Muscle Flashcards

1
Q

What is an agonist muscle?

A

Prime mover of any skeletal muscle movement

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2
Q

What is an antagonist muscle?

A

Flexors and extensors that act on the same joint to produce opposite actions

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3
Q

What is the epimysium?

A

Tendon connective tissue extends muscle in an irregular arrangement to form this fibrous sheath

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4
Q

What are the columns of muscle fibers inside the epimysium?

A

Fascicles

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5
Q

What is each fascicle surrounded by?

A

Perimysium

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6
Q

What are the striations in muscle’s appearance produced by?

A

Alternating A and I bands

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7
Q

What stimulates the muscle fiber to contract?

A

Motor neuron stimulates muscle fiber to contract by liberating Ach at the neuromuscular junction (motor end plate)

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8
Q

What is a motor unit?

A

Each somatic motor neuron, together with all of the muscle fibers that it innervates

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9
Q

What is each muscle fiber innervated by?

A

Each muscle fiber receives a single axon terminal from a somatic motor neuron
-Each axon can produce a number of collateral branches to innervate an equal number of muscle fibers

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10
Q

How is innervation ratio related to strength of muscle contraction?

A

Small motor units -> fine neural control (one neuron per small amount of muscle fibers), i.e. in extraocular muscles that position eyes
-Larger motor units (recruitment) -> stronger and more powerful contractions, i.e. in gastrocnemius

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11
Q

What is each myofibril composed of?

A

Myofilaments

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12
Q

What are the thick filaments primarily composed of?

A

Myosin

-Thick filaments are in A bands

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13
Q

What are then thin filaments primarily composed of?

A

Actin

  • Thin filaments are in I bands
  • Center of each I band is Z disc
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14
Q

What is a sarcomere?

A

Subunit from Z disc to Z disc

-M lines are produced by protein filaments in a sarcomere, they anchor myosin during contraction

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15
Q

What is titin?

A

A type of elastic protein that runs through the myosin from the M lines to the Z lines
-Contributes to elastic recoil of muscle

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16
Q

What is the sliding filament theory of contraction?

A

Muscle contraction results from shortening of the sarcomeres, which is produced not by shortening of filaments but rather by the sliding of thin filaments over and between thick filaments (action of cross bridges)

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17
Q

What causes a myofiber to shorten?

A

Shortening of the distance from Z disc to Z disc

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18
Q

Which bands shorten during contraction?

A
I bands (distance between A bands of successive sarcomeres) and H bands (thick filaments, contain only myosin) decrease in length
-A bands do NOT shorten, they move closer together (toward the origin of the muscle)
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19
Q

What action produces the sliding of the filaments?

A

Action of numerous cross bridges that extend out from the myosin toward the act
-These cross bridges are part of the myosin proteins that extend from the axis of the thick filaments to form “arms” that terminate in globular “heads”

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20
Q

What serves as cross bridges in the myosin protein?

A

Its 2 globular heads

  • Each myosin head has an ATP-binding site and an actin-binding site
  • The heads function as myosin ATPase enzymes, splitting ATP into ADP and Pi
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21
Q

When are the myosin heads attached to actin?

A

During contraction only

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22
Q

What must occur before the myosin heads can bind to actin?

A

ATP must be hydrolyzed to ADP and Pi

-Phosphate binds to the myosin head, phosphorylating it -> “cocked” conformation -> energized myosin can bind to actin

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23
Q

What happens once the myosin head binds to actin?

A

A cross bridge is formed, the bound Pi is released (myosin head becomes dephosphorylated) -> conformational change in the myosin -> cross bridge produces a power stroke
-This is the force that pulls the thin filaments toward the center of the A band

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24
Q

After the power stroke is completed, what is required for the myosin head to break its bond with actin?

A

The bound ADP is released as a new ATP molecule binds to the myosin head -> ready to bind again

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25
Q

Why is the action of the cross bridges described as asynchronous?

