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HSC1007 A&P > Muscle physiology > Flashcards

Muscle physiology Flashcards

1
Q

What are muscles?

A

Specialised tissues that can develop tension & shorten (contraction) –> produce movements

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2
Q

Functions of muscles

A
  1. Produce purposeful movements
  2. Propulsion of contents through hollow internal organs (e.g. bld vessels, intestines)
  3. Emptying of contents to external env. (e.g. faeces, urine)
  4. Maintain posture & body position
  5. Stabilise joints
  6. Generate heat (by-product of contraction)
  7. Helps in circulation, digestion & breathing
  8. Protect internal organs
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3
Q

What are the types of muscles?

A
  1. Skeletal muscles
  2. Cardiac muscles
  3. Smooth muscles
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4
Q

Properties of skeletal muscles

A
  • Voluntary control
  • Striated (contracts uniformly)
  • Bundles of long, cylindrical, multinucleate cells
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5
Q

Properties of cardiac muscles

A
  • Involuntary control
  • Striated
  • Interlinked network of short, slender, cylindrical, branched cells
  • Connected cell to cell by intercalated discs
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6
Q

Properties of smooth muscles

A
  • Involuntary
  • Unstriated
  • Loose network of short, slender, spindle-shaped cells
  • Arranged in sheets
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7
Q

Skeletal muscle organisation

A

Whole muscle –> Muscle Fascicle –> Muscle fiber (cell) –> myofibril –> Sarcomere

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8
Q

What is sarcomere?

A

Functional unit
- Arranged in series
- Bordered by Z disc line
- Consists of thin (actin) & thick (myosin) filaments

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9
Q

What is the A band?

A

Overlapping thin and thick filaments

Dark band under light microscope

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10
Q

What is the I band?

A

Mostly thin filament with Z line running through it

Light band under light microscope

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11
Q

What is the H zone?

A

Myosin filament not covered by actin filament

Within the A-band; M line runs through H zone

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12
Q

What is the Z line?

A

Borders the sarcomere unit

Located in the middle of the I band

Dark line within the I band (light band)

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13
Q

How many actin filaments surrounds 1 myosin filament?

A

6 actin filaments

1 myosin can pull on 6 actin filaments to create shortening effect

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14
Q

What happens when Ca2+ binds to troponin?

A

The shape of troponin is changed in a way that causes the tropomyosin to slip away from its blocking position –> exposes binding site for myosin

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15
Q

What is tropomyosin?

A

Elongated protein that coils around the length of the actin & covers the myosin cross bridge binding site –> so actin cannot interact with myosin (thick filament)

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16
Q

How are actin arranged in an actin filament?

A

Arranged in a helix manner

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17
Q

What does one myosin protein consist of?

A

Two identical intertwined, golf club like subunits –> two heads

The heads form the CROSS BRIDGE

Each head has: Actin-binding site & Myosin ATPase site

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18
Q

What is the myosin ATPase site?

A

Enzymatic site
Uses ATP as energy currency –> enable myosin cross-bridge to move back & forth –> allows pulling action of myosin onto actin filament

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19
Q

How does ATP release energy?

A

ATP is converted to ADP –> releases one phosphate ion

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20
Q

What are the pathways for ATP production?

A
  1. Transfer of a high-energy phosphate from creatine phosphate to ADP
  2. Glycolysis
  3. Oxidative phosphorylation
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21
Q

Transfer of high-energy phosphate from creatine phosphate to ADP

A
  • Phosphocreatine –> contains high-energy phosphate ion
  • ADP can react with phosphocreatine with the help of enzyme creatine kinase
  • Regenerates ATP during exercise

Basically, to regenerate ATP, just need to add phosphate ion back to ADP

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22
Q

Is transferring a high-energy phosphate from creatine phosphate to ADP a long term solution?

A

No, short term solution

Phosphocreatine found in very limited pools within skeletal muscles –> useful for only a few seconds

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23
Q

What is glycolysis?

A

Anaerobic pathway

  • Production of small amount of ATP w/o O2 in cytosol (outside mitochondria)
  • Glucose broken down into 2 pyruvic molecules –> generates small amount of ATP
  • w/o sufficient O2, pyruvate is converted to lactate through lactic acid fermentation = allows glycolysis to continue temporarily
  • Occurs during short, high-intensity exercise
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24
Q

What is oxidative phosphorylation?

