (protein arranged into fibres)
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11
Q

skeletal muscle structure

A
  • outer connective tissue - epimysium
  • contains bundles of muscle tissue - fascicles
    – fascicles are covered by the perimysium -> a connective tissue sheath
    – nerves and blood vessels
  • muscle fibres (muscle cells) are found within each fascicle
    – covered by an innermost connective tissue sheath - endomysium
    – within the muscle fibres are the functional units of skeletal muscle -> Myofibrils
    – contain so many myofibrils, little room for other organelles
    – cytosol contains lots of glycogen & mitochondria
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12
Q

structure of a muscle fibre

A
  • long cylindrical cell
  • several hundred nuclei on surface of fibre
  • cell membrane = sarcolemma
  • majority of space is myofibrils (contractile and elastic protein bundles)
  • contains a specialized ER = sarcoplasmic reticulum
    – associated with SR are T-tubules
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13
Q

T-tubules

A

series of branching tubes
AKA transverse tubes -> lumen continuous with ECF
- closely associated with terminal cisternae (sequester Ca)
- one T-tubule with flanking terminal cisternae = triad

allow rapid AP diffusion into muscle fibre

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14
Q

muscle equivalents for:
muscle cell
cell membrane
cytoplasm
modified ER

A

muscle fibre
sarcolemma
sarcoplasm
sarcoplasmic reticulum (SR)

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15
Q

myofibrils occupy ____ of the space in a muscle fibre

A

most

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16
Q

components of myofibril

A

contractile proteins (generate movement)
- actin
- myosin

regulatory proteins
- tropomyosin
- troponin

accessory proteins
- titin
- nebulin

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17
Q

one repeated pattern of a striated unit forms a _____

A

sarcomere

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18
Q

a sarcomere is made up of:

A

Z-line (disks)
I band - isotropic -> reflects light uniformly
A band - anisotropic -> scatters light unevenly
H zone - (part of A band)
M line - middle

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19
Q

what causes these striations?

A

organization of myofibril protein components (Actin and myosin) cause striations

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20
Q

myosin

A

a motor protein that consists of two coiled protein molecules (chains) with head & tail region (joined by a flexible hinge)
- arranged so the heads are at the ends and tails are together
- convert ATP to movement

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21
Q

about 250 myosin molecules join ->

A

a thick filament

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22
Q

actin

A
  • subunits G-actin (globular actin)
  • G-actin subunits polymerize to form chain (F-actin) -> filamentous
  • 2 F-actin chains twist together to form basis of thin filament
  • the coiled F-actin associates with troponin and tropomyosin (regulate muscle contraction, form completed thin filament)
  • myosin heads interact directly with actin filaments
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23
Q

actin and myosin interactions are called

A

crossbridges

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24
Q

Z-line (disks)

A

site of attachment for thin filaments
- one sarcomere is made of 2 Z discs & the filaments between them

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25
Q

I band

A

region containing only thin filaments
- a Z disc runs through middle of I band -> each 1/2 of I band is part of a different sarcomere

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26
Q

A band

A

region containing thick and thin filaments
- thick and thin filaments overlap at outer edges of A band
- centre occupied by thick filaments only

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27
Q

H zone (part of A band)

A

region containing only thick filaments
-central region is lighter than outer edges

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28
Q

M line

A

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

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29
Q

cross-sections: focus on one thin/thick filament

A

thin filament: surrounded by 3 thick filaments
thick filament: surrounded by 6 thin filaments

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30
Q

titin

A

largest known protein
- elastic protein, stretches from one Z disc to M-line in a sarcomere
- stabilizes position of contractile filaments
- returns stretched muscles to resting length

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31
Q

nebulin

A
  • non-elastic, attaches to Z disc
  • helps to align actin filaments in sarcomere
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32
Q

muscle tension

A

the force created by a contracting muscle whereas the load is a weight or force that opposes the contraction

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33
Q

muscles ____ when they contract

A

shorten

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34
Q

an early theory of muscle contraction:

A

muscles were made up of molecules that shorten when active and stretch when at rest
- molecule was thought to be myosin, because it shortens when heated

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35
Q

Andrew Huxley and Rold Niedeigerke

A
  • observed that length of A band remains constant throughout muscle contraction
  • A band represents myosin filament -> therefore myosin shortening could not be responsible for muscle contraction
  • explanation: the sliding filament theory of contraction
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36
Q

sliding filament theory

A
  • at rest, the ends of thick (myosin) and thin (actin) filaments overlap slightly within each sarcomere
  • thick and thin filaments slide past each other with no change in length of filaments
  • the thin (actin) filaments slide along the thick (myosin) filaments towards M line of sarcomere; brings Z discs closer together
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37
Q

how do actin filaments move?