A

Only 50% of the cross bridges are attached at any given time

-Like the actions of a team engaged in tug-of-war

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26
Q

When is the cross bridge not attached to actin?

A

Resting fiber

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27
Q

What works together to regulate the attachment of cross bridges to actin, and thus serve as a switch for muscle contraction and relaxation?

A

Tropomyosin (lies within groove between double row of G-actin) and troponin (attached to tropomyosin)

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28
Q

How do the troponin and tropomyosin attach during muscle relaxation?

A

When sarcoplasmic [Ca2+] is low, Ca2+ is not bound to troponin -> tropomyosin is in a position that blocks myosin binding to actin -> prevent muscle contraction

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29
Q

What is the role of Ca2+ in muscle contraction?

A

Ca2+ attaches to troponin -> movement of troponin-tropomysin complex -> exposes binding sites on actin -> myosin cross bridges can attach to actin and undergo a power stroke

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30
Q

What happens when a somatic motor neuron releases ACh?

A

Binds to nicotinic ACh receptors in the sarcolemma, causing a depolarization that stimulates voltage-gated channels -> Na+ diffuses in, producing depolarizing stimulus (+ ions are attracted to negative plasma membrane) -> if depolarization sufficient, threshold occurs -> APs

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31
Q

Once an AP is produced what happens to produce muscle contraction?

A

APs travel down sarcolemma and T tubules -> stimulates opening of voltage-gated Ca2+ channels in T tubulues -> these channels are mechanically coupled to Ca2+ release channels in the SR, causes them to open -> Ca2+ diffuses out of the SR so it can bind to troponin in the myofibrils -> muscle contraction

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32
Q

T or F: As long as APs continue to be produced–which is as long as neural stimulation of the muscle is maintained–the Ca2+ release channels in the SR will remain open, Ca2+ will passively diffuse out of the SR, and the SR [Ca2+] will remain high. Thus, Ca2+ will remain attached to troponin, and the cross-bridge cycle will continue to maintain contraction.

A

True

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33
Q

What is necessary for the muscle to relax?

A

APs must cease

1) ACh-esterase degrades ACh
2) Ca2+ release channels close -> Ca2+ pumped back into SR through Ca2+-ATPase pumps
3) Choline recycled to make more ACh

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34
Q

What is a twitch?

A

When the muscle is stimulated with a single electric shock of sufficient voltage, it quickly contracts and relaxes

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35
Q

What is summation?

A

If second electrical shock is administered before complete relaxation of muscle -> produces a second twitch that may partially “ride piggyback” on the first

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36
Q

What is incomplete tetanus?

A

If the stimulator is set to deliver an increasing frequency of electric shocks automatically, the relaxation time between successive twitches will get shorter and shorter as the strength of contraction increases in amplitude

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37
Q

What is complete tetanus?

A

At a particular “fusion frequency” of stimulation, there is no visible relaxation between twitches -> contaction is smooth and sustained
-If the stimulation is continued, the muscle will demonstrate fatigue

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38
Q

What is treppe (the staircase effect)?

A

If a series of electrical shocks are delivered at maximum voltage -> each shock produces a separate twitch, each of the twitches evoked will be successively stronger, up to a higher maximum

  • Due to increase in intracellular Ca2+
  • Represents “warm-up”
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39
Q

What must happen in order for muscle fibers to shorten when they contract?

A

They must generate a force that is greater than the opposing forces that act to prevent movement of the muscle’s insertion

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40
Q

What is isotonic contraction?

A

Force of contraction remains constant throughout the shortening process
-Velocity of muscle shortening decreases as the load increases

41
Q

What is isometric contraction?

A

Length of muscle fibers remain constant, if the number of muscle fibers activated is too few to shorten the muscle
-Velocity of shortening is 0

42
Q

What is the force-velocity curve?

A

Inverse relationship between force opposing muscle contraction and velocity of muscle shortening

43
Q

What is an eccentric contraction?

A

Force exerted on a muscle to stretch is greater than the force of muscle contraction -> muscle will lengthen as it contracts

44
Q

Why do tendons provide a series-elastic component?