A

Aerobic pathway

  • Occurs in mitochondria & requires O2
  • Pyruvic acid (from glycolysis) is converted to acetyl-CoA
  • Enters Krebs cycle –> produces CO2 & electron carriers
  • Electron carriers transfer electrons to the Electron Transport Chain –> O2 is used to produce significant amt of ATP (32 ATP molecules!)
  • Supports prolonged exercise
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25
Q

What is the sliding filament theory?

A

Thick and thin filaments will overlap onto each other –> movement is the sliding filament theory

Sliding filaments over one another –> pull closer to each other –> shortening effect –> generate contraction of a muscle

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26
Q

How does the myofibril change during the shortening of a sarcomere?

A

Changes in size of sarcomere bands

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27
Q

What happens to the I band during shortening of a sarcomere?

A

Becomes shorter –> thin filament more overlapped with thick filament

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28
Q

What happens to the A band during shortening of a sarcomere?

A

Same width –> thick filaments remain the same length (not the one being pulled)

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29
Q

What happens to the H zone during shortening of a sarcomere?

A

Shorter –> thick filament overlapped by thin filament

Remember –> H zone is area of thick filament NOT overlapped by thin filament

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30
Q

What does the presence of Ca2+ do in the shortening of a sarcomere?

A

Conformational change that exposes myosin cross-bridge binding site

  • allows attachment of myosin head to thin filament
  • action of myosin head pulling against it will cause shortening of sarcomere

Presence of Ca2+ important to allow interaction b/w the thin & thick filaments

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31
Q

What is a power stroke?

A

When thick filament is bound to thin filament –> initiates pulling/stroking action, involves tilting of attached myosin

Pulling action = power stroke

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32
Q

Steps in a power stroke

A
  1. Myosin cross bridge binds to actin molecules
  2. Cross bridge bends, pulling actin inwards/towards centre of sarcomere (tilt attached head of myosin = dist b/w 2 Z lines shorten)
  3. Cross bridge detaches at end of power stroke (by binding to ATP) –> returns to original conformation
  4. Cross bridge binds to more distal actin molecule –> cycle repeats
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33
Q

What is the role of ATP in the power stroke?

A
  1. Detachment of myosin head –> binds to myosin head causing detachment –> myosin head can bind to more distal actin molecules
  2. “Cocking” of myosin head –> be ready for power stroke (hydrolysis of bound ATP provides energy for conformational change/cocking of myosin head)
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34
Q

Steps in the cross-bridging cycle

A
  1. ATP hydrolysis = ATP split by myosin ATPase
    ADP & Phosphate ion remain attached to myosin + energy stored in cross bridge (energy “cocks” cross bridge)
  2. Binding = Ca2+ released on excitation = removes inhibitory influence from actin (by binding to tropomyosin –> conformational change –> exposes cross bridge binding sites )= enables binding with cross bridge
  3. Bending = Power stroke of cross bridge triggered on contact b/w myosin & actin; Phosphate ion released during & ADP released after power stroke
  4. Detachment = Linkage b/w actin & myosin broken –> fresh molecule of ATP binds to myosin cross bridge –> cross bridge returns to original conformation + ATP hydrolyzed

Repeats

2b. Resting = no excitation = no Ca2+ released = acting & myosin prevented from binding = no cross-bridge cycle = muscle fiber remains at rest

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35
Q

What happens when there is no ATP for skeletal muscle contraction?

A

E.g. Death = rigor mortis
- Dying cells stop producing fresh ATP
- Due to Ca+ influx into cytosol (due to deterioration of sarcoplasmic reticulum), muscle contractions occur
- BUT myosin heads CANNOT detach from actin filaments because NO ATP = remain attached
- So muscles remains stiff & contracted = rigor mortis

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36
Q

Asynchronous cross-bridge cycling

A

Cross bridges DO NOT stoke in unision

  • Only some of myosin heads will perform the power stroke
  • Others return to original conformation (ready to bind to distal actin molecules)
  • If all stroke tgt = myosin heads will detach at the same time –> sarcomere suddenly loses tension before next power stroke can be initiated = causes a “jerky” contraction instead of smooth contraction
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37
Q

How does smooth muscle contraction differ from skeletal muscle?

