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Physiology 208 > Skeletal Muscle > Flashcards

Skeletal Muscle Flashcards

1
Q

Skeletal Muscles

A
  • primarily voluntary by somatic motor neurons
  • multinucleated
  • striations
  • usually attached to bones by tendons
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2
Q

Origin vs. Insertion

A

Origin:
- closest to the trunk or to more stationary bone
Insertion:
- more distal or more mobile attachment

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3
Q

Flexor vs. Extensor

A 
- antagonistic muscle groups
Flexor:
- brings bones together
Extensor:
- moves bones away
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4
Q

Breakdown of Skeletal Muscle

A

Largest to smallest

  1. Muscle
  2. Connective tissue, blood vessels, *Fascicles
  3. muscle fibres
  4. myofibrils
  5. sarcomere
  6. myosin (thick) and actin (thin)
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5
Q

Striations

A

correspond to ordered arrays of thick and thin filaments within the myofibrils

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6
Q

F-Actin

A
  • back bone of thin filaments
  • double stranded alpha helical polymer of G-actin molecules
  • contains binding site for thick filaments (myosin)
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7
Q

Tropomyosin

A
  • two identical helices that coil around each other and still in the two grooves formed by actin strands
  • regulates the binding of myosin to actin
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8
Q

Troponin Complex

A
  • situated ~every 7 actin molecules
    Heterotrimer consisting of:
    1. troponin T (TnT): binds to a single molecule of tropomyosin
    2. troponin C (TnC): Ca2+ binding site
    3. troponin I (TnI): under resting conditions is bound to actin inhibiting contraction
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9
Q

Thick Filaments

A
  • consists of bundles of Myosin molecules
  • two intertwined heavy chains (two alpha helical rods wrapped around each other)
  • each consist of two light chains
  • Myosin head has region for binding actin as well as a site for binding and hydrolyzing ATP (ATPase)
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10
Q

Regulatory Light Chain

A

regulates ATPase activity of myosin

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11
Q

Essential Light Chain

A

stabilizes myosin head

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12
Q

Titin

A
  • very large protein extending from M line to Z line

- involved in stabilization and the elastic recoil behaviour of muscle

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13
Q

Nebulin

A
  • large protein that wraps around the thin filament
  • regulates the length of thin filaments
  • contribute to the structural integrity of myofibrils
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14
Q

Sarcomere Structure

A
  1. Z disk: zigzag protein; attachment for thin filaments
  2. I bands: occupied only by thin filaments
  3. A band: entire length of thick filaments; thin and thick overlap
  4. H zone: only thick filaments
  5. M line: attachment for thick filament
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15
Q

Sliding Filament Model

A
  • sarcomere shortens during contraction
  • actin and myosin don’t change length, they slide past one another
  • H zone and I band both shorten while A band remains constant
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16
Q

Tension

A

the force generated by a contracting skeletal muscle

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17
Q

Initiation of Skeletal Muscle Contraction

A
  1. events at neuromuscular junction
  2. excitation-contraction coupling
  3. Ca2+ signal
  4. contraction-relaxation cycle
  5. muscle twitch OR sliding filament theory
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18
Q

Neuromuscular Junction

A

point of synaptic contact between somatic motor neurone and individual muscle fibre

  • the synapse of a lower motor neuron to a muscle fibre
  • consists of axon terminals, motor end plates on muscle membrane, Schwann cell sheaths
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19
Q

Excitation-Contraction Coupling

A

an action potential initiated in the skeletal muscle fibre results in an increase in intracellular (sarcoplasmic) Ca2+

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20
Q

Brain Regions Involved in Voluntary Movements

A
  • Primary Motor Cortex
  • premotor cortex (motor association)
  • basal ganglia
  • thalamus
  • midbrain
  • cerebellum
    Corticospinal tract
  • ventral and interior lateral white matter
    Upper motor neuron
  • brain to spinal cord
    Alpha (lower) motor neuron
  • spinal cord to muscle
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21
Q

Alpha (lower) motor neuron

A
  • from spinal cord to muscle
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22
Q