A

thin filaments are propelled/pulled along by myosin heads
- the heads “walk” along the thin filaments, but since myosin is fixed, thin filaments move

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38
Q

crossbridge cycling steps (4)

A
  1. myosin tightly bound to actin (rigor state - 45 degrees). ATP binds to myosin head -> myosin releases from actin
  2. myosin ATPase hydrolyzes ATP -> ADP + Pi, causing myosin head to swing over and bind weakly to new actin molecule 1-3 molecules away (relaxed state - 90 degree) (closer to Z disc); waiting for Ca signal
  3. Pi released, myosin head rotates on hinge, swings back, pulling actin (thin filament) along with it towards M line (POWER STROKE)
  4. ADP then released, return to step 1
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39
Q

myosin head binding sites (2)

A
  • active subunit (Thin filament)
  • ATP
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40
Q

what would happen if all crossbridges released together

A

thin filaments would slip back into original positions & contraction would not occur

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41
Q

what stops muscles from contracting whenever ATP is available?

A

troponin and tropomyosin

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42
Q

tropomyosin regulation

A
  • coils around F-actin molecules and can cover/uncover each G-actin molecule
  • when covering G-actin, blocks myosin binding site
43
Q

tropomyosin positions (2)

A

“off” - blocking binding site for myosin head
“on” - allows free access to actin for myosin

44
Q

at rest, tropomyosin is in ___ position

A

off

45
Q

troponin

A
  • regulates position of tropomyosin
  • consists of 3 protein subunits; troponin c is important in troponin regulation
  • Ca2+ binds to troponin -> causes conformational change in troponin -> moves tropomyosin to “on”
46
Q

concentrations of Ca2+ in cytosol regulates muscle contraction

A

Ca2+ levels high -> contraction
Ca2+ levels decrease -> relaxation

47
Q

excitation-contraction coupling

A

series of electrical and mechanical events in a muscle that leads to muscle contraction
- occurs through an AP in muscle membrane

48
Q

excitation-contraction coupling steps

A
  1. ACh released by neuron into synaptic cleft at neuromuscular junction and binds to nicotinic cholinergic receptors on motor end plate
  2. receptors are Na+/K+ channels
    - binding of ACh opens channels -> both Na+ and K+ move across membrane
    - ACh removed by acetylcholinesterase
    - Na+ influx exceeds K+ efflux -> local depolarization occurs at synapse
  3. end plate potential (AP) moves down T-tubule
    - T-tubule membrane contains dihydropyridine receptors (DHP receptors) -> L-type calcium channel
    - depolarization changes conformation of DHP receptors
    - DHP receptors are mechanically linked to Ca2+ channels of SR, known as ryanodine receptors (RyR)
  4. DHP receptor changes RyR conformation, opening Ca2+ channels of SR -> Ca2+ leaves SR
    - increases cystolic [Ca2+]
  5. Ca2+ binds to troponin -> moves tropomyosin out of way
  6. myosin powerstroke
  7. actin filament slides toward M line -> contraction
  8. relaxation of skeletal muscle when Ca2+ pumped back into SR through Ca2+-ATPase
  9. lower cystolic [Ca2+] causes troponin and Ca2+ to unbind
  10. tropomyosin “off”
    - elastic elements pull filaments back to relaxed position when myosin unbinds
49
Q

skeletal muscle: (excitation-contraction coupling) local depolarization occurs at synapse called?

A

End Plate Potential (EPP)

50
Q

EPPS are almost always ____ threshold

A

above -> results in contraction

51
Q

ATP (glucose -> ATP methods)

A
  • glycolysis occurs aerobically or anaerobically
    (2 ATP/glucose), produces lactic acid without oxygen
  • oxidative metabolism requires oxygen (15x more ATP/glucose), no toxic end products
52
Q

phosphocreatine

A
  • high energy phosphate molecule in addition to ATP
  • muscles have a high concentration of phosphocreatine (rapid source of energy)
  • easily donates Pi to ADP -> limited amount of ATP
  • used to buffer [ATP] over short time scales
  • resting muscles store energy in phosphocreatine
53
Q

phosphocreatine reaction + catalyzed by?

