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HLSC 126 - Human Physiology I > Chapter 8 > Flashcards

Chapter 8 Flashcards

1
Q

Voluntary Muscles

A

-controlled by the somatic nervous system
-skeletal muscle

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2
Q

Involuntary Muscles

A

-innervated by autonomic nervous system
-cardiac muscle
-smooth muscle

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3
Q

Striated Muscle

A

-alternating light and dark bands are seen under microscope
-overlapping proteins
-skeletal muscle
-cardiac muscle

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4
Q

Unstriated Muscle

A

-smooth appearance; no bands
-smooth muscle

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5
Q

Skeletal Muscle

A

-most abundant
-32-40% of body weight
-make up the muscular system

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6
Q

Muscle Fibre

A

-single skeletal muscle cell
-muscle consists of several muscle fibres bundled together via connective tissue

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7
Q

Myoblasts

A

-smaller cells that make muscle fibres during embryonic development
-have multiple nuclei in a single muscle cell
-high amounts of mitochondria to meet energy demands

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8
Q

Myofibrils

A

-predominant structural feature of a muscle fibre
-80% of muscle fibre volume

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9
Q

Sarcolemma

A

-the plasma membrane

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10
Q

T-Tubules

A

-aka transverse tubules
-dips or hollow regions at the junction of an A band and an I band
-run perpendicular to the surface of the muscle cell membrane
-action potentials spread here to interior of muscle fibre

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11
Q

Presence of Nuclei

A

-muscle fibres have their own nucleus
-hence they can regenerate

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12
Q

Presence of Mitochondira

A

-in high amounts to meet energy demands

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13
Q

Skeletal Muscle Organization

A

Whole muscle (organ)➡️muscle fibre (cell)➡️myofibril (specialized intercellular structure)➡️thick and thin filaments (cytoskeletal elements)➡️myosin and actin (protein molecules)

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14
Q

Connective Tissue Covering

A

-covers each muscle
-primarily collagen and to the lesser extent, elastin
-provides structure to the muscle
-allows transfer of force to the bone
-tension for movement/stabilization

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15
Q

Epimysium

A

-covers whole muscle

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16
Q

Peromysium

A

-divides muscle fibres into bundles

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17
Q

Endomysium

A

-covers each muscle fibre

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18
Q

Tendons

A

-connect muscle to bone

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19
Q

Glycogen Reserves

A

-glycogen breaks down to produce glucose
-glucose is the substrate for ATP production

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20
Q

Sarcoplasmic Reticulum (SR)

A

-modified smooth endoplasmic reticulum
-stores calcium in terminal cisternae (aka lateral sacs)

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21
Q

Role of Calcium

A
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22
Q

Proteins

A

-make up contractile and regulatory regions

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23
Q

Contractile Proteins

A

-form filaments
-actin and myosin

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24
Q

Thick Filaments (myosin)

A

-assemblies of myosin protein
-look like golf clubs
-250 to 300
-head has ATP and actin binding sites
-hinge region allows for binding to occur and cross bridges to from
-considered a motor protein

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25
Q

Thin Filaments (actin)

A

-assemblies of actin protein
-pearl chain
-actin is the primary structural component of thin filaments
-bulbs have myosin binding sites
-thin filament also consists of troponin and tropomyosin

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26
Q

Cross Bridge

A

-where actin and myosin join together
-myosin heads
-results in contraction of the muscle fibre

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27
Q

Regulatory Proteins

A

-troponin and tropomyosin

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28
Q

Tropomyosin

A

-cover/hide the actin binding site on thin filaments
-blocks action that leads to muscle contraction

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29
Q

Troponin

A

-binds to calcium ions
-has three polypeptide units with three different binding sites, one for each: tropomyosin, calcium, actin
-exposes the actin binding site so the cross bridge can form

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30
Q

Binding of Troponin Units

A

-when troponin not bound to calcium: the protein stabilizes tropomyosin, blocking binding sites
-when calcium binds to troponin, protein shape is changes so tropomyosin slips away from blocking position
-this unblocking forms the cross bridge, then the contraction