Motor unit

A
  • a single motor neuron and all the muscle fibres it innervates
  • each axon branches and innervates several muscle fibres (cells)
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23
Q

Amyotrophic Lateral Sclerosis

A
  • neurodegenerative motor neuron disease
  • upper and/or lower motor neurone degenerate leading to muscle atrophy and weakness from disuse
  • 10% genetically inherited
    - dominant traits
    - mutation in gene(s) producing superoxide dismutase (enzymes that catalyze disputation of superoxide into oxygen and hydrogen peroxide)
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24
Q

Three components of Neuromuscular Junction

A
  1. presynaptic motor neuron filled with synaptic vesicles
  2. the synaptic cleft
  3. the postsynaptic membrane of the skeletal muscle fibre
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25
Q

Motor End Plate

A
  • region of the sarcolemma at the neuromuscular junction
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26
Q

Junctional Folds

A

on sarcolemma to increases surface area

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27
Q

Acetylcholine

A
  • contained in motor neuron vesicles
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28
Q

Nicotinic Acetylcholine Receptors

A
  • in the muscle sarcolemma
  • member of cys-loop receptor family of ligand gated ion channels
  • classified as monovalent cation channel (permeable to Na+ and K+)
  • opening requires 2 acetylcholine molecules
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29
Q

Opening one ACh receptor

A
  • the nicotinic cholinergic receptor binds to 2 ACh molecules, opening a nonspecific monovalent cation channel
  • allow Na+ and K+ to pass
  • net Na+ influx depolarizes muscle fibre
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30
Q

Excitatory End-Plate Potential

A
  • generated by the entry of Na+ through nACh
  • spreads to adjacent voltage gated Na+ channels on the sarcolemma and initiates an action potential
  • always causes an AP in a muscle fibre because of high amount of ACh
  • same as EPSP
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31
Q

When AP’s Stop Firing

A
  • acetylcholine in synaptic cleft must be removed and will either
    • diffuse away
    • be broken down to acetate and choline by the enzyme acetylcholinesterase
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32
Q

Acetylcholinesterase

A

an enzyme that breaks down acetylcholine into acetate and choline

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33
Q

Choline Acetyltranferase

A

an enzyme that makes acetylcholine from:

  • choline is transported back into motor neuron
  • Acetyl CoA produced from mitochondria
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34
Q

Myasthenia Gravis

A
  • severe weakness of muscle
  • disorder of neuromuscular transmission
  • can be redistricted to extra ocular muscles or generalized
  • AUTOIMMUNE: body produces antibodies that bind to ACh receptors
  • impedes activation of AChR and eventually decreases #
  • degeneration of post-junctional folds
  • treatment: acetylcholinesterase inhibitors or immunosuppressant
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35
Q

Action Potentials in Skeletal Muscle

A
  • propagate from the sarcolemma to the interior muscle fibres along the transverse tubule network
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36
Q

Sarcolemma

A
  • penetrates into the muscle fibre in the form of T-tubules and wrap around each myofibril in specific regions
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37
Q

Sarcoplasmic Reticulum

A
  • specialized Ca2+ storage organelles

- strategically organized with the T-tubules

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38
Q

Excitation-Contraction Coupling

A
  • the process by which electrical excitation of the surface membrane triggers an increase of [Ca2+]I in muscle
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39
Q

T-Tubules

A
  • penetrate the muscle fibres and surround the myofibrils at two point in each sarcomere, at the A and I band junctions
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40
Q

Triad

A
  • formed by the tubules and two cisternae that are associated with it
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41
Q

Cisternae

A
  • specialized end regions of the sarcoplasmic reticulum
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42
Q

DHP

A
  • dihydropyridine L-type Ca2+ channel

- voltage sensitive

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43
Q

RyR

A
  • ryanodine receptor

- Ca2+ release channel on SR

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44
Q

Initiation of Muscle Action Potential

A
  1. somatic motor neurone releases ACh at neuromuscular junction
  2. net entry of Na+ through ACh receptor-channel initiates a muscle action potential
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45
Q