A

phosphocreatine + ADP -> ATP + creatine
- catalyzed by creatine kinase (CK)

reverse also works: ATP + creatine -> ADP + phosphocreatine

54
Q

2 important muscle contraction periods

A

twitch and latent period

55
Q

twitch

A

single contraction-relaxation cycle

56
Q

latent period

A

short delay between the AP and beginning of muscle tension
(time it takes for excitation-contraction coupling to occur)

57
Q

is ATP used for relaxation phase? if so what for?

A

yes, to pump Ca2+ back

58
Q

3 general types of muscle fibres

A
  1. slow-twitch fibres (type I)
    - oxidative, redder from myoglobin
  2. fast-twitch oxidative-glycolytic fibres (type IIA)
  3. fast-twitch glycolytic fibres (type IIX)
    - no myoglobin, paler
59
Q

oxidative fibres usually appear red due to ____

A

myoglobin

60
Q

myoglobin

A

oxygen-carrying haeme protein

61
Q

oxidative fibres vs glycolytic fibres

A

oxidative fibres are smaller, have numerous mitochondria, and are better vascularized -> more blood vessels (for oxygen!)

62
Q

what does “fast” or “slow” refer to in muscle fibre types?

A

rate of myosin ATPase activity
- fast fibres can split ATP more quickly and can contract/develop tension faster (result of presence of diff isoforms of myosin, don’t last long)

63
Q

duration of contraction varies between fibres:

A
  • fast fibres have shorter twitches (more twitches per unit time)
  • twitch duration determined by rate of removal of Ca2+ from cytosol (contraction AND relaxation phase)
  • short (fast) twitch duration is useful for rapid, small muscle contractions (e.g. piano, typing)
  • long (slow) twitch duration good for long sustained movements (e.g. standing upright)
64
Q

which type of muscle fibre has highest rate of Ca2+ removal from cytosol?

A

fast twitch muscles

65
Q

tension exerted by a muscle during a single twitch is influenced by: (2)

A
  1. muscle type (due too structure, fast twitch fibres can generate more tension)
  2. sarcomere length at start of contraction
66
Q

diff situations of sarcomere overlap

A

too little overlap
- few crossbridges
- little force can be generated

too much overlap
- actin filaments start to interfere with each other
- less force generated

way too much overlap
- thick filaments collide with Z disk
- force rapidly decreases

67
Q

does a single twitch represent the maximum force the muscle fibre can develop?

A

no, the force of a muscle fibre can be increased by increasing the rate of APs that stimulate the fibre

68
Q

summation

A
  • increase in force generated by a muscle
  • due to repeated stimulation from APs that occur before the muscle has fully relaxed
69
Q

tetanus (2 types)

A

state of muscle when maximum force of contraction is reached

  • incomplete (unfused) tetanus: slow stimulation rate -> fibre relaxes slightly between stimuli
  • complete (fused) tetanus: fast stimulation rate -> fibre does not have time to relax (fatigue after a while, lose tension despite stimulus)
70
Q

motor unit

A

basic unit of contraction in an intact skeletal muscle
- a muscle is made up of many different motor units

71
Q

motor unit components (2)

A
  • a group of muscle fibres -> # fibres varies
  • somatic motor neuron that controls them -> only ONE

note: all muscle fibres in a motor unit are the same type (fast or slow-twitch)
- an AP in the somatic motor neuron -> contraction of all muscle fibres in motor unit (all-or-none)

72
Q

contraction of muscle can be varied by: (motor units) (2)

A
  1. changing the type of motor unit activated
  2. changing the # motor units that are active
73
Q

recruitment (motor units)

A
  • force of contraction is increased by using more motor units
  • different muscle fibres are recruited at different times
  • slow oxidative fibres have a low threshold for stimulation
  • fast glycolytic fibres have a high threshold for stimulation
74
Q

which would have more muscle fibres per motor unit, fine movements or coarse movements?

A

coarse! (more power)

75
Q

2 main types of muscle contraction

A
  1. isotonic
  2. isometric
76
Q

isotonic

A
  • creates forces and MOVES a load
  • load is usually constant, and the muscle length changes
77
Q

isometric

A
  • creates force WITHOUT movement
  • muscle length constant
  • load usually greater than force that can be applied
78
Q

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

A

even though sarcomeres shorten, muscle length stays constant because these elastic elements stretch to take up force until fully stretched

79
Q

where is smooth muscle found in body?