A
  • Modification of smooth muscle activity is done via autonomic nervous system (instead of somatic nervous system)
  • Arrangement of thick & thin filaments is different
  • Ca2+ dependent phosphorylation of myosin (interacts with thick filaments instead of thin filaments)
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38
Q

What is a single unit of smooth muscle?

A

Myogenic –> can generate own contractile activity

Has pacemaker cells within the tissue –> generate slow-wave potential for coordination of diff motor patterns of contractions

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39
Q

How are the thick & thin filaments arranged in smooth muscle?

A
  • Network of fibers forms a diamond-shaped lattice (X striated)
  • Filaments overlay onto each other
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40
Q

What are the types of filaments in a smooth muscle cell?

A
  • Thick myosin filaments: longer than in skeletal
  • Thin actin filaments: contains tropomyosin but lack troponin
  • Intermediate filaments: X participate in contractions but cytoskeletal framework –> support cell shape
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41
Q

What happens during contraction in a smooth muscle cell?

A

The pulling of myosin head on upper & lower actin filaments will cause the whole network (diamond-shaped lattice) to compress tgt = shortening of muscle

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42
Q

What is a myosin light chain?

A

Chain of protein molecules wrapped around the neck region of myosin head

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43
Q

What is Ca2+ role in muscle contraction?

A
  1. Calcium-induced calcium release (from SR lateral sacs –> effects on dihydropyridine & ryanodine receptors) = excitation-contraction coupling
  2. Binding to troponin = conformational change = expose cross-bridge binding sites
  3. Calcium-dependent phosphorylation of myosin light chain (smooth muscle)
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44
Q

What are the steps in Ca2+-dependent phosphorylation of myosin light chain?

A
  1. Ca2+ binds to calmodulin (intracellular protein) = complex that activates enzyme myosin light chain kinase
  2. Myosin light chain kinase adds a phosphate group to myosin light chain = generates phosphorylated myosin cross bridge
  3. Allows the binding of myosin head to actin filament = initiation of power stroke
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45
Q

What are some characteristics of smooth muscles?

A
  • Smooth muscle can produce tension even when stretched
  • Can develop near-maximal tension over greater range of muscle length (than skeletal)
  • Stress-relaxation response
  • Slow & economical
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46
Q

What is the late phenomenon of smooth muscle?

A

Contractile response is slower & uses less energy for same amt of contractile activity (than skeletal)

  • Latch phenomenon: cross-bridges latch onto actin filaments for longer time each cycle –> allows smooth muscles to maintain tension with less ATP consumption
  • Each cross-bridge cycle uses 1 ATP molecule
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47
Q

What is the stress relaxation response of smooth muscle?

A

Initially inc. tension when suddenly stretched –> can quickly rearrange cross-bridge attachments to restore tension (e.g. when suddenly stretched)

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48
Q

What are cardiac muscles made up of?

A
  • Blend of both skeletal & smooth muscle (also myogenic)
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49
Q

What are the gap junctions for in cardiac muscles?

A

(Interconnected by gap junctions found in intercalated discs that join cells tgt)

Allows small molecules & ions to pass from one cell to another
- Action potential spread quickly from one cell to another through gap junctions = super quick electrical coupling b/w cardiac cells = contract simultaneously

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50
Q

How do we voluntarily control & generate muscle contractions?

A
  1. Primary motor cortex (brain) sends motor command
  2. Signal is transmitted from brain to spinal cord then to lower motor neuron = innervates specific muscle
  3. Motor neuron meets & terminates onto skeletal muscle tissue via motor end plate (aka neuromuscular junction)
  4. Action potential from lower motor neuron release neurotransmitters –> acetylcholine
  5. NT travel across synaptic cleft & bind to specialised receptors on muscle tissue
  6. Bound NT open ion channels on postsynaptic mbn = depolarisation (aka excitation event)
  7. AP triggered will propagate along mbn & eventually trigger contraction of entire muscle
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51
Q

What is the link between excitation (depolarization at postsynaptic mbn) and contraction?