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31
Q

Accessory Proteins

A

-nebulin and titin

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32
Q

Nebulin

A

-runs through thin filaments to stabilize them

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33
Q

Titin

A

-runs through thick filament to stabilize it
-largest protein in the body
-30 000 amino acid chain
-acts like a spring to augment muscle elasticity

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34
Q

Dystrophin Protein

A

-stabilizes entire structure
-attaches to sarcolemma

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35
Q

Sarcomere

A

-single unit of contraction
-functional unit of skeletal muscle (smallest component that can perform all the functions)

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36
Q

Z Lines

A

-zig zag line of proteins
-in the middle of each I band
-where thin filaments attach/anchor
-sarcomeres reside between the two Z lines

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37
Q

I Band

A

-remaining portion of the thin filament that does not project into the A band
-actin/thin filament

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38
Q

M Line

A

-middle line
-supporting proteins that hold the thick filaments together vertically

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39
Q

A Band

A

-overlapping region
-made of a stacked set of thick filaments
-thick filaments extend entire width of A band

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40
Q

H Zone

A

-lighter area in the middle of the A band where the thin filaments don’t reach
-central portions of thick filaments found in this region

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41
Q

Light Regions

A

-not over lapping

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42
Q

Dark Regions

A

-where thin and thick filaments overlap

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43
Q

Neuromuscular Junction (CH 5)

A

-gets excited with acetylcholine
-starts an action potential which originated as a graded potential

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44
Q

Sarcoplasmic Reticulum and T-Tubule Receptor Coupling

A

-are both in close proximity to each other
-both have receptors
that snap together like buttons
-troponin binds to the releases calcium ions (released from lateral sacs)
-tropomyosin is removed from the actin binding site
-several cross bridges are formed:)

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45
Q

Sarcoplasmic Reticulum and Contraction

A

-contains 4 receptor proteins that join with the T Tubule receptors
-“ryanodine proteins” aka foot proteins (calcium release channels)
-get excited by action potential

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46
Q

T-Tubules and Contraction

A

-contain 4 receptors that join with SR receptors
-“dihydropyridine” aka DHP receptors
-leads to the release of calcium

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47
Q

Power Stroke

A

-caused by cross bridge bending
-uses ATP constantly
-SR releases calcium into sarcoplasm
-hydrolysis of ATP transfers energy to myosin head
-myosin heads bind to actin
-sarcomere pulled inward
-fresh ATP binds to myosin head and detaches it from actin

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48
Q

Cross Bridge Cycling

A

-pulls thin filaments inward relative to stationary thick filaments
-one myosin head attaches to actin at a time
-bridge changes shape and bends inward and pulls thin filament inward
-this cycle repeats and completes shortening
-at the end of one cycle the actin and myosin cross bridge breaks, then it binds to the next molecule
-ie. pulling a rope in hand over hand

49
Q

What prevents the thin filaments from slipping away?

A

-cross bridges don’t stroke in unison
-it is a staggered system between the six surrounding thin filaments
-some hold on while others let go

50
Q

Sliding Filament Theory

A

-increase in calcium starts filament sliding
-thin filaments on each side of the sarcomere slide inward over stationary thick filaments toward the centre of A band
-sarcomere shortens simultaneously

51
Q

Z Lines during Sliding Filament Mechanism

A

-come closer together

52
Q

I Bands during Sliding Filament Mechanism

A

-become shorter and almost disappear

53
Q

M Line during Sliding Filament Mechanism

A

-remains the same

54
Q

A band during Sliding Filament Mechanism

A

-width remains the same

55
Q

H Zone during Sliding Filament Mechanism

A

-shrinks from over lap

56
Q

Do the thick or thin filaments change length ever?

A

No, they just slide closer together.

57
Q

Where does the energy come from?

