Chapter 12: Muscle Physiology Flashcards

1
Q

what is the somatic motor division?

A
  • supplies motor impulses to the skeletal muscles.
  • voluntarily controls skeletal muscles
  • ALWAYS excitatory
  • is functionally and anatomically different from the autonomic pathways
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2
Q

anatomy of the somatic nervous system

A
  • a single motor neuron travels from the CNS to innervate skeletal muscle cells
  • a motor neuron originates in the ventral horn of the spinal cord
  • a single motor neuron innervates several muscle fibres (cells) via branching axons
  • a single muscle fibre can only be innervated by one neuron
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3
Q

what is a motor unit?

A

a motor neuron plus all the muscle fibres that it innervates

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4
Q

what is a neuromuscular junction?

A

the location of a synapse between a motor neuron and a skeletal muscle fiber in the somatic nervous system

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5
Q

what is a terminal bouton?

A

the axon terminal of a motor neuron in the somatic nervous system that stores and releases acetylcholine

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6
Q

what is a motor end plate?

A
  • a specialized region of the muscle fibers plasma membrane
  • has a large number of nicotinic cholinergic receptors (respond to acetylcholine)
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7
Q

what are the components of the neuromuscular junction?

A
  • axon terminal (terminal bouton)
  • motor end plates (on muscle membrane)
  • schwann cell sheaths
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8
Q

how does signal transmission occur at neuromuscular junctions in the somatic nervous system?

A
  • when a motor neuron is activated by converging synaptic input, action potentials are propagated to the terminal boutons of all muscle fibers in the motor unit located at the neuromuscular junctions
  • the arrival of the AP causes voltage-gated Ca2+ channels in the boutons to open
  • calcium enters the cytosol and triggers synaptic vesicles with ACh to fuse with the pre-synaptic membrane
  • acetylcholine is released via exocytosis and diffuses across the synaptic cleft
  • ACh binds to nicotinic cholinergic receptors at the motor end plate on post-synaptic membrane, causing cation channels to open
  • the open channel allows Na+ to flow into and K+ to flow out of the the muscle fibre simultaneously
  • the net influx of Na+ produces a depolarization called an end-plate potential (EPP)
  • if the end-plate potentials depolarizes the muscle fiber to threshold, an action potential in the muscle cell plasma membrane occurs
  • this triggers contraction of the muscle fiber
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9
Q

comparison between the somatic and autonomic motor divisons

A
  • somatic has 1 neuron in efferent path, autonomic has 2 neurons in efferent path
  • somatic has only ACh/nicotinic receptor/transmitter but autonomic has ACh/cholinergic and NE/adrengenic
  • somatic targets skeletal muscle, autonomic targets smooth and cardiac muscle, endocrine/exocrine glands and adipose tissue
  • somatic only has excitatory effect but autonomic has excitatory and inhibitory effects on target tissue
  • somatic only has axons in peripheral but autonomic has pre-ganglionic neurons, ganglia and post-ganglionic neurons
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10
Q

3 types of muscles

A
  • skeletal muscle
  • cardiac muscle
  • smooth muscle
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11
Q

what does skeletal muscle look like?

A
  • large, multi-nucleated cells
  • appear striped or striated under the microscope
  • is attached to the skeletal system (bones)
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12
Q

what are the functions of muscle tissue?

A
  • produce skeletal movement
  • maintain body position
  • support soft tissues
  • maintain body temperature
  • store nutrient reserves
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13
Q

what are the three layers of the muscle fibers?

A
  • epimysium
  • perimysium
  • endomysium

–> the ends of these muscles come together to form tendons(bundle) or aponeurosis (sheet)

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14
Q

what is epimysium?

A
  • connective tissue that surrounds the entire body of the muscle
  • it defines the muscles volume
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15
Q

what is perimysium?

A
  • connective tissue that extends into the body
  • divides muscle into numerous bundles (called fascicles) of individual muscle cells
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16
Q

what is endomysium?

A
  • a shin sheath of connective tissue that encases muscle fibres
  • separates single muscle fibres from one another
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17
Q

what is a fasisicle?

A
  • bundles of individual muscle cells
  • contains 100’s to 1000’s of muscle cells called muscle fibres (due to their elongated shape)
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18
Q

what is a muscle fiber?

A
  • individual/single muscle cells
  • wrapped by a layer of endomysium
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19
Q

how large are skeletal muscle fibers?

