Chapter 8 Flashcards
(119 cards)
1
Q
Voluntary Muscles
A
-controlled by the somatic nervous system
-skeletal muscle
2
Q
Involuntary Muscles
A
-innervated by autonomic nervous system
-cardiac muscle
-smooth muscle
3
Q
Striated Muscle
A
-alternating light and dark bands are seen under microscope
-overlapping proteins
-skeletal muscle
-cardiac muscle
4
Q
Unstriated Muscle
A
-smooth appearance; no bands
-smooth muscle
5
Q
Skeletal Muscle
A
-most abundant
-32-40% of body weight
-make up the muscular system
6
Q
Muscle Fibre
A
-single skeletal muscle cell
-muscle consists of several muscle fibres bundled together via connective tissue
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
8
Q
Myofibrils
A
-predominant structural feature of a muscle fibre
-80% of muscle fibre volume
9
Q
Sarcolemma
A
-the plasma membrane
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
11
Q
Presence of Nuclei
A
-muscle fibres have their own nucleus
-hence they can regenerate
12
Q
Presence of Mitochondira
A
-in high amounts to meet energy demands
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)
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
15
Q
Epimysium
A
-covers whole muscle
16
Q
Peromysium
A
-divides muscle fibres into bundles
17
Q
Endomysium
A
-covers each muscle fibre
18
Q
Tendons
A
-connect muscle to bone
19
Q
Glycogen Reserves
A
-glycogen breaks down to produce glucose
-glucose is the substrate for ATP production
20
Q
Sarcoplasmic Reticulum (SR)
A
-modified smooth endoplasmic reticulum
-stores calcium in terminal cisternae (aka lateral sacs)
21
Q
Role of Calcium
A
22
Q
Proteins
A
-make up contractile and regulatory regions
23
Q
Contractile Proteins
A
-form filaments
-actin and myosin
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
25
Thin Filaments (actin)
-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
26
Cross Bridge
-where actin and myosin join together
-myosin heads
-results in contraction of the muscle fibre
27
Regulatory Proteins
-troponin and tropomyosin
28
Tropomyosin
-cover/hide the actin binding site on thin filaments
-blocks action that leads to muscle contraction
29
Troponin
-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
30
Binding of Troponin Units
-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
31
Accessory Proteins
-nebulin and titin
32
Nebulin
-runs through thin filaments to stabilize them
33
Titin
-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
34
Dystrophin Protein
-stabilizes entire structure
-attaches to sarcolemma
35
Sarcomere
-single unit of contraction
-functional unit of skeletal muscle (smallest component that can perform all the functions)
36
Z Lines
-zig zag line of proteins
-in the middle of each I band
-where thin filaments attach/anchor
-sarcomeres reside between the two Z lines
37
I Band
-remaining portion of the thin filament that does not project into the A band
-actin/thin filament
38
M Line
-middle line
-supporting proteins that hold the thick filaments together vertically
39
A Band
-overlapping region
-made of a stacked set of thick filaments
-thick filaments extend entire width of A band
40
H Zone
-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
41
Light Regions
-not over lapping
42
Dark Regions
-where thin and thick filaments overlap
43
Neuromuscular Junction (CH 5)
-gets excited with acetylcholine
-starts an action potential which originated as a graded potential
44
Sarcoplasmic Reticulum and T-Tubule Receptor Coupling
-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:)
45
Sarcoplasmic Reticulum and Contraction
-contains 4 receptor proteins that join with the T Tubule receptors
-"ryanodine proteins" aka foot proteins (calcium release channels)
-get excited by action potential
46
T-Tubules and Contraction
-contain 4 receptors that join with SR receptors
-"dihydropyridine" aka DHP receptors
-leads to the release of calcium
47
Power Stroke
-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
48
Cross Bridge Cycling
-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
What prevents the thin filaments from slipping away?
-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
Sliding Filament Theory
-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
Z Lines during Sliding Filament Mechanism
-come closer together
52
I Bands during Sliding Filament Mechanism
-become shorter and almost disappear
53
M Line during Sliding Filament Mechanism
-remains the same
54
A band during Sliding Filament Mechanism
-width remains the same
55
H Zone during Sliding Filament Mechanism
-shrinks from over lap
56
Do the thick or thin filaments change length ever?
No, they just slide closer together.
57
Where does the energy come from?