A

Release of Ca2+ –> mediator for conformational change in tropomyosin –> expose cross-bridge binding sites

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52
Q

Where is Ca2+ stored?

A

Sarcoplasmic reticulum (specialised sacs)
- Modified endoplasmic reticulum –> forms network of interconnected mbn & closed compartments)

Lateral sacs: enlarged regions at both ends (of myofibrils)
- release Ca2+ upon receiving excitation signal

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53
Q

What are t-tubules?

A

Specific points where mbn dips into muscle fibre & runs perpendicularly from mbn surface

Continuous with sarcolemma (specialised cell mbn around muscle fibers)

54
Q

How is Ca2+ released from sarcoplasmic reticulum?

A
  1. Action potential travels along the sarcolemma (surface mbn)
  2. At specific points, AP will travel into T-tubule
  3. T-tubules travel along lateral sacs of sarcoplasmic reticulum so upon excitation = induce release of Ca2+ from sarcoplasmic reticulum
55
Q

What are dihydropyridine receptors?

A

Voltage-sensitive receptors
They are also voltage-gated calcium channels

56
Q

How is action potential propagated into the T-tubules?

A

via communication b/w physically coupled receptors

  1. When AP arrives in T-tubules, dihydropyridine receptors picks up the electrical activity
  2. Dihydropyridine receptors directly signal adjacent receptors positioned on sarcoplasmic reticulum (bc close proximity b/w T-tubules & lateral sac mbn) = Ryanodine receptors
  3. Lead to opening of RYR = release Ca2+ stored in internal compartment of SR

https://www.youtube.com/watch?v=3Wc7I-H5stQ

57
Q

What are ryanodine receptors?

A

Calcium releasing channels found on SR mbn

58
Q

What is calcium-induced calcium release?

A

The whole calcium release process (with the dihydropyridine & ryanodine receptors)

Activation of ryanodine receptors mediated by calcium –> means a SMALL amt of calcium released & comes into contact with ryanodine receptors = more Ca2+ released

59
Q

What happens if Ca2+ is always present?

A

Ca2+ will always bind to troponin –> induce contractions persistently (if sufficient ATP supply for contractile activity)

60
Q

What is the active reuptake of Ca2+ via SERCAs?

A

SERCAs = Sarco/Endoplasmic Reticulum Ca2+-ATPase

  • ATP required to drive active tpt of Ca2+ back into SR –> Re-uptake/storing of Ca2+
  • Once Ca2+ removed, tropomyosin returns to original blocking position = prevent interaction b/w thick & thin filaments = muscle relaxation
61
Q

How long does it take to have full contractile activity brought about by a single stimulation?

A

30 - 100 msec

62
Q

How long does one action potential last?

A

~ 1-2 msec

63
Q

Why does contraction outlasts the electrical activity (AP) that initiated it?

A
  1. Takes time for onset of contraction –> a lot of processes are involved before Ca2+ is released
  2. Takes time to generate tension by cross-bridge activity –> certain length that thick & thin filaments need to slide over e/o before achieving peak muscle tension
  3. Takes time for Ca2+ reuptake
64
Q

What are the types of muscle fibers?

A
  1. Slow-oxidative (Type I)
  2. Fast-oxidative (Type IIa)
  3. Fast-glycolytic (Type IIx)
65
Q

Which type of muscle fibers are slow twitch?

A

Slow oxidative (Type I)

Generate peak twitch tension in 50-100 msec

66
Q

Which type of muscle fibers are fast twitch?

A

Fast-oxidative (Type IIa)
Fast-glycolytic (Type IIx)

Generate peak twitch tension in 15-40 msec

67
Q

What is the composition of muscle fiber types?

A

Mixture of all three types of muscle fibers
All three types present (usually) but composition might be different (e.g. Biceps brachii primarily type 2; soleus primarily type 1)

68
Q

What are fiber characteristics dependent on?