A
  • 3 to 4 inches long (attach at a tendon)
  • 0.05mm to 0.15mm wide (diameter)
  • contain hundreds of nuclei, not just one
  • develop through the fusion of mesodermal cells (myoblasts)
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20
Q

what are the major structural features of a skeletal muscle cell?

A
  • sarcolemma
  • myofibrils
  • sacroplasmic reticulum
  • transverse tubules (T-tubules)
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21
Q

what is the sarcolemma?

A
  • is the plasma/cell membrane of muscle fiber cells
  • surrounds the sarcoplasm (cytoplasm in muscle fibers)
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22
Q

what are transverse tubules?

A
  • t-tubules are invaginations of the sarcolemma
  • they’re the structures that transmit action potentials rapidly from the sarcolemma to the myofibrils
  • electrical signals that reach the T-tubule trigger the release of Ca2+ from the sarcoplasmic reticulum causing depolarization
  • T-tubules ensure that the entire length of the muscle fiber is depolarized so it can contract simultaneously
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23
Q

what are myofibrils?

A
  • made up of bundles of protein filaments called myofilaments
  • a result of a collection of 2 protein myofilaments called myosin and actin
  • these myofilaments are responsible for muscle contraction (shortening of a muscle fibre)
  • composed of a fundamental unit called a sarcomere that repeats over and over
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24
Q

what is the sarcoplasmic reticulum?

A
  • the sac-like, membranous structure surrounding each myofibril
  • helps transmit action potentials to myofibrils
  • form chambers (called cisternae) that attach to T-tubules which store calcium
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25
Q

what is a triad in skeletal muscle?

A
  • arrangement of three components: 2 terminal cisternae of the sarcoplasmic reticulum and one t-tubule
  • responsible for the regulation of excitation-contraction coupling
  • the cisternae concentrate Ca2+ via ion pumps and release Ca2+ into sarcomere to begin muscle contraction
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26
Q

why are muscles striped?

A
  • appearance is refered to as “striated”
  • caused by the orderly arrangement of protein fibers called thick and thin filaments (actin and myosin)
  • the fibers run parallel to the long axis of the muscle
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27
Q

what are sarcomeres?

A
  • the basic contractile unit of muscle fiber
  • they’re the repeating units that make up myofibrils
  • each sarcomere is composed of two main protein filaments (actin and myosin) responsible for muscle contraction
  • sarcomeres are bordered by Z lines on either side
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28
Q

what are thick and thin filaments?

A

actin = THIN
myosin = THICK
- referred to as contractile proteins because they are the machinery that generates contractile forces in muscles

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29
Q

what are the regions that appear on a sarcomere?

A
  • A band
  • I band
  • H zone
  • Z line
  • M line
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30
Q

what do the regions of the sarcomere represent?

A
  • Z line = anchor thin filaments (actin) and define the borders of sarcomeres at either end
  • M lines = connect thick filaments (actin) together and runs down the middle of the sarcomere
  • I band = light band with only thin filaments (actin)
  • A band = dark band represents the length ofthick filaments (myosin), and where it overlaps with thin (actin) filaments
  • H zone = centre of the sarcomere band where only thick filaments (myosin) are present
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31
Q

what is the structure of a thin filament (actin)?

A
  • basic component of thin filaments are actin monomers called G-actin which each have an active myosin binding site
  • G-actins link together end-to-end to form F-actin (filamentous actin)
  • F actin is composed of 2 rows of 300-400 G-actin molecules to form a twisted double helix arrangement
  • 2 regulatory proteins (tropomyosin and troponin) are found in thin filaments
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32
Q

what proteins are found in thin filaments? what do they do?

A

–> tropomyosin and troponin are regulatory proteins that enable muscles to start/stop contracting

  • tropomyosin is a long fibrous muscle that extends over numerous actin monomers (G-actin) and blocks myosin-binding sites (prevents binding from occuring)
  • troponin is a complex of 3 proteins:
    (1) attaches to actin
    (2) attaches to tropomyosin protein
    (3) binds to Ca2+ reversibly
  • Ca2+ binding triggers skeletal muscle contraction
  • occurs when Ca2+ binds to troponin, and a conformational change occurs. This influences the position of tropomyosin and as a result, tropomyosin shifts its position. This exposes the myosin-binding sites on the actin filaments and they can interact
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33
Q

what is the structure of a thick filament (myosin)?