A

-the splitting of ATP

58
Q

Role of ATP during Power Stoke

A

-break down of ATP occurs on the myosin cross bridge before it links with actin

59
Q

Role of ATP: Step 1

A

-ADP and P1 remain tightly bound to myosin, the generated energy is stored within the cross bridge
binds with actin molecule

60
Q

Role of ATP: Step 2a

A

-when the muscle fibre is excited, calcium pulls troponin-tropomyosin complex out of its blocking position
-myosin cross bridge

61
Q

Role of ATP: Step 3

A

-contact between myosin and actin “pulls the trigger” causing the cross bridge bending
-inorganic phosphate is released from cross bridge during power stroke
-ADP is released after the power stroke is completed

62
Q

Role of ATP: Step 2b

A

-when muscle is not excited, calcium is not released, blocking position remains, no power stroking takes place

63
Q

Role of ATP: Step 4a

A

-after P1 and ADP are released from myosin following power stroke: myosin ATPase site is free for attachment of another ATP molecule
-cross bridge remains linked until a fresh ATP attached to myosin to detach the cross bridge
-cross bridge is ready for another cycle

64
Q

Role of ATP: Step 4b

A

-if no fresh ATP is available, actin and myosin remain together in RIGOR COMPLEX

65
Q

Rigor Mortis

A

-muscle stiffness upon death
-locking of muscle in place
-no fresh ATP = no movement/separation of cross bridge
-calcium re-uptake doesn’t occur
-enzymatic degradation eats flesh

66
Q

Relaxation

A

-the opposite of contraction
-acetylcholinesterase breaks down ACh at the neuromuscular junction
-action potential stops
-SR and T-tubules release from each other
-no action potential = calcium moves back into SR via the calcium ATPase pump
-tropomyosin back into blocking position
-cross bridge stops

67
Q

Muscle Twitch

A

-a brief, weak contraction
-produced from a single action potential
-too short and weak to be useful
-doesn’t normally take place

68
Q

Twitch Summation

A

-results from sustained elevation of cytosolic calcium
-sustained stimulation of the fibre before it has time to relax
-possible because duration of action potential is shorter than the twitch – action potential needs to finish before next one

69
Q

2 factors to adjust gradation of a muscle

A
  1. number of fibres contracting
  2. firing frequency of each fibre
70
Q

Most Tension

A

-larger muscles have more muscle fibres and hence generate more tension than smaller muscles

71
Q

Motor Neurons

A

-have branches at their ends that supply each group of muscle fibres = motor unit

72
Q

Tetanus (not the infection)

A

-occurs if muscle fibre is stimulated so rapidly that it doesn’t have a chance to relax between stimuli
-sustained contractile activity
-smooth contraction of maximal strength

73
Q

Optimal Muscle Length

A

-form best cross bridges
-lots of power stroking
-myosin heads are in line with actin body
-relationship between length and tension before onset of contraction
-optimal = maximal forced achieved at subsequent tetanic contraction
-more tension achieved when beginning at optimal length

74
Q

Lengths Greater than Optimal Length

A

-thin filaments pulled out from the thick
-decreases number of actin sites available for binding = less tension
-when muscle stretched 70% longer; no sites available = no contraction

75
Q

Less than Optimal Length

A

-less tension because:
1. thin filaments from opposite side are overlapped = less available binding sites
2. ends of thick filaments forced against z lines = further shortening impeded
3. muscle lengths at less than 80%; not as much calcium is released = fewer sites are uncovered

76
Q

Muscle Origin

A

-end of muscle attached to stationary part of the skeleton

77
Q

Muscle Insertion

A

-end of the muscle attached to the skeletal part that moves

78
Q

How is tension created?