A
  • walls of hollow organs & tubes -> not attached to bones of skeleton
  • fewer in % body weight, but much more important
  • some important smooth muscles -> bladder sphincter, intestine, walls of blood vessels
80
Q

smooth muscle can be arranged in 2 ways:

A
  1. single unit -> cells coupled by gap junctions
    - not necessary to electrically stimulate each individual fibre
    - found on walls of internal organs -> e.g. blood vessels
  2. multi-unit -> no gap junctions
    - each individual muscle fibre is separately innervated
    - e.g. eye iris, parts of reproductive organs
81
Q

smooth muscle vs skeletal muscle: muscle level (3)

A
  1. contraction of smooth muscle changes muscle shape, not just length
  2. smooth muscle develops tension (force) slowly
  3. smooth muscle can maintain contraction longer without fatiguing -> important because some are contracted most of the time (e.g. internal bladder sphincter)
82
Q

smooth muscle vs skeletal muscle: cellular level (6)

A
  1. fibres much smaller in smooth muscle than skeletal muscle fibres
    - about same diameter as a single myofibril in skeletal muscle fibre
  2. actin & myosin are not arranged into sarcomeres, so no striations
  3. actin & myosin arranged in long bundles diagonally around periphery of cell
  4. actin anchored at cell membrane structures called DENSE BODIES
    - not attached to Z lines like in skeletal muscle
  5. no T-tubules in sarcolemma, not much SR
    - smooth muscle cells have special vesicles (CAVEOLAE - sequester Ca2+) that are invaginations of sarcolemma, specialized for cell signalling
  6. force of contraction is related to amount of Ca2+ released
83
Q

what is the effect of not having T-tubules (smooth muscle)?

A

no direct coupling of the AP to Ca2+ release from SR through DHP receptor-ryanodine receptor coupling as in skeletal muscle
- instead Ca2+ entering through cell membrane causes Ca2+ release from SR

84
Q

smooth muscle vs skeletal muscle: molecular level (5)

A
  1. less myosin per unit actin in smooth muscle than skeletal muscle
  2. actin and myosin filaments are longer and overlap more in smooth muscle
  3. myosin ATPase activity much slower in smooth muscle
  4. myosin heads are located along all parts of myosin molecule in smooth muscle (not just ends like in skeletal muscle)
  5. no troponin in smooth muscle
85
Q

how do properties of myosin in smooth muscle contribute to characteristics of smooth muscle?

A

contract more slowly & for longer periods of time than skeletal or cardiac muscle
- in part due to slower myosin ATPase activity
- longer actin and myosin filaments allow longer contractions and allow smooth muscle to be stretched yet still be able to contract

remember: in skeletal muscle, too much stretching leads to too little overlap and an inability to contract

86
Q

Smooth Muscle Contraction Steps (5)

A
  • major difference between contraction of smooth muscle & cardiac muscle is the role of phosphorylation in regulating the smooth muscle contraction process
  1. signal to initiate contraction is increase in cystolic Ca2+
    - cytosolic Ca2+ levels control contraction
    - Ca2+ entry from ECF results in release of SR Ca2+ and Ca2+ from caveolae (calcium-induced calcium release)
  2. Ca2+ binds to calmodulin (CaM) in cytosol
  3. Ca2+/CaM activates enzyme myosin light chain kinase (MLCK)
  4. MLCK activates myosin by phosphorylating light chain of myosin molecule in the head using energy and Pi from ATP -> this ATP is used to activate myosin through phosphorylation, NOT crossbridge cycling
  5. phosphorylated myosin (active) can now interact with actin and go through crossbridge cycling, and allow contraction to occur in smooth muscle cell -> remember, additional ATP is needed for each crossbridge cycle

Note: MLCK uses Pi from ATP to activate myosin, but additional ATP is needed to go through crossbridge cycling for contraction

87
Q

smooth muscle contraction: how does Ca2+ enter from ECF?

A
  • Ca2+ enters from ECF through:
    – voltage-gated channels -> open when cell depolarizes
    – stretch-activated channels -> open when membrane stretched
    – chemically-gated channels -> open in response to hormones
88
Q

smooth muscle contraction: myosin phosphorylated/unphosphorylated?

A
  • when myosin is not phosphorylated, ATPase activity is blocked
  • when myosin is phosphorylated, ATPase is active
89
Q

smooth muscle regulation vs skeletal muscle regulation

A

smooth muscle: myosin is regulated by phosphorylation of myosin

skeletal muscle: actin is regulated by troponin/tropomyosin

90
Q

what would happen to contraction if a smooth muscle cell were placed in a Ca2+-free saline solution?