Excitation-Contraction Coupling Process

A
  1. Action potential in t-tubule alters conformation of DHP receptor
  2. DHP receptor open RyR Ca2+ release channels in sarcoplasmic reticulum and Ca2+ enters cytoplasm
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46
Q

Ca2+ induced Ca2+ release

A
  • can enter sarcoplasm through L-type channels
  • RyR can be activated by Ca2+
  • NOT vital in skeletal muscle
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47
Q

Increase in [Ca2+]i

A
  • triggers contraction
  • Ca2+ binds low affinity sites on TnC (conformational change)
  • troponin complex and tropomyosin moves to reveal myosin binding site on actin
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48
Q

Cross Bridge Cycle

A
  • once intracellular Ca2+ is elevated tropomyosin shifts allowing myosin to tightly bind actic
    1. ATP Binding
    2. ATP Hydrolysis
    3. The Power Stroke
    4. ADP Release
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49
Q

ATP Binding

A
  • ATP binds to the head of myosin heavy chain reducing affinity of myosin for actin
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50
Q

ATP Hydrolysis

A
  • ATP is broken down to ADP and inorganic phosphate (Pi) resulting in the myosin head pivoting around into cocked state
  • cocked head is now aligned with and binds to a new actin molecule on thin filament
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51
Q

The Power Stroke

A
  • dissociation of Pi from myosin head strengthens bond between actin and myosin AND triggers power stroke
  • a conformational change in which the myosin head returns to its un-cocked state
  • pulls actin filaments generating force and motion
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52
Q

ADP Release

A
  • dissociation of ADP from myosin causes to remain bound to actin until ATP initiates the cycle again
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53
Q

Termination of Contraction

A
  • requires removal of Ca2+

- Ca2+ must be removed so myosin binding site on actin can be covered by tropomyosin

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54
Q

Removal of Ca2+

A
  • can be removed to the extracellular space by:
    • Na-Ca exchanger
    • Ca2+ pump (uses ATP)
  • eventually would deplete the cell of any Ca2+, leaving SR empty and because this play a minor role
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55
Q

Ca2+ Reuptake in the SR

A
  1. Na-Ca exchanger and Ca2+ pump in the plasma membrane both extrude Ca2+ from the cell
  2. Ca2+ pump sequesters Ca2+ within the SR
  3. Ca2+ is bound in the SR by calreticulin and calsequestrin
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56
Q

Mediation of Ca2+

A
  • mediated by sarcoplasmic and endoplasmic reticulum Ca2+ -ATPase (SERCA)-type Ca2+ pump
  • high Ca2+ in SR inhibits this pump
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57
Q

Calsequestrin and Calreticulin

A
  • Ca2+ binding proteins in SR to delay inhibition
  • maximize Ca2+ uptake by the SR
  • up to 50 Ca2+ binding sites per molecule
58
Q

Rigor Mortis

A
  • development of rigid muscle several hours after death
  • permanent formation of cross bridges
  • Ca2+ leaks into the sarcoplasm and binds troponin
  • ATP production stops
59
Q

When ATP Production Stops

A
  • Ca2+ can’t be removed (SERCA pump is ATP powered)
  • ATP needed to release myosin head from actin
  • remains latched cross bridge formation until muscles begin to deteriorate
60
Q

Latent Period

A
  • the slight delay between motor neuron AP and muscle fibre AP (synaptic release)
  • delay between muscle fibre AP and contraction time when Ca2+ is being released and binding troponin
61
Q

ATP needed for in skeletal muscles

A
  • myosin ATPase (contraction)
  • Ca2+ ATPase (relaxation)
  • Na+/K+ ATPase (after AP in muscle fibre)
62
Q

Sources of ATP in skeletal muscles

A
  1. Free intracellular ATP (few seconds)
  2. ATP stored as phosphocreatine (10 sec)
  3. Glycolysis (anaerobic metabolism)
  4. Aerobic (oxidative) metabolism
63
Q