A

by the tightening of the series elastic component that are the non-contractile tissues of the muscle (tendons)

79
Q

Isotonic Contraction

A

-equal stretch
-tension is constant
-force production is unchanged
-consists of concentric and eccentric contraction

80
Q

Concentric Contraction

A

-bring weight toward the body
-create tension
-flexion
-usually muscle shortening
-actin pulled together

81
Q

Eccentric Contraction

A

-weight goes away from centre of the body
-extension
-muscle lengthening
-usually results in injury when done poorly
-actin pulled apart

82
Q

Isometric Contraction

A

-length is unchanged
-muscle fibre is prevented from shortening
-tension at constant length
-static
-ie. holding a heavy box in a constant position or plank

83
Q

Dynamic Contraction

A

-changing force contraction
-length changes
-both concentric and eccentric

84
Q

Static Contraction

A

-not in motion contraction
-increased tension but no change in body position

85
Q

Creatine Phosphate

A

-source of energy
-involves the transfer of a high-energy phosphate from creatine phosphate to ADP
-aka creatine kinase enzyme breaks down creatine phosphate to get creatine + ATP

86
Q

Glycolysis

A

-a source of energy
-splitting of glucose into 2 pyruvate molecules
=2 ATP molecules

87
Q

Oxidative Phosphorylation

A

-citric acid/krebs cycle and ETC
-metabolize acetyl CoA to two CO2 molecules, resulting in NADH and FADH2
=34 ATP molecules

88
Q

Creatine as a Supplement

A

-can cause severe GI disturbances
-dehydration
-muscle stores = weight gain

89
Q

3 processes that require ATP

A
  1. provides energy for power stroke
  2. allows bridge to detach so cycle can be repeated
  3. active transport of calcium back to the SR during relaxation
90
Q

Muscle Fibres

A

-classified based on differences in ATP hydrolysis and synthesis

91
Q

Fast Twitch (type II)

A

-2-3x faster
-faster ATP use (splitting)
-faster calcium release
-used occasionally
-ie. pianist
-innervated by a1 motor neurons (are larger)

92
Q

Slow Twitch (type I)

A

-slower in general
-slower ATP use
-slower calcium release
-frequently used
-ie. maintaining posture or walking
-innervated by a2 motor neurons

93
Q

Oxidative Muscle Fibres

A

-need oxygen
-glycolysis, krebs cycle, etc = ATP
-more mitochondria
-high conc. of blood vessels
-increased oxygen
-myoglobin binds to oxygen giving a rich red color
-fatigue less often

94
Q

Glycolytic Muscle Fibres

A

-oxygen doesn’t matter
-stops at glycolysis (anaerobic) = 2 ATP
-less mitochondria
-fewer blood vessels
-lower myoglobin = pale white color
-fatigue more often

95
Q

Types of Muscle fibres

A

-these categories combine to create:
a. slow-oxidative (type 1) fibres
b. fast-oxidative (type 2a) fibres
c. fast-glycolytic (type 2x) fibres

96
Q

Muscle Fatigue

A

-occurs when exercising muscle can no longer respond to stimulation with the same degree of contractile activity
-underlying causes unclear
-2 types: a. central fatigue & b. peripheral fatigue

97
Q

Central Fatigue

A

-CNS no longer adequately activates motor neurons (somatic motor neuron/ANS issue)
-psychological (muscles still physically able to perform)
-monotony - same thing over and over again ie. assembly line

98
Q

Peripheral Fatigue

A

-NMJ is vulnerable (Ch 5)
-SR and T-tubules
-can be a lack of ATP
-build up of lactic acid
-depleted glycogen levels

99
Q

Circumventing Fatigue - EPOC

A

Excess
Post-exercise
Oxygen
Consumption
aka recharging

100
Q

Control of Motor Movement

A

-three levels of input can control motor-neuron output:
1. input from afferent neurons
2. input from primary motor cortex
3. input from brain stem

101
Q

Afferent Neurons

A

-input from afferent neurons usually through intervening interneurons at the level of the spinal cord: spinal reflexed
-ie. reflexes

102
Q

Primary Motor Cortex

A

-fibres originating from neuronal cell bodies, pyramidal cells, descend directly to terminate on motor neurons without synaptic interruption
-basal nuclei: ie. parkinsons
-thalamus: a “loop”
-cerebellum: skilled, procedural memories