A

Non-contractile tendons and connective tissue absorb tension as the muscle contracts

  • Tendons have elasticity (resist distension) and display recoil (spring back to resting length)
  • Tendons first must be pulled tight, before the muscle contraction results in shortening
45
Q

What is the strength of muscle contraction influenced by?

A
  • # of fibers within the muscle that are stimulated to contract
  • Frequency of stimulation
  • Thickness of each muscle fiber (thicker fibers have more myofibrils and can exert more power)
  • Initial length of muscle fiber
46
Q

What is ideal resting length?

A

Length which can generate maximum force

  • If overlap is too small -> few cross bridges can attach
  • If there is no overlap -> no cross bridges can attach -> zero tension
47
Q

What do increases or or decreases in muscle lengths result in?

A

Rapid decreases in tension

48
Q

When is maximum relative tension achieved?

A

When the muscle is 100% to 120% of its resting length

49
Q

In the first 45-90 secs of moderate to heavy exercise how do skeletal muscles get ATP?

A

Anaerobic respiration

  • Cardiopulmonary system requires this amount of time to increase O2 supply to exercising muscles
  • If exercise is moderate, aerobic respiration contributes the majority of skeletal muscle requirements following the 1st 2 mins of exercise
50
Q

What is the maximum oxygen uptake (aerobic capacity)?

A

Maximum rate of oxygen consumption (V02 max) determined by age, gender, and size

51
Q

What does exercise of greater intensity and duration cause?

A

Increased blood glucose uptake into the exercising muscles

  • Due to the ability of muscle contraction to stimulate the insertion of GLUT4 carriers into the sarcolemma
  • Also promotes inhibition of glycogenesis and increased uptake and oxidation of fatty acids
  • Liver increases glycogenolysis
52
Q

Where is most energy derived from during light exercise?

A

Aerobic respiration of fatty acids

-Derived mainly from stored fat in adipose tissue and to a lesser extent from triglycerides stored in the muscle

53
Q

Where is most energy derived from during moderate exercise?

A

Equally from aerobic respiration of fatty acids and glucose

54
Q

What is the lactate (or anaerobic) threshold?

A

The percentage of the maximal oxygen uptake at which a significant rise in blood lactate levels occurs
-In a healthy person: a significant amount of blood [lactate] appears when exercise is performed at about 50-70% of V02 max

55
Q

When a person stops exercising, why does he/she continue to breathe heavily for some time afterward?

A

The rate of oxygen uptake is returning slowly to pre-exercise levels
-This extra oxygen is used to repay the “oxygen debt” incurred during exercise

56
Q

What does the oxygen debt include?

A
  • Oxygen that was withdrawn from savings deposits (hemoglobin in blood and myoglobin in muscle)
  • The extra oxygen required for metabolism by tissues warmed during exercise
  • The oxygen needed for metabolism of the lactic acid produced during anaerobic metabolism
57
Q

What serves as a muscle reserve of high-energy phosphate, used for the rapid formation of ATP?

A

Phosphocreatine (creatine phosphate)

  • [Phosphocreatine] in muscle cells 3x higher
  • So efficient that even though rate of ATP breakdown rapidly increases from rest to exercise, muscle ATP concentrations decrease only slightly in aerobically adapted muscle
58
Q

During times of rest how can the depleted reserve of phosphocreatine be restored?

A

By the reverse reaction: phosphorylation of creatine with phosphate derived from ATP

59
Q

How can skeletal muscle fibers be divided?

A

Based on contraction speed:

  • Slow-twitch (type I fibers) vs. fast-twitch (type II fibers)
  • Differences due to different myosin ATPase isoenzymes that are slow or fast
60
Q

Why are slow-twitch (type I fibers) also referred to red fibers? What is characteristic of slow-twitch fibers ?

A

High [myoglobin] ; High oxidative capacity for aerobic respiration, resistant to fatigue, rich capillary supply, numberous mitochondria and aerobic enzymes
-i.e. soleus muscle in the leg

61
Q

Why are fast-twitch (type IIX fibers) also referred to white fibers? What is characteristic of them?