A
  • thick filament is made of 100’s of myosin molecules (look like golf clubs)
  • a myosin molecule is composed of 2 intertwined subunits, and each have a long tail and fat head
  • has an additional protein called titin
  • myosin has 2 binding sites located on the head

–> the head is referred to as the “crossbridge” because they sometimes bridge the gap between thick and thin filaments
–> the middle of the filament lacks heads (crossbridges), it is called the bare area

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34
Q

what is function of the 2 binding sites on thick filaments?

A

(1) actin binding site
- capable of binding to the actin monomers in the thin filament (forming cross-bridges)

(2) nucleotide binding site for ATP and ATPase
- ATP can attach
- ATPase activity means it can hydrolyze ATP into ADP and inorganic phosphate (Pi).
- this provides the energy required for the myosin to undergo a conformational change, allowing it to bind to actin

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35
Q

what proteins are found in thick filaments? what do they do?

A
  • titin is found in thick filaments
  • it’s a very elastic protein that provides elastciity to the sarcomere
  • that extends along the thick filament from M line to Z line
  • works to anchor thick filaments in their proper position relative to thin filaments
  • helps return muscles back to original state after being subjected to a stretching force
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36
Q

how does titin contribute to the response of muscles when subjected to stretching forces?

A
  • when a muscle is stretched, the titin strands elongates as the sarcomere lengthens.
  • eventually, the strands acts like a spring and resists further stretching.
  • when the stretching force is removed, titin pulls the muscle fibers back to their original length by bringing Z lines and thick filaments closer together and causes the sarcomeres to shorten.
  • this helps the muscle return to its normal state after being stretched
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37
Q

what is the sliding filament model?

A
  • the original theory was that when a muscle contracts, the thin and thick protein filaments shorten
  • the new theory is that when contraction occurs, thick and thin filament slide past each other and overlap, and do not actually change in length
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38
Q

how does the sliding filament model work?

A

when a muscle contracts, the sarcomere within a myofibril undergoes the following changes:
- the A band stays the same length (length of myosin)
- the I band shortens (where actin overlaps myosin)
- the H zone shortens (area of only myosin)
- overall, the entire sarcomere shortens BUT the filaments themselves don’t shrink

–> sliding of thin filaments toward the M line

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39
Q

how do the filaments slide during contraction?

A
  • the sliding of filaments and shortening of a sarcomere is due to the cyclical formation and breaking of cross bridges (links between actin and myosin)
  • is powered by ATP hydrolysis (into ADP and Pi)
  • the cross bridge cycle!
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40
Q

what are the 5 steps to the cross-bridge cycle?

A

1) binding of myosin to actin
- myosin begins in its high energy form = ADP + Pi is bound to the ATPase site of myosin head
- the ATP has been hydrolyzed already
- myosin has high affinity for actin
- the myosin head binds to the actin monomer in the adjacent thin filament
- only occur in presence of Ca2+

2) power stroke
- the binding of myosin to actin triggers the release of Pi and ADP from the ATPase site on myosin
- at this time, the myosin head pivots toward the middle of the sarcomere and pulls the thin filament along with it

3) rigor
- after the powerstroke ends, and ADP and Pi are gone, myosin goes back to a low energy state
- myosin and actin are tightly bound together (called rigor) and are stuck.

4) unbinding of actin and myosin
- a new ATP enters the ATPase site on myosin head and causes a conformational change of the myosin head
- this causes affinity for actin to decrease
- therefore, myosin detaches from the actin binding site

5) cocking of myosin head
- soon after a new ATP binds to myosin ATPase, it is split via hydrolysis into ADP and Pi
- this process releases energy
- some of it is captured by the myosin molecule and goes into it’s high energy state
- if calcium is present, the cycle will continue

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41
Q

how does the crossbridge cycle relate to the sliding filament theory?

A

–> the crossbridge cycle is a series of events that underlies the sliding filament theory

  • in the resting state, myosin heads are in a low-energy configuration with ATP bound.
  • using energy via ATP hydrolysis (ADP + Pi), the myosin heads repeatedly bind and form cross bridges with actin
  • this initiates a power stroke movement which slides the actin (thin) filaments past the myosin (thick) filaments toward the center of a sarcomere
  • these cross bridges repeatedly break and reform which cause myosin filaments repeatedly attach to and pull on thin actin filaments
  • this causes the sarcomere to shorten and cause a muscle contraction.
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42
Q

how long could the cross-bridge cycle continue for?

A
  • could continue indefinitely as long as their is enough ATP and Ca2+ available to bind troponin
  • however, to stop it, regulatory proteins (troponin and tropomyosin) interact with calcium to control the availability of myosin-binding sites on actin
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43
Q

what is excitation-contraction coupling?