A

no contraction -> no Ca2+ entry from extracellular environment

91
Q

relaxation in smooth muscle (2) steps

A
  1. Ca2+ removed from cytosol
    - pumped back into SR using ATP to extra-cellular environment through -> Ca2+-Na+ antiport, Ca2+-ATPase
  2. decrease in Ca2+ levels in cytosol causes Ca2+ to unbind from calmodulin (CaM) -> inactivates MLCK
    - myosin light chains are dephosphorylated by myosin light chain phosphatase (MLCP)

Note: dephosphorylation of myosin does not automatically relax muscle
- allows smooth muscle to enter “LATCH STATE”, not fully understood
- tension is maintained (myosin remains bound to actin) but with minimal ATP consumption

92
Q

cardiac muscle cells are called ___ ___

A

myocardial cells

93
Q

most myocardial cells are typical ___ muscle

A

striated
- contractile fibres organized into sarcomeres

94
Q

myocardial muscle have intercalated disks, which include? (2)

A

gap junctions
desmosomes

95
Q

cardiac muscle vs skeletal muscle: (3)

A
  • cardiac muscle cells are much smaller with single nucleus and ~1/3 cell volume occupied by mitochondria
  • T-tubules are much larger and branched, and SR is smaller
  • adjacent cells are joined by intercalated discs with desmosomes
96
Q

about 1% of cardiac muscle cells are NOT involved in contraction. they are?
how are they connected to other cardiac cells?

A

autorhythmic/pacemaker cells!
- involved in electrical excitation of heart (known as electrical conducting system of heart)
- they initiate heartbeat & allow electrical excitation to spread rapidly throughout heart
- connected to other cardiac cells via gap junctions

97
Q

cardiac muscle contraction (like skeletal muscles EXCEPT?) (3)

A
  1. Ca2+ enters through Ca2+ channel son cell membrane as well as SR
    - first: calcium enters through external calcium channels
    - next: calcium-induced calcium release -> release of stored Ca2+ from SR
    - SR calcium provides 90% needed Ca2+ for contraction
  2. cardiac cells have Na/Ca2+ antiport (in addition to Ca2+-ATPase)
    - removes Ca2+ from cytosol and pumps into extracellular space
  3. exhibit GRADED contraction -> force generated proportional to number of active crossbridges
    - # active crossbridges proportional to cystolic [Ca2+]
    - therefore, force generated proportional to cystolic [Ca2+]
98
Q

factors influencing cardiac muscle contraction force (2):

A
  1. changes in [Ca2+]
    - regulated by epinephrine and norepinephrine -> bind to & activate beta1-adrenergic receptors
    – binding then activates cAMP second messenger signalling pathway that leads to:
    a. phosphorylation of voltage-gated Ca2+ channels (increases probability of opening, which increases cystolic [Ca2+])
    b. phosphorylation of phospholamban (leads to increased SR Ca2+-ATPase activity, which increases SR Ca2+ (overall more forceful & shorter contraction)
  2. sarcomere length
    - tension generated proportional to length of muscle fibre
    - due to degree of overlap between actin and myosin -> there is optimal amount of overlap
  • Note: stretching a myocardial muscle cell may also allow more Ca2+ to enter through cell membrane Ca2+ channels -> contributing to a more forceful next contraction
99
Q

cardiac muscle is an excitable tissue, meaning?

A

can generate APs

100
Q

cardiac muscle generates APs: (5 phases, starting with 4 then 0-3)

A

phase 4: resting membrane potential

phase 0: depolarization -> AP opens voltage-gated Na+ channels, causing a rapid increase in membrane Na+ permeability (close again)

phase 1: initial repolarization -> open fast K+ channels allow intial repolarization

phase 2: the plateau -> initial depolarization triggered voltage-gated Ca2+ channels to slowly open, causing an increase in Ca2+ permeability and the fast K+ channels close

phase 3: rapid repolarization -> the Ca2+ channels close and slow voltage-gated K+ channels open, resting stage ion permeability restored

101
Q

cardiac muscle contraction AP: sustained depolarization is due to?

A

slow opening of voltage-gated Ca2+ channels

102
Q

cardiac muscle contraction AP: result of sustained depolarization?

A

longer AP in cardiac muscle
- important! prevents tetanus and allows heart to relax between contractions (needs to last long time, cannot fatigue)

103
Q

why don’t cardiac muscle cells undergo summation and tetanus?

A

because of the longer refractory period -> cell has finished contracting before next AP

BIOL 273 Physiology (6 decks)

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