A

Fewer myoglobin; adapted to respire anaerobically, have large stores of glycogen, few capillaries, few mitochondria
-i.e. extraocular muscles that position the eye

62
Q

What is characteristic of the intermediate (type IIA fibers)?

A
  • Great aerobic ability

- Resistant to fatigue

63
Q

T or F: People have the same proportion of fast- and slow-twitch fibers in their muscles.

A

False; people genetically vary tremendously

64
Q

What is muscle fatigue?

A

A reversible, exercise-induced reduction in the ability of a muscle to generate force

65
Q

What is sustained muscle contraction fatigue due to?

A

An accumulation of ECF [K+]

-Repolarization phase of AP

66
Q

During moderate exercise, when does fatigue occur?

A

When slow-twitch fibers deplete their glycogen reserve

-Fast-twitch fibers are recruited -> converting glucose to lactic acid (nterferes with Ca2+ transport)

67
Q

What is central fatigue?

A

Muscle fatigue caused by changes in CNS rather than fatigue of muscles themselves

68
Q

In trained endurance athlete, the maximum O2 uptake during strenuous exercise increases from the average 50 mL of 02/min up to 86 ml of 02/min. What does this adaptation affect?

A
  • Increases lactate threshold (less lactic acid produced -> less fatigue)
  • Increases proportion of energy derived from aerobic respiration of fatty acids
  • Lowers depletion of glycogen stores
  • All fibers adapt to endurance training (increase # of mitochondria)
69
Q

What does endurance training increase?

A

Increase in type IIA fibers and a decrease in type IIX fibers
-Does NOT increase size of muscles

70
Q

What is muscle enlargement produced by?

A

Frequent periods of high-intensity exercise in which muscles work against high-resistance
-Type II fibers become thicker (may split into 2 myofibrils)

71
Q

What is lower motor neuron activity influenced by?

A
  • Sensory feedback from the muscles and tendons
  • Facilitory and inhibitory effects of upper motor neurons (cell bodies in spinal cord and axons within neurons that stimulate muscle contractions)
72
Q

What is said to be the final common pathway by which sensory stimuli and higher brain centers exert control over skeletal movements?

A

Lower motor neurons

73
Q

In order for the NS to control skeletal movements properly, it must continuously receive what sensory feedback information?

A

1) Tension that the muscle exerts on its tendons (provided by the Golgi tendon organs)
2) Muscle length (provided by the muscle spindle apparatus)

74
Q

What does the spindle apparatus function as?

A

Muscle length detector

  • Contains thin muscle cells called intrafusal fibers
  • Spindles insert into tendons on each end of the muscle
75
Q

T or F: Unlike the extrafusal fibers, which contain myofibrils along their entire length, the contractile apparatus is absent from the central regions of the intrafusal fibers.

A

True

-The central, noncontracting part of an intrafusal fiber contains nuclei

76
Q

What are the two types of intrafusal fibers?

A

1) Nuclear bag fibers - nuclei arranged in a loose aggregate in the central regions of the fibers
2) Nuclear chain fibers - nuclei arranged in rows

77
Q

What type of sensory neurons serves the intrafusal fibers and is most stimulated at onset of stretch?

A

Primary, annulospiral sensory endings

-Wrap around the central regions of both nuclear bag and chain fibers

78
Q

What type of sensory neurons serves the intrafusal fibers and responds to tonic (sustained) stretch?

A

Secondary, flower-spray endings

-Located over the contracting poles of nuclear chain fibers

79
Q

When are both types of intrafusal sensory neurons stimulated?

A

Sudden, rapid stretching of a muscle causes spindle to stretch
-Produces more forceful muscle contraction

80
Q

What are the extrafusal fibers?

A

Ordinary muscle fibers outside the spindles

  • Contain myofibrils along entire length
  • Only fibers strong and numberous enough to cause muscle contraction
  • Spindles are arranged in parallel with the extrafusal muscle fibers
81
Q

What are the 2 types of lower motor neurons in the spinal cord?