A

the process by which the action potential of the motor neuron leads to the synchronous contraction of the myofibrils

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44
Q

what are the steps to excitation-contraction coupling

A

1) the motor neuron synapses with the muscle cell at the neuromuscular junction
2) the motor neuron transmits an action potential and secretes neurotransmitter acetylcholine from the axon terminal
3) ACh diffuses to the sarcolemma of the muscle cell and binds to the nicotinic receptors on the motor end plate. the binding elicits an end plate potential (EPP) which triggers an action potential in the muscle fiber cell
2) the action potential propagates along the sarcolemma and down the t-tubules
3) DHP receptors in the t-tubule membrane undergo a conformational change, which transmits a signal to ryanodine receptors in sarcoplasmic reticulum to open Ca2+ channels in the lateral cisternae sacs.
4) Ca2+ leaves the sarcoplasmic reticulum and enter the cytosol, which increases cytosolic concentration of Ca2+
5) the Ca2+ binds to troponin causing a conformational change and shifts tropomyosin out of normal resting position, which exposes the myosin-binding sites on actin.
6) the myosin heads can now bind to actin, which allows the cross bridge cycle to begin and sarcomere (muscle fiber) to contract.
7) Ca2+ is actively transported via ATPase into the lumen of SR following the action potential

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45
Q

what is the role of Ca2+, troponin and tropomyosin in excitation-contraction coupling?

A

if no calcium is present = troponin holds tropomyosin over (and blocks) the myosin binding sites on actin
- no cross bridges can form between actin and myosin
- the muscle is relaxed

if calcium is present = Ca2+ binds to troponin causing conformation change of troponin, causing movement of tropomyosin and exposes the myosin binding sites on actin
- cross bridges can form between actin and myosin
- the muscle contract because the cross bridge cycle can occur

46
Q

how does a muscle contraction stop?

A

(1) the action potential must stop
- the muscle fiber cell has stopped receiving input from the motor neuron
- no more ACh is released into the neuromuscular junction = no more action potential
- causes repolarization of the the sarcolemma and T-tubules
- simultaneously, acetylcholinesterase degrades ACh in the synaptic cleft

(2) t tubule voltage gated Ca2+ channels close
- when membrane potential returns to normal (repolarizes due to no more action potential), ryanodine receptors (voltage sensitive) in sarcoplasmic reticulum close so no more Ca2+ can be released

(3) Ca2+ must be removed from the sarcoplasm
- ATPase pumps actively transports Ca2+ out of the sarcoplasm back into the sarcoplasmic reticulum
- the myosin binding sites on actin can be “reshielded” by the troponin/tropomyosin complex

(4) availability of ATP
- ATP breaks the bond between the myosin heads and the actin filament to stop the cross bridge cycle

47
Q

what occurs at a cellular level during muscle relaxation?

A

the muscle contraction ends when calcium dissociates from troponin and the number of exposed sites on the actin filament decreases, leading to a decline in the number of active cross bridges

48
Q

how is the concentration of calcium related to strength of muscle contraction?

A
  • strength of contraction ultimately depends on the amount of calcium in the cytosol
  • if theres more calcium, more myosin binding sites can be exposed which in turn allows more cross bridge cycling to occur
49
Q

what is the role of ATP in excitation-contraction coupling?

A
  • ATP needed for cross bridge formation
  • ATP needed for unbinding of actin and myosin
  • ATP needed for Ca2+ pump back into sarcoplasmic reticulum from the sarcoplasm
50
Q

what is the role of acetylcholine in excitation-contraction coupling?

A

initiates muscle contraction!!!

  • ACh is released by the motor neuron into synaptic cleft
  • binds to receptor on motor end plate which opens ion channels, allowed Na+ into cell causing an EPP
  • if it reaches threshold, an action potential is propagated along the sarcolemma and muscle contraction can occur
51
Q

what is rigor mortis?

A
  • the state of muscular rigidity and stiffness
  • occurs 2-3 hours after death and lasts about 24 hours
  • result of cross-bridging
52
Q

what occurs during rigor mortis?

A
  • after death, Ca2+ ions leak out of the sarcoplasmic reticulum and allow myosin heads to bind to actin
  • ion pumps cease to function (no ATP)
  • as ATP synthesis has ceased, cross bridges cannot detach from actin and stay in high energy state
  • therefore muscles stay contracted because the cross-bridge cannot be broken (usually occurs when ATP binds and pushes to low energy state)
  • need proteolytic enzymes to begin digesting decomposing cells
53
Q

what does the force of muscle contraction depend on?