A

Primarily dependent on ATP hydrolysis & synthesis

69
Q

What is the oxidative phosphorylation capacity like for:
- Slow-oxidative (type I)
- Fast-oxidative (type IIa)
- Fast-glycolytic (type IIx)

A
  • Slow-oxidative (type I) : High (aerobic)
  • Fast-oxidative (type IIa): High (aerobic)
  • Fast-glycolytic (type IIx): Low
70
Q

How do the amount of enzymes for anaerobic glycolysis differ for:
- Slow-oxidative (type I)
- Fast-oxidative (type IIa)
- Fast-glycolytic (type IIx)

A
  • Slow-oxidative (type I): Low
  • Fast-oxidative (type IIa): Intermediate
  • Fast-glycolytic (type IIx): High
71
Q

Why do type IIx fibers have low amounts of mitochondria, capillaries & myoglobin content?

A

These are machinery for oxidative pathways bc type IIx uses anaerobic pathways

72
Q

Fast vs Slow fibers

A

Higher myosin-ATPase activity = more rapid splitting of ATP & faster rate at which energy is available for crossbridge cycling

Fast fibers –> higher myosin-ATPase activity

73
Q

Oxidative vs glycolytic fibers

A

Oxidative - use O2 to generate ATP (aerobic; oxidative phosphorylation)
Glycolytic - use anaerobic pathways

Oxidative muscle fibers more resistant to fatigue (can produce ATP for longer duration)

74
Q

How does genetic endowment affect muscle fibers?

A

The % of each type of muscle fiber is determined by:
- genetics (some built as “sprinters” or “marathoners”)
- type of activity the muscle is specialised

75
Q

An Improvement in oxidative capacity of muscle fibers due to _________

A

Aerobic endurance exercises

76
Q

Muscle hypertrophy due to _________

A

Anaerobic high intensity resistance training

77
Q

How do muscles adapt in response to demands placed on them?

A
  1. Improvement in oxidative capacity
  2. Muscle hypertrophy
  3. Influence of testosterone
  4. Interconversion b/w fiber types
  5. Repair of muscle
  6. Muscle atrophy
78
Q

How does muscle hypertrophy occur?

A

When muscle protein synthesis exceeds muscle protein breakdown

79
Q

How does testosterone influence muscle fibers?

A
  • Promotes synthesis & assembly of myosin & actin
  • Boost muscle growth
  • Inc. cross-sectional area
80
Q

Can there be interconversion b/w muscle fiber types?

A

yes!

Type IIa fibers ↔ Type IIx fibers
(e.g. sprint training –> can convert IIa to IIx)

Slow & fast fibers are generally not interconvertible (EXCEPT under special circumstances –> e.g. spinal cord injury/lower gravity in space)

81
Q

Repair mechanism for muscle

A

Satellite cells
- become myogenic precursor cells under muscle damage
- Muscle stem cell –> expand & differentiate

(usually when cells start to die off)

82
Q

What is muscle atrophy?

A

Loss of muscle tissue = Dec. in size/mass of muscle
- Disuse
- Denervation (e.g. Amyotrophic Lateral Sclerosis –> ALS)
- Aging

Use it or lose it !!!

83
Q

What is sarcopenia?

A
  • Gradual muscle around 40 y/o (involuntary)
  • Inactivity comprises 1% loss per year (loss accelerates after 50 y/o, esp in males)
  • Loss in both SIZE and NUMBER of muscle fibers
  • Loss of muscle mass is permanent! –> can affect activities of daily living & bone mass (poor balance/muscle coordination = inc. fall risk)
84
Q

Where is tension produced?

A

Produced internally within sarcomeres

85
Q

How are muscles attached to bones?

A

Whole muscles = group of muscle fibers bundled tgt

Muscles attached to bones by tough, collagenous tendons

86
Q

How is muscle tension transmitted to bone?

A

Transmitted to bone as it tightens the series-elastic component (aka tendon) –> then can move

87
Q

Can muscles do a pushing action?

A

NO
Can only do pulling action

88
Q

Lever system

A

Bones = levers
Joints = fulcrums
Skeletal muscles = provide force to move bones

89
Q

What is the key advantage of the lever system?

A

The velocity that the load is moving is significantly faster than the shortening velocity of masses = amplification of velocity & distance (7x)

BASICALLY, muscle needs to contract 1cm to move load by 7cm

90
Q

What is the disadvantage of the lever system?