A

1) alpha motor neurons

2) gamma motor neurons

82
Q

What do the alpha motor neurons innervate?

A

Extrafusal fibers

  • Fast conducting fibers
  • Only stimulation of these neurons cause skeletal muscle movements
83
Q

What do the gamma motor neurons innervate?

A

Intrafusal fibers

  • Too few in # to cause muscle to shorten -> only cause isometric muscle contraction
  • Activity of gamma motor neurons is maintained to keep muscle spindles under proper tension while muscles are relaxed
84
Q

Do upper motor neurons stimulate alpha or gamma motor neurons?

A

Usually stimulate alpha and gamma simultaneously

85
Q

What does the reflex contraction of skeletal muscles occur in response to?

A

Sensory input

-Does not depend on activation of upper motor neurons

86
Q

What is the simplest of all reflexes?

A

Muscle stretch reflex (monosynaptic-stretch reflex)

-Only one synapse within the CNS (sensory neuron directly synapses with the motor neuron)

87
Q

What produces the knee jerk?

A

Monosynaptic-stretch reflex

  • Striking patellar ligamament passively stretches the spindles -> stimulates primary endings in spindles -> activating sensory neurons -> synapse with alpha motor neurons stimulating extrafusal fibers -> isotonic contraction
  • Negative feedback (stretching of muscles stimulates shortening of muscles)
88
Q

What is the Golgi tendon organ reflex?

A

Disynaptic reflex (2 synapses are crossed in CNS)

  • Sensory neurons synapse with interneurons
  • Inhibitory reflex helps prevent dangerous tension on a tendon from excessive muscle contraction, or from muscle contraction that could add to the tension on a tendon during passive stretching of the muscle
89
Q

What is reciprocal innervation?

A

Sensory neuron STIMULATES motor neuron and interneuron -> interneuron INHIBITS motor neurons of antagonistic muscles
-When limb is flexed, antagonistic extensor muscles are passively stretched

90
Q

What is the crossed-extensor reflex?

A

Double reciprocal innervation

  • Affects muscles on the contralateral side of the cord
  • Step on tack -> same foot is withdrawn by contraction of flexors and relaxation of extensors
  • Contralateral leg instead extends to support the body
91
Q

The upper motor neurons influence the lower motor neurons via what?

A

Pyramidal and extrapyramidal tracts

92
Q

How does the cerebellum influence motor activity?

A

Only indirectly (has no no descending tracts)

  • All output is inhibitory
  • Aids motor coordination
93
Q

What area of the brain has profound inhibitory effects on the activity of lower motor neurons?

A

Basal nuclei

-Damage to this area -> increased muscle tone

94
Q

How are cardiac muscle cells similar to skeletal muscle cells?

A
  • Contain actin and myosin filaments arranged in sarcomeres

- Contract by sliding filament mechanism

95
Q

How are cardiac muscle cells different from skeletal muscle cells?

A
  • Short, branched, and interconnected via gap junctions -> APs travel through gap junctions (behaves as one unit; all cells contribute to contraction)
  • Skeletal muscle cells are long, fibers structurally and functionally separated from each other
96
Q

How are smooth muscle cells similar to skeletal muscle cells?

A

Contain actin and myosin that produce contractions

97
Q

How are smooth muscle cells different than skeletal muscle cells?

A
  • Lack sarcomeres
  • Contain > content of actin than myosin (ratio 16:1)
  • Myosin filaments (which are really long) attached at ends of the cell to dense bodies
  • Contains gap junctions
98
Q

What does smooth muscle contraction depend on?

A

Rise in free intracellular Ca2+

  • Ca2+ binds with calmodulin
  • Ca2+ calmodulin complex joins with and activates myosin light chain kinase
  • Myosin heads are phosphorylated
  • Myosin heads binds with actin
99
Q

When does smooth muscle relaxation occur?

A

When [Ca2+] decreases