A
  • number of myosin binding sites on actin that are exposed = increase number of active cross bridging sites
  • more cross bridges = generate more force
54
Q

what 2 factors affect the force generated in a muscle?

A

1) the force generated in individual muscle fibers
2) the number of muscle fibers contracting

55
Q

what 4 factors affect the force of muscle contraction in individual muscle fibers?

A

1) the frequency of stimulation (high or low)
2) muscle fiber diameter
3) changes in muscle fiber length (been stretched or shortened)
4) recruitment of motor units

56
Q

how does frequency affect the force of muscle contraction?

A
  • frequency of MU activation can either increase or decrease tension in a muscle
  • temporal summation = higher frequencies of activation through rapid stimulation leads to temporal summation, where individual twitches add up, resulting in increased tension.
57
Q

describe how frequency of motor unit stimulation affect can affect the force of a muscle contraction

A
  • at higher frequencies, the rate of calcium released from the sarcoplasmic reticulum into the cytosol EXCEEDS the rate of calcium being actively transported from the cytosol back into the sarcoplasmic reticulum
  • this leads to an increase in peak tension (the maximum force a muscle can generate during a contraction)
  • the more calcium in the cytosol, the more calcium that is able to bind to troponin, which moves the tropomyosin to expose more myosin-binding sites on actin
  • the more myosin-binding sites exposed, the more cross that can participate in cross cycling
  • therefore the greater the tension development in the muscle = bigger contraction
58
Q

how does motor unit recruitment affect the force of muscle contraction?

A
  • recruiting more motor units increases the force of muscle contraction
  • therefore, the higher the recruitment the stronger the muscle contraction will be.
  • 5 fibers vs 7 fibers vs 12 fibers
  • spatial summation = the recruitment of multiple motor units simultaneously so as the intensity of a contraction increases, more motor units are recruited to contribute to force production
59
Q

how does length of a muscle fiber affect the amount of tension a muscle produces?

A
  • twitch force depends on the length of individual sarcomeres before contraction (not the number of sarcomeres)
  • each muscle fiber has an optimum length that it generates the most force due to maximum participation of myosin cross-bridges
  • if a fiber shortens beyond or stretched beyond the optimum range, the force-generating capacity decreases
  • the changes in fiber length alter the length of the sarcomeres = there is limited potential for myofilaments to overlap (sliding filament theory) = less cross bridges can form = reduce their ability to generate force
60
Q

how does fiber diameter affect force of muscle contraction?

A
  • diameter is a crucial variable that determines its force-generating capacity
  • the greater the fiber diameter is directly related to the amount of force it can generate
  • larger diameter muscle fiber = greater cross-sectional area = contains more myofibrils = more sarcomeres = more potential for cross bridging = greater force of contraction
61
Q

what is a muscle twitch?

A
  • the response of a muscle to a single action potential = a single contraction-relaxation cycle
  • follows all-or-none principle = when a muscle fiber is stimulated, it will contract maximally in response to a threshold stimulus
62
Q

3 key phases of a muscle twitch

A

1) latent period
- delay that occurs between the action potential in a muscle cell and contraction
- the time required for the release of Ca2+ and binding to troponin

2) contraction phase
- muscle tension increases to a maximum value
- cytosolic concentration of calcium increases
- cross-bridge cycle interaction occurs (myosin heads bind to actin)

3) relaxation phase
- muscle tension decreases
- cytosolic concentration of calcium decreases

63
Q

what is the main characteristic of a muslce twitch?

A
  • its reproducibility!!!
  • relates to the all-or-nothing character of a muscle cell’s action potential
  • an action potential always triggers the same degree of calcium release from SR, causes same rise in cytosolic calcium concentration, exposes the same number of binding sites for myosin cross bridge = SAME FORCE
64
Q

two types of twitches

A

1) isometric twitch
2) isotonic twitch

65
Q

what is an isometric twitch?

A
  • a muscular contractions in which there is no change in the length of the muscle, an no limb moves
  • load > tension = muscle creates tension but maintains the same (iso) length (metric) because the load is greater than the force generated by the muscle
  • some pure isometric contractions occur
66
Q

what is an isotonic twitch?