A

Since muscle is closer to the fulcrum, more force is needed

The further the force is exerted away from the fulcrum, the greater the turning effect that can generate

91
Q

What are the primary types of contraction?

A
  1. Isotonic (Constant tension)
  2. Isometric (Constant length)
  3. Isokinetic (Constant motion)
92
Q

What is isotonic contraction?

A

Load remains constant as muscle length changes –> normal muscle contraction (e.g. bicep curls)

93
Q

What is isometric contraction?

A

Muscle length remains constant as tension increases (e.g. holding a weight w/o raising/lowering it, wall squat)

94
Q

What is isokinetic contraction?

A

Velocity remains constant as muscle fibers shorten –> use of equipment = externally controls velocity of movement

95
Q

Other types of contraction

A

Concentric contraction = muscle shortens under load

Eccentric contraction = muscle lengthens under load

96
Q

What kind of exercises more likely to damage muscles?

A

Eccentric exercises = delayed onset of muscle soreness (DOMS)

97
Q

What is ultrastructural damage?

A

Caused by tension exerted when muscle lengthening

E.g.
- Sarcomere disruption
- Loss of Z lines
- Z line streaming
- Widening of dist b/w thick & thin filaments

(organised structure disrupted)

98
Q

Which type of muscle fibers more susceptible to eccentric exercise induced damage?

A

Fast twitch/type II fibers
Due to smaller sarcomeric proteins

99
Q

What % of energy use by muscles is converted to heat?

A

75% converted to heat (bc thermoregulation)
25% external work (aka muscle contraction)

100
Q

What is the load-velocity relationship?

A

The heavier the load, the slower you lift it
- Power stroke slows when the myosin tilts against a greater load
- Basically speed of shortening is fastest when X load –> speed will dec. with inc. load

101
Q

What is graded contractions?

A

Contractions can be of varying strengths

Basically, normal muscle contraction can be modified to produce different amounts of force

102
Q

What are graded contractions based on?

A
  1. Number of muscle fibers contracting
  2. Amount of tension developed by each contracting fiber
103
Q

What allows the number of contracting muscle fibers to vary?

A

PNS innervates muscle fibers in bundles = one single motor neuron innervates multiple muscle fibers

So based on the no. of motor neurons being activated by motor cortex, can recruit different number of motor units
(more motor units recruited = inc. no. of muscle fibers contracting = stronger contraction)

104
Q

What does 1 motor unit consist of?

A

One motor neuron + all muscle fibers it innervates

105
Q

Which motor units are recruited first?

A

Smaller motor units are recruited first (bc smaller motor neurons more excitable)

Least fatigable motor units are recruited first (type I) to most fatigable (type II)

106
Q

What are the factors influencing amount of muscle tension?

A
  1. Frequency of stimulation
  2. Length of fiber at onset of contraction
  3. Extent of fatigue
  4. Thickness of fiber
107
Q

What happens if a muscle fiber is restimulated after it has completely relaxed?

A

One AP = one twitch

If muscle given time to recover before next AP = second twitch will have the same magnitude as the first twitch

No twitch summation

108
Q

What happens if muscle fiber is restimulated before it has completely relaxed?

A

2nd AP is introduced before muscle completely relaxes:
The second twitch is added on to the first twitch = twitch summation

2nd twitch summits onto 1st twitch = create higher tension level

109
Q

What causes tetanus?

A

When a muscle fiber is stimulated so rapidly that it X have opportunity to relax AT ALL between stimuli = maximal sustained contraction (3-4x stronger than a single twitch)

110
Q

What influences summation of tension?

A
  1. Sustained elevation in cystolic CA2+ (drive continual cross-bridge cycling = inc tension progressively)
  2. More time in stretch series-elastic (tendon) component (allow transmission of greater tension to bone)
111
Q

What is the optimum muscle length?

A

The length that allows the maximum no. of myosin cross bridges & actin accessible for binding & pulling

112
Q

What happens in muscle length that is too short?

A

Undesirable overlapping = non-ideal mechanics for shortening = dec. in tension produced

113
Q

What happens in muscle length that is too long?