Muscles at Rest

A
  • resting muscle stores energy from ATP in the high-energy bonds of phosphocreatine
  • ATP from metabolism + creatine -> ADP + phosphocreatine
64
Q

Working Muscles

A
  • working muscles use the stored energy made when at rest

- phosphocreatine + ADP -> creating + ATP

65
Q

Muscles need a steady supply of ATP to function

66
Q

Glycogenesis

A
  • a large amount of glucose is stored in muscle cells in the form of glycogen
67
Q

Glycogenolysis

A
  • when ATP is needed glycogen is then converted back to glucose
  • one glucose molecule can be broken down to pyruvate by glycolysis resulting in 2 ATP molecules
68
Q

Anaerobic Metabolism

A
  • process of of making ATP
  • occurs in the absence of oxygen
  • pyruvate is further broken down to lactate
  • takes place in sarcoplasm of muscle
69
Q

Oxidative (aerobic) Metabolism

A
  • if oxygen and mitochondria are present
  • after glycolysis pyruvate enters citric acid cycle producing 2 more ATP molecules and high energy electrons and H+
  • high energy electrons and H+ combine with O2 in the electron transport chain to produce additional 26-28 molecule of ATP
  • occurs in mitochondria
  • oxygen is necessary
70
Q

Muscle Fatigue

A
  • a decrease in muscle tension as a result of previous contractile activity that is reversible with rest
71
Q

Central Fatigue

A
  • CNS
  • feeling of tiredness and desire to cease activity
  • precedes physiological cell fatigue
  • low pH from acid production during ATP hydrolysis may influence the sensation of fatigue perceived by the brain
  • likely only the case during maximal exertion
72
Q

Connection between Fuel Status and Central Fatigue

A
  • subjects who rinse their mouths with solutions of carbohydrates are able to exercise significantly longer before exhaustion than subjects who rinse with water alone
73
Q

Peripheral Fatigue at Neuromuscular Junction

A
  • PNS
  • at the neuromuscular junction
    - proposed ACh synthesis can’t keep up with neuron firing rate, decreased neurotransmitter release > decrease AChR activation on muscle > muscle fails to reach threshold for firing AP
  • neuromuscular fatigue unlikely
74
Q

Peripheral Fatigue at Excitation-Contraction Coupling

A
  • most experimental evidence points to problems with excitation-contraction coupling
  • depleting of ATP or glycogen stores are not usually a limiting factor
  • change in membrane potential
75
Q

Peripheral Fatigue at the T-Tubule

A
  • with repeated AP firing, K+ builds up in the T-Tubules (extracellular space) changing the threshold for AP’s in the muscle fibre
76
Q

Peripheral Fatigue within the Muscle Fibre

A
  • build up of inorganic phosphate, ADP, H+ and reduction of ATP
  • substances can act directly or indirectly to cause fatigue
77
Q

Peripheral Fatigue in the SR

A
  • reduced Ca2+ reuptake and release (SERCA and RyR or formation of calcium phosphate)
78
Q

Peripheral Fatigue with Troponin C

A
  • decreased Ca2+ sensitivity leading to decreased cross-bridge cycling
79
Q

Peripheral Fatigue at the Myosin Head

A
  • release of Pi and ADP during cross bridge cycle slowed by sarcoplasmic accumulation
80
Q

Peripheral Fatigue

A
  • failed excitation-contraction coupling at the T-tubule
  • decrease in the rate of Ca2+ release, reuptake, and storage by the SR
  • decreased activation of thin filament proteins by Ca2+
  • direction inhibition of the binding and power-stroke motion of the myosin cross-bridges
81
Q

Skeletal Muscle Classification

A
  1. Maximal velocity of shortening (fast or slow)

2. Pathway they use to form ATP

82
Q

Maximal Velocity of Shortening

A
  • velocity of shortening dependent on ability to hydrolyze ATP
  • differs with different isoforms of myosin heavy chain
  • slow fibres and fast fibres
83
Q