A
  • a muscular contraction that occurs when the muscle changes length, producing limb motion
  • tension > load = the muscle generates a constant (iso) tension (tonic) just greater than any forces opposing it (a load)
  • pure isotonic contractions are rare
  • 2 types: eccentric and concentric
67
Q

what are the two types of isotonic twitches?

A
  • two types: (1) concentric and (2) eccentric contraction
    –> concentric = shortening of the muscle
    –> eccentric = lengthening of a muscle
68
Q

what is the difference in elastic elements in a isometric and isotonic contraction?

A
  • in an isometric contraction, sarcomeres shorten and generate force BUT the elastic elements in the muscle stretch which result in the muscle length to stay the same
  • in an isotonic contraction, sarcomeres shorten more but because the elastic elements are already stretched, the muscles shorten
69
Q

what is tension?

A

the force exerted by a contracting muscle

70
Q

what is a load?

A

the force opposing contraction (i.e a dumbbell)

71
Q

why is a pure isotonic or isometric contraction rare?

A
  • because many practical day to day activities requires limb movement, and load is generally not constant
  • therefore requires both isometric contraction followed my isotonic contraction
72
Q

what is the transition from isometric to isotonic phases?

A
  • when an external load/resistance is constant, a muscle often begins its contraction with an isometric phase
  • isometric tension continues to build up until tension exceeds the external load/resistance
  • when this occurs, the muscle transitions from the isometric phase to the isotonic phase
  • tension remains constant allowing for controlled shortening or lengthening of the muscle
  • this allows for dynamic movement of the body
73
Q

what are the different types of muscle fibres?

A

1) slow twitch = type I
- fatigue resistant,
- lower force/ power

2) fast twitch = type II
- intermediate fibres
- more fatigue resistant than IIX but less than I
- intermediate force/power

3) fast fibers = type IIB or IIX
- powerful
- fatigable

74
Q

how do muscles vary contraction?

A
  • changing types of active motor units
  • changing number of active motor units
75
Q

what is treppe?

A
  • occurs at a frequency of muscle stimulation where independent twitches follow one another closely
  • it will cause the peak tension (maximum force of muscle contraction) rises in a stepwise fashion until it eventually plateaus to a constant level
76
Q

what is twitch summation?

A
  • occurs when a muscle is stimulated repetitively and doesn’t allow muscle to relax fully
  • when additional action potentials arrive before twitches can be completed so the twitches sum and yielding a force greater than that of a single twitch
77
Q

what causes twitch summation to occur?

A
  • summation happens whenever twitches occur at a frequency such that calcium cannot be removed from the cytosol as rapidly as it is released from the sarcoplasmic reticulum
  • this causes a buildup of calcium ions in the cytosol
  • this is why calcium removal is necessary for relaxation (without it, the muscle fiber can’t relax between twitches)
78
Q

what is tetanus?

A
  • occurs when a muscle is being stimulated at high frequencies
  • tetanus is the point when summation reaches a peak and plateaus = the tension is relatively constant
79
Q

what is incomplete tetanus? how does this occur?

A
  • the frequency of stimulation is too low so the muscle is able to briefly relax between each stimuli = causes small oscillations
  • causes the muscle fibre not to fire at maximum value
  • the peaks are only reached when calcium levels are great enough to saturate troponin, and move tropomyosin, exposing all myosin-binding sites on actin = cross bridging can occur
80
Q

what is complete tetanus? how does this occur?

A
  • if the frequency of stimulus is high enough then the muscle never gets an opportunity to relax
    -in this state, the muscle is contracting at maximal force and remains contracting as long as the high-frequency stimulation continues.
  • occurs because calcium levels are great enough to continually saturate troponin such that all myosin-binding sites on actin are continually exposed = continuous cross bridging
81
Q

what is the length-tension curve?

A

the visual representation of how the force of contraction varies when the length of a muscle fiber increases or decrease beyond optimum length

82
Q

potential differences in motor units

A
  • the number of motor units varies in different muscle
  • the size of motor units varies
  • the fiber diamter (and strength) varies in a motor unit
83
Q

what are the different sizes of motor units?

A

size of motor unit:
- small = for delicate movements
- large = for strength movements

diameter of motor unit:
- small = for weaker movements
- large = for stronger movements

84
Q

what is the size principle?

A
  • the order of motor unit recruitment is related to the size of motor units
    –> small units are recruited first = small neurons excited first
    –> large units are recruited last = large neurons are excited after (via spatial and temporal summation)
  • larger units are recruited last because they are harder to depolarize to threshold and require greater excitatory synaptic input in order to fire
85
Q

what is asynchronous recruitment?