103
Q

Brainstem

A

-midbrain
-pons
-MO
-final link in multineuronal pathways

104
Q

Muscular Dystrophy

A

-genetic disease; carried in x chromosome, males more prone
-missing dystrophin protein that attaches sarcomere to sarcolemma
-sarcomere deforms when it tries to shorten
-affects hip muscles
-wheelchair bound
-leads to death
-gene therapy: manipulate gene that makes dystrophin

105
Q

Parkinsons Disease

A

-basal nuclei disorder
-tremors, reptilian stare, shuffled gait, confusion, cognitive failure, sleep issues
-treatment = leva dopa

106
Q

Muscle Spindle Structure

A

-consist of collections of specialized muscle fibres known as intrafusal fibres
-each spindle has its own private efferent and afferent nerve supply
-pay a key role in stretch reflex: how much a muscle can stretch

107
Q

Intrafusal Fibres

A

-lie within spindle shaped connective tissue capsules, parallel to extrafusal fibres
-has noncontractile central portion
-contractile portion is limited to the ends

108
Q

Extrafusal Fibres

A

-contain contracile elements (myofibrils) throughout its entire length

109
Q

Pathways of the muscle spindle

A

-CNS➡️ a) gamma motor neuron➡️intrafusal fibre (receptor) or b) alpha motor neuron➡️extrafusal fibre

110
Q

Golgi Tendon Organ

A

-in the tendons of the muscle
-respond to changes in tension rather than length
-consist of ending of afferent fibres intertwined with connective tissue = tendon
-tension causes golgi tendon organ receptors stretch causing afferent fibres to fire at the frequency of the developed tension
-reaches conscious awareness
-aware of tension but not length
-protect from injury: muscle stops creating force it can’t handle

111
Q

Smooth Muscle

A

-found in the hollow tubes of internal organs
-no striations
-no sarcomere structure
-have actin and myosin
-form cross bridges
-no troponin; instead calmodulin
-has tropomyosin to hide actin binding site
-poor SR (stores calcium) and no T-tubules
-spindle shaped cells with a single nucleus arranged in sheets
-no z lines; instead has button like proteins called Dense bodies that hold actin and myosin together called

112
Q

Smooth Muscle: Mechanism of Contraction

A

-globular structure creates forward motion
-calmodulin binds with calcium from SR and ECF
-calmodulin binds to inactive myosin light chain kinase (MLC kinase) enzyme and activates it
-breaks down ATP to do a power stroke (ATP = ADP + P1)
-activates myosin head which binds to actin
=cross bridge

113
Q

2 Types of Smooth Muscle

A

a. multi unit smooth muscle
b. single unit smooth muscle

114
Q

Multi Unit Smooth Muscle

A

-neurogenic (contraction is nerve produced; same as skeletal muscle)
-consists of discrete units that must be separately stimulated to contract
-found in: iris of the eye, large blood vessels, muscles in eye that adjust the lens

115
Q

Varicosity

A

-stores neurotransmitters
-open during action potentials

116
Q

Single Unit Smooth Muscle

A

-self-excitable
-aka visceral smooth muscle
-fibres become excited and contract as a single unit
-cells are electrically linked by gap junctions
-also described as a functional syncytium (1 cell)
-contraction is slow and energy efficient
-found in all hollow organs (ie. GI tract)

117
Q

Pacemaker Potentials

A

-membrane potential gradually depolarizes on its own because of shifts in passive ionic fluxes
-when depolarized to threshold, action potential is initiated
-after repolarizing, depolarizes again
-cyclically generates action potentials
-dont have to reach tetanus
-stay in cross bridge longer

118
Q

Slow Wave Potential

A

-gradually alternating hyperpolarizing and depolarizing swings in potential

119
Q

Cardiac Muscle

A

-found only in walls of the heart
-striated
-cells interconnected by gap junctions
-fibres joined in branching network
-innervated by ANS
-held together by inter calculated discs

HLSC 126 - Human Physiology I (5 decks)

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