-the splitting of ATP
58
Role of ATP during Power Stoke
-break down of ATP occurs on the myosin cross bridge before it links with actin
59
Role of ATP: Step 1
-ADP and P1 remain tightly bound to myosin, the generated energy is stored within the cross bridge
binds with actin molecule
60
Role of ATP: Step 2a
-when the muscle fibre is excited, calcium pulls troponin-tropomyosin complex out of its blocking position
-myosin cross bridge
61
Role of ATP: Step 3
-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
Role of ATP: Step 2b
-when muscle is not excited, calcium is not released, blocking position remains, no power stroking takes place
63
Role of ATP: Step 4a
-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
Role of ATP: Step 4b
-if no fresh ATP is available, actin and myosin remain together in RIGOR COMPLEX
65
Rigor Mortis
-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
Relaxation
-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
Muscle Twitch
-a brief, weak contraction
-produced from a single action potential
-too short and weak to be useful
-doesn't normally take place
68
Twitch Summation
-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
2 factors to adjust gradation of a muscle
1. number of fibres contracting
2. firing frequency of each fibre
70
Most Tension
-larger muscles have more muscle fibres and hence generate more tension than smaller muscles
71
Motor Neurons
-have branches at their ends that supply each group of muscle fibres = motor unit
72
Tetanus (not the infection)
-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
Optimal Muscle Length
-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
Lengths Greater than Optimal Length
-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
Less than Optimal Length
-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
Muscle Origin
-end of muscle attached to stationary part of the skeleton
77
Muscle Insertion
-end of the muscle attached to the skeletal part that moves
78
How is tension created?
by the tightening of the series elastic component that are the non-contractile tissues of the muscle (tendons)
79
Isotonic Contraction
-equal stretch
-tension is constant
-force production is unchanged
-consists of concentric and eccentric contraction
80
Concentric Contraction
-bring weight toward the body
-create tension
-flexion
-usually muscle shortening
-actin pulled together
81
Eccentric Contraction
-weight goes away from centre of the body
-extension
-muscle lengthening
-usually results in injury when done poorly
-actin pulled apart
82
Isometric Contraction
-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
Dynamic Contraction
-changing force contraction
-length changes
-both concentric and eccentric
84
Static Contraction
-not in motion contraction
-increased tension but no change in body position
85
Creatine Phosphate
-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
Glycolysis
-a source of energy
-splitting of glucose into 2 pyruvate molecules
=2 ATP molecules
87
Oxidative Phosphorylation
-citric acid/krebs cycle and ETC
-metabolize acetyl CoA to two CO2 molecules, resulting in NADH and FADH2
=34 ATP molecules
88
Creatine as a Supplement
-can cause severe GI disturbances
-dehydration
-muscle stores = weight gain
89
3 processes that require ATP
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
Muscle Fibres
-classified based on differences in ATP hydrolysis and synthesis
91
Fast Twitch (type II)
-2-3x faster
-faster ATP use (splitting)
-faster calcium release
-used occasionally
-ie. pianist
-innervated by a1 motor neurons (are larger)
92
Slow Twitch (type I)
-slower in general
-slower ATP use
-slower calcium release
-frequently used
-ie. maintaining posture or walking
-innervated by a2 motor neurons
93
Oxidative Muscle Fibres
-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
Glycolytic Muscle Fibres
-oxygen doesn't matter
-stops at glycolysis (anaerobic) = 2 ATP
-less mitochondria
-fewer blood vessels
-lower myoglobin = pale white color
-fatigue more often
95
Types of Muscle fibres
-these categories combine to create:
a. slow-oxidative (type 1) fibres
b. fast-oxidative (type 2a) fibres
c. fast-glycolytic (type 2x) fibres
96
Muscle Fatigue
-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
Central Fatigue
-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
Peripheral Fatigue
-NMJ is vulnerable (Ch 5)
-SR and T-tubules
-can be a lack of ATP
-build up of lactic acid
-depleted glycogen levels
99
Circumventing Fatigue - EPOC
Excess
Post-exercise
Oxygen
Consumption
aka recharging
100
Control of Motor Movement
-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
Afferent Neurons
-input from afferent neurons usually through intervening interneurons at the level of the spinal cord: spinal reflexed
-ie. reflexes
102
Primary Motor Cortex
-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
Brainstem
-midbrain
-pons
-MO
-final link in multineuronal pathways
104
Muscular Dystrophy
-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
Parkinsons Disease
-basal nuclei disorder
-tremors, reptilian stare, shuffled gait, confusion, cognitive failure, sleep issues
-treatment = leva dopa
106
Muscle Spindle Structure
-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
Intrafusal Fibres
-lie within spindle shaped connective tissue capsules, parallel to extrafusal fibres
-has noncontractile central portion
-contractile portion is limited to the ends
108
Extrafusal Fibres
-contain contracile elements (myofibrils) throughout its entire length
109
Pathways of the muscle spindle
-CNS➡️ a) gamma motor neuron➡️intrafusal fibre (receptor) or b) alpha motor neuron➡️extrafusal fibre
110
Golgi Tendon Organ
-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
Smooth Muscle
-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
Smooth Muscle: Mechanism of Contraction
-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
2 Types of Smooth Muscle
a. multi unit smooth muscle
b. single unit smooth muscle
114
Multi Unit Smooth Muscle
-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
Varicosity
-stores neurotransmitters
-open during action potentials
116
Single Unit Smooth Muscle
-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
Pacemaker Potentials
-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
Slow Wave Potential
-gradually alternating hyperpolarizing and depolarizing swings in potential
119
Cardiac Muscle
-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