A
  • the idea that motor units fire at different times (some are active while others are inactive to rest)
  • this prevents fatigue while maintain contraction of a muscle
  • as motor units fatigue, the body is unable to maintain the same tension on, the muscle so the force output decreases
86
Q

what is the velocity of shortening? what were the findings?

A
  • defined as the rate of change of the distance shortened
  • a muscle is stimulated to contract isotonically to measure the muscles velocity of shortening
  • found 3 effects
    (1) the latent period of shortening increases with increasing load
    (2) the duration of shortening decreases with increasing load
    (3) the velocity of shortening muscle decreases with increasing load (as something gets heavier, it can’t be lifted as quickly)
87
Q

what is the relationship between load and velocity?

A
  • as the load increases, the velocity of shortening gradually decreases
  • velocity eventually reaching zero when the load is equal to or greater than the maximum tension that can be generated by the muscle
  • velocity of shortening is greatest when no load is placed on the muscle
88
Q

key aspects of neural control of skeletal muscles

A
  • upper motor neurons in the CNS influence the activity of lower motor neurons and skeletal muscles = send facilitatory or inhibitory signals to control motor activity
  • the motor center in the CNS serves as the command center for voluntary muscle contraction/movements
  • neural control is also influenced by continuous sensory feedback from muscles and surrounding tissues via sensory receptors
89
Q

what are the different proprioceptors that help with neural control?

A
  • muscle spindle apparatus
    –> sensory receptor located in skeletal muscle that monitor changes in muscle length like stretching or contracting
  • golgi tendon organs
    –> sensory receptor located near the junction between muscle and tendon that detects changes in muscle tension
  • joint receptors
    –> sensory receptor located in capsules and ligaments that monitor the position of joints and give information about limb position in space
90
Q

what is the pathway for skeletal muscle reflexes?

A
  • proprioceptors located in skeletal muscle, joint capsules and ligament send input signals to the CNS through sensory neurons
  • the CNS integrates the input signal
  • somatic motor neurons carry output signals via alpha motor neurons
  • effector organs receiving input are contractile muscle fibers or extrafusal muscle fibers
91
Q

what is a monosynaptic reflex in skeletal muscle?

A
  • a reflex that has a single synapse between the afferent and efferent neuron
92
Q

what is a polysynaptic reflex in skeletal muscle?

A
  • a reflex with two or more synapses
  • the somatic motor reflex has both synapses in the CNS
93
Q

types of fibers in muscle spindle receptors

A

1) intrafusal fibers
- specialized muscle fibers found within the muscle spindle
- are the contractile cells of the muscle spindle
- adjust the sensitivity of the muscle to stretch
- innervated by gamma motor units

2) extrafusal fibers
- are the regular, contractile muscle fibers that generate force and produce movement.
- responsible for skeletal muscle contraction
- innervated by alpha motor neurons

94
Q

2 types of sensory endings of muscle spindles

A

(1) an annulospiral ending
- is wrapped around the central bag area
- is connected to type Ia afferent fibers

(2) flower-spray endings
- located to the side of the central bag of certain muscle spindles
- connected to type II afferent fibers

95
Q

what are alpha and gamma motor neurons?

A

alpha motor neurons (fast)
- innervate extrafusal fibers
- responsible for initiating contraction of skeletal muscles

gamma motor neurons (slow):
- innervate intrafusal fibers
- responsible for inducing some level of tension
- increases sensitivity of a muscle to passive stretch and enhances proprioceptive feedback

96
Q

how do muscle spindles respond to changes in muscle length?

A
  • when a muscle is stretched, the intrafusal fibers are stretched.
  • this activates the receptors, causing the frequency of action potentials to increase in proportion to the degree of stretch
  • likewise, a decrease in the length of the muscle, such as occurs during muscle contraction, decreases the frequency of action potentials in the afferent neurons
  • in this case, contraction of muscle fibers causes the muscle spindle to go slack, which would make them inefficient detectors of any further changes in muscle length
  • to maintain their effectiveness (and length), gamma motor neurons stimulate contraction of intrafusal fibers
97
Q

what is the importance of coactivation of alpha and gamma motor neurons in muscle spindles?

A
  • they work together to maintain spindle function when a muscle contracts
  • ensures that muscle spindles maintain sensitivity to stretch over a wide range of muscle lengths
  • helps to maintain normal muscle tone by preventing the muscle spindle from going slack during periods of muscle contraction
98
Q

what happens when alpha and gamma motor neurons are coactivated?