Slow Fibres

A
  • contain mysin with slower ATPase activity

- TYPE I

84
Q

Fast Fibres

A
  • contain myosin with more rapid ATPase activity

- TYPE II

85
Q

Pathway Used to Form ATP

A
  • classifying according to the enzymatic machinery available for synthesizing ATP
  • Oxidative fibres and Glycolytic fibres
86
Q

Oxidative Fibres

A
  • fibres containing a large amount of mitochondria have a high capacity for aerobic (oxidative) metabolism
  • surrounded by blood vessels and contain a large amount of myoglobin to aid in oxygen delivery
87
Q

Glycolytic Fibres

A
  • fibres containing few mitochondria but an abundance of glycolytic enzymes and a large store of glycogen
88
Q

Type I (Red Muscle)

A
  • slow-twitch oxidative
  • slow speed of max tension
  • slow myosin ATPase activity
  • small diameter
  • longest contraction duration
    moderate Ca2+ ATPase activity in SR
  • fatigue resistant
  • most used: posture
  • oxidative: aerobic
  • capillary density: high
  • numerous mitochondria
  • dark red (myoglobin)
89
Q

Type IIA (Red Muscle)

A
  • fast-twitch oxidative-glycolytic
  • intermediate speed of max tension
  • fast myosin ATPase activity
  • medium size diameter
  • short contraction duration
  • high Ca2+ ATPase activity in SR
  • fatigue resistane
  • use: standing, walking
  • glycolytic but becomes more oxidative with endurance training
  • capillary density: medium
  • moderate amount of mitochondria
  • red colour
90
Q

Type IIX (White Muscle)

A
  • fast-twitch glycolytic
  • fastest speed of max tension
  • fast myosin ATPase activity
  • large diameter
  • short contraction duration
  • high Ca2+ ATPase activity in SR
  • easily fatigued
  • least used: jumping, quick, fine movements
  • glycolytic; more anaerobic than fast-twitch oxidative-glycolytic type
  • capillary density: low
  • few mitochondria
  • colour: pale
91
Q

Determinants of Muscle Force in Muscle Cell

A
  • fibre diameter
  • fatiguability
  • initial resting length
  • frequency of activation
92
Q

Determinants of Muscle Force of Entire Muscle

A
  • number of muscle cells activated
    • number of muscle cells/motor unit
    • number of motor units activated
93
Q

Length-Tension Relationship

A
  • muscle length influences tension development by determining the degree of overlap between actin and myosin filaments
  • too much or too little overlap of thick and thin filaments in resting muscle results in decreased tension
  • amount of tension developed is directly proportional to the number of cross bridges formed
94
Q

Twitch

A
  • a single action potential in a single muscle fibre results in an individual muscle twitch
  • a single twitch does not represent the maximal force that a muscle fibre can develop
  • a single action potential in a muscle fibre last approx. 1-3ms but a muscle twitch can last up to 100ms
95
Q

Summation

A
  • occurs when a subsequent action potential occurs before the muscle fibre is allowed to relax, which results in a more forceful contraction due to a summation of single twitches
96
Q

Force

A
  • developed by a muscle fibre is increased by summation of multiple twitches
97
Q

Tetanus

A
  • a maintained contractile response to repeated stimuli
98
Q

Unfused Tetanus

A
  • reaches steady state of contraction but stimuli are far enough apart that the muscle fibre slightly relaxes between stimuli
99
Q

Fused Tetanus

A
  • the stimulation rate is fast enough that the fibre does not relax, instead it reaches maximum tension and remains there
100
Q

Increase Tension by One Single Muscle Fibre

A
  • increase the rate at which action potentials occur in the fibre
101
Q

Force Increased in a Whole Skeletal Muscle

A
  • increased by the recruitment of additional motor units
102
Q

Motor Unit

A
  • a single motor neuron and all the muscle fibres it innervates, one motor neuron innervates one fibre type
103
Q

Motor Neuron Pool

A
  • the group of all motor neurons innervating a single muscle
104
Q

Weak Stimulus to Motor Pool

A
  • recruits smallest motor neurons first
105
Q

Size Principle

A
  • as the stimulus onto the motor neuron pool increases, additional larger motor neurons recruited
  • all muscle fibres within one motor unit are the same type
106
Q