A

“Unused/unmatched” cross bridges & actin
X participate in contraction = dec. tension produced

If no overlap at all = no muscle tension generated (bc X interaction b/w myosin & actin)

114
Q

What is fatigue?

A

Inability to maintain muscle tension at a given level
- peripheral (muscle) origin or central origin (dec. motor drive; nervous system)

115
Q

Central fatigue

A

CNS no longer adequately activates motor neurons (dec. central drive due to inc. serotonin, tryptophan)

Defence mechanism = X muscles to reach a point where cannot produce ATP = catastrophic failure

116
Q

What is peripheral fatigue?

A

Exercising muscles can no longer respond to stimulation with same degree of contractile activity
- local inc. in phosphate, leakage of Ca2+, depletion of glycogen

117
Q

How does thickness of fiber affect muscle tension?

A
  1. Size of myofibers (AKA myofiber hypertrophy) = the thicker the fiber, the stronger tension it can generate (e.g. strength/resistance training)
  2. Number of myofibers (AKA myofiber splitting/hyperplasia) = muscle thickness remains the same but inc. in no. of muscle cells/fibers (e.g. testosterone, steroids, vigorous weight training)
118
Q

What are the 3 typical types of movement?

A
  1. Voluntary (goal-directed, involves motor outputs)
  2. Reflexes (automatic)
  3. Rhythmic (central pattern generators to drive rhythmic patterned outputs independently –> walking, ANS)
119
Q

What is proprioception?

A

Understanding relative position & movement of body

120
Q

What are muscle spindles?

A

Sensory structures that convey info on muscle length –> detects muscle stretch

Primary type of proprioceptors (stretch receptors)

121
Q

What are golgi tendon organs?

A

Proprioceptors located in tendons (near junction of tendons & muscle)

Sense & convey info on muscle tension –> activated when muscle shortens

122
Q

What are the extrafusal fibers?

A

“ordinary” muscle fibers

123
Q

What are intrafusal fibers?

A

Muscle spindles
Communicate muscle length by sending info through assoc. sensory neuron

124
Q

What neuron is the extrafusal skeletal muscle fiber innervated by?

A

Alpha Motor Neuron
- Provides signals to contract the masses

125
Q

What neuron is the intrafusal skeletal muscle fiber (aka muscle spindles) innervated by?

A

Gamma Motor neuron = efferent neuron
- Sense stretch & send impulse to spinal cord
- Causes contraction of muscle spindles

126
Q

What causes muscle spindles remain taut?

A

Activation of gamma motor neuron

Alpha-gamma co-activation important in maintaining a “taut” muscle spindle (so during normal muscle contraction, both alpha & gamma neurons are activated)

127
Q

Why can’t muscle spindles be loose & slack?

A

X communicate any change in length bc they are meant to detect any stretch

128
Q

How does the golgi tendon organ detect muscle tension?

A

When there is contraction in the muscle, there is transmission of the tension to the tendon & bone = Golgi tendon organ is in the tendon = can sense the transmission of tension

–> can provide constant feedback to brain on the level of force being exerted = allow precise control of muscle strength

129
Q

What happens in a patellar tendon reflex (stretch reflex)?

A
  1. Force exerted from the hit will pull on attached extensor muscles = creates a stretch
  2. Stretch stimulus detected by muscle spindles = efferent signal transmitted along sensory neuron = directly synapse onto alpha motor neurons that innervates the same extensor muscles
  3. Sensation of stretch directly leads to contraction of muscles

Stretch reflex is monosynaptic = 1 sensory neuron

130
Q

Importance of stretch reflex?

A

To sense & resist changes in muscle length = stabilize our balance & maintain posture

E.g. External force (bus stops suddenly) –> stretch reflex helps to keep body upright –> prevent falls

131
Q

What happens in withdrawal reflex?

A
  1. Harmful stimulus stimulates pain receptor
  2. Pain stimulus transmitted along efferent pathway to spinal cord (some of the info sent to brain also)
  3. This reflex is mediated at spinal cord level = synapse with interneuron
  4. Interneuron signals appropriate motor neuron
  5. Muscle contraction = sends signal to flexor muscle to contract & extensor muscle