A
  • during voluntary muscle contraction, alpha and gamma motor neurons are coactivated by upper motor neurons to cause contraction of extrafusal and intrafusal muscle fibers almost simultaneously
  • because axons of alpha motor neurons are larger in diameter than gamma motor neurons, action potentials will be conducted to the extrafusal fibers more quickly than to the intrafusal fibers
  • the extrafusal fibers will contract, creating slack on the muscle spindle, which in turn responds with a decrease in the frequency of action potentials in the afferent neuron.
  • however, the intrafusal fibers contract, removing the slack in the muscle spindle.
  • in this manner, the muscle spindle is reset to detect any further changes in muscle length
99
Q

what are golgi tendon organs?

A
  • they are sensory capsules within tendons
  • located in series with muscle fibers and detect muscle tension
100
Q

what is the golgi tendon organ reflex?

A

the golgi tendon organ will inhibit a muscle from creating any force (causing it to relax) if there is too much muscle tension to protect from injury

  • when muscle contraction stretches the tendon, golgi tendon organs are activated and a reflex occurs
  • when the tension in the muscle reaches a certain threshold, golgi tendon organs send inhibitory signals to the alpha motor neurons that innervate the muscles
  • this reflex relaxes the muscle and limits excessive muscle contraction
101
Q

what are the 3 types of movement

A

1) reflex
2) voluntary
3) rhythmic

102
Q

what is smooth muscle?

A
  • the type of muscle found in internal organs, blood vessels, and other structures that are not under voluntary control
  • the fibers are arranged in layers (circular and/or longitudinal)
  • lacks the striations (lines)
103
Q

what are the characteristics of smooth muscle?

A
  • important for homeostasis
  • has great ability to stretch
  • low fatiguability
  • controlled by hormones, paracrines and autonomic nervous system
104
Q

how is smooth muscle organized?

A
  • smooth muscle consists of thick and thin filaments that are not arranged into sarcomeres giving it a non-striated pattern
  • filaments tend to run obliquely in various directions, which means that contraction occurs along several axes
105
Q

what are dense bodies?

A
  • points where the thin filaments (actin) are anchored within the muscle cell
  • they transmit contractile force to the cell’s exterior
106
Q

how is smooth muscle categorized?

A
  • by location
  • by contraction pattern
  • by their communication
107
Q

where is smooth muscle found?

A

1) vascular (walls of blood vessels)
2) gastrointestinal (wall of digestive tract and organs)
3) urninary (walls of bladder and ureters)
4) respiratory (airway passages)
5) reproductive
6) ocular

108
Q

how does smooth muscle contract?

A
  • uses actin/myosin cross bridging to create force
  • contraction is initiated by the release Ca2+
109
Q

what are the steps of excitation-contraction coupling in smooth muscle?

A
  • most Ca2+ ions come from outside the cell as a result of voltage gated calcium channels in the plasma membrane
  • Ca2+ triggers the release of more calcium from the sarcoplasmic reticulum
  • calcium binds to calmoduilin (there is no evidence of troponin and tropomyosin)
  • The binding triggers a conformational change that causes the calcium/calmodulin complex to bind to and activate an enzyme called myosin light chain kinase (MLCK)
  • MLCK catalyzes the phosphorylation of myosin crossbridges, activating the crossbridges and thereby initiating crossbridge activity
110
Q

how does smooth muscle relax?

A
  • the phosphate groups attached to myosin are covalently bound and do not dissociate readily
  • to terminate the cross bridge cycle, the phosphatase enzyme removes phosphate from myosin
  • phosphatases compete with MLCK so activation of myosin occurs only when enough calcium is present to activate MLCK to a degree sufficient to overcome the phosphatase action
  • Ca2+ is removed from the cytoplasm via ATPase and sodium/potassium counter transport
111
Q

contraction time of smooth vs skeletal muscle

A
  • smooth muscle is slower to contract
  • Myosin ATPase activity in smooth muscle is anywhere from 10 to 100 times slower than the corresponding activity in skeletal muscle
112
Q

what is the concept of neural regulation of smooth muscle contraction

A
  • innervated by the autonomic nervous system (sympathetic or parasympathetic or both)
  • can be excitatory or inhibitory
  • the responses of smooth muscle depends on the of neurotransmitter receptors found on the muscle cells
  • neurotransmitter is released from varicosities along the axons