Small-diameter motor neuron

A
  • Rm is high
  • conduction velocity is low
  • slow oxidative fibres (type I)
  • action potential
  • innervate smaller muscle fibres (innervate the least number)
  • constitute smaller motor units
107
Q

Large-diameter motor neuron

A
  • Rm is low
  • conduction velocity is high
  • fast-glycolytic fibres (type II)
  • EPSP
  • doesn’t go above threshold
  • innervate a large number of (large diameter) muscle fibres making up large motor units
108
Q

Intermediate Size Motor Neurons

A
  • fast oxidative glycolytic fibres

- innervate an intermediate number of (medium diameter) muscle fibres establishing intermediate sized motor units

109
Q

Tension

A
  • the force tending to pull the attachment points of a muscle toward one another
110
Q

Isotonic Contractions

A
  • the muscle contracts, shortens, and creates enough force to move the load
  • creates force to generate movement
111
Q

Concentric Contraction

A
  • involved in Isotonic contractions

- muscle shortens while generating force

112
Q

Eccentric Contraction

A
  • involved in Isotonic contractions
  • muscle lengthens while generating force
  • acts to decelerate the joint at the end of a movement
113
Q

Isometric Contractions

A
  • sarcomeres shorten without changing muscle length through elastic elements in tendons, last and connective tissue in and around muscle fibres
114
Q

Muscle Contraction Process

A
  1. muscle at rest
  2. Isometric contraction: muscle has not shortened
  3. Isotonic contraction: the entire muscle shortens
115
Q

Constant Remodling of Muscle Mass by:

A
  • changing rates of contractile protein synthesis and degradation
  • regulated by pathways influenced by mechanical stress, physical activity, availability of nutrients, growth factors and age
116
Q

Increasing Muscle Mass

A

PROTEIN SYNTHESIS > PROTEIN DEGRADATION

117
Q

Two mechanisms to increase muscle mass

A
  1. hypertrophy

2. hyperplasia

118
Q

Myosatellite Cells

A
  • involved in muscle repair may form new muscle fibres
  • occurs in development
  • response to an injury
  • become active and proliferate
  • migrate to damaged region and fuse to the existing muscle fibre to cause regeneration
119
Q

Muscle Hypertrophy

A
  • when skeletal muscle is subjected to an overload stimulus, it causes perturbations in muscle fibres and the related extracellular matrix
  • sets off a chain of myogenic events that lead to:
    • increase in size and # of contractile proteins (myosin, actin)
    • increased # of sarcomeres in a muscle length
    • increased sarcoplasmic storage (glycogen)
  • greater rate of myofiber hypertrophy for type II fibre
120
Q

Skeletal Muscle Atrophy

A
  • PROTEIN DEGRADATION > PROTEIN SYNTHESIS
  • can occur due to disuse:
    • immobilization, bed rest, unloading, food deprivation, age (sarcopenia)
121
Q

Cachexia

A
  • skeletal muscle atrophy disease
  • weakness and/or wasting due to chronic disease
  • cancer is often associated with a loss of weight and weakness of muscles
122
Q

Skeletal Muscle Reflexes

A
  • involved in almost all movements
  • receptors sense change in joint movements, muscle tension and muscle length and feed info into the CNS which responds in one of two ways:
    1. if muscle contraction is needed the CNS activates motor neurons to the muscle fibres
    2. if relaxation is needs the sensory input activates inhibitory interneurons in CNS which inhibit activity in motor neuron leading to relaxation
123
Q

Four Components of Skeletal Muscle Reflexes

A
  1. Sensory Receptors
  2. Integrating Center
  3. Efferent Neurons
  4. Effectors
124
Q

Monosynaptic Reflex

A
  • has a single synapse between the afferent and efferent neurons
125
Q

Polysynaptic Reflexes

A
  • have two or more synapses

- this somatic motor reflex has both synapses in the CNS

126
Q

Proprioceptors

A
  • provide info into the CNS about the position of our limbs in space, movements, and the effort exerted by skeletal muscles
  • muscle spindles, Golgi tendon organ, joint receptors
127
Q

Joint Receptors

A
  • these are found in the capsules and ligaments around joints and are stimulated by mechanical distortion that accompany changes in the position of bones
128
Q

Muscle Spindles

A
  • small elongated stretch receptors
  • scattered among and arranged parallel to skeletal muscle fibres
  • send info to CNS about muscle length and changes in muscle length
  • made up of sensory neuron wrapped around intrafusal muscle fibres
  • tonically active (muscle tone) and firing even when relaxed
129
Q

Extrafusal Muscle Fibres

A
  • regular muscle fibres innervated by alpha motor neurons
130
Q

Muscle Spindle Reflex

A
  • the addition of a load stretches the muscle and the spindles, creating a reflex contraction
131
Q

Parts Involved in Muscle Spindles

A
  • Gamma motor neurons from CNS innervate intrafusal fibres
  • tonically active sensory neurons send info to CNS
  • Gamma neurons from CNS control contraction in intrafusal fibres
  • intrafusal fibres are found in muscle spindles
132
Q

Muscle Spindles without Gamma Motor Neurons

A

ensure that muscle spindles maintain their sensitivity over wider ranges of muscle lengths

  • muscle stretches = muscle spindle contracts
  • muscle contracts = muscle spindle stretches
133
Q

Alpha-Gamma Coactivation

A
  • maintains spindle function when muscle contracts
    1. alpha motor neuron fires and gamma motor neuron fires
    2. muscle and intrafusal fibres both contract
    3. stretch on enters of intrafusal fibres unchanged.
    • firing rate of afferent neuron remains constant
134
Q

Golgi Tendon Organ

A
  • sensory neuron interwoven among collagen fibres inside a connective tissue capsule
  • respond to muscle tension
  • originally proposed to control inhibitory reflexes to prevent muscle damage
  • control force within muscles and stability around joints
135
Q

Golgi Tendon Reflex

A
  • protects the muscle from excessively heavy loads by causing the muscle to relax and drop the load
    1. neuron from Golgi tendon organ fires
    2. motor neuron is inhibited
    3. muscle relaxes
    4. load is dropped
136
Q

Patellar Tendon (Knee Jerk) Reflex

A
  • monosynaptic stretch reflex and reciprocal inhibition of the antagonistic muscle
137
Q

Stimulus of Sensory Receptors

A
  • can lead to contraction of one muscle and inhibition in the antagonistic muscle (reciprocal inhibition)
138
Q

Patellar Tendon Reflex Process

A
  1. stimulus: tap to tendon stretch muscle
  2. receptor: muscle spindle stretches and fires
  3. afferent path: AP travels through sensory neuron
  4. integrating center: sensory neuron synapses in spinal cord
  5. efferent path 1: somatic motor neuron
    efferent path 2: interneuron inhibiting somatic motor neuron
  6. effector 1: quadriceps muscle
    effector 2: hamstring muscle
  7. response 1: quadriceps contract, swinging leg forward
    response 2: hamstring stays relaxed, allowing extension of leg (reciprocal inhibition)
139
Q

Flexion Reflexes

A
  • pulls limbs away from painful stimuli
140
Q

The Crossed Extensor Reflex

A
  • a flexion reflex in one limb causes extension in the opposite limb
  • the coordination of reflexes with postural adjustments is essential for maintain balance
141
Q

The Crossed Extensor Reflex Process

A
  1. painful stimulus activates nociceptor
  2. primary sensory neuron enters spinal cord and diverges
    3a. one collateral activates ascending pathways for sensation (pain) and postural adjustment (shift in center of gravity)
    3b. withdrawal reflex pulls foot aways from painful stimulus
    3c. crossed extensor reflex supports body as weight shifts away form painful stimulus
142
Q

Proteins in SR

A

Calsequestrin and Calreticulin

Physiology 208 (11 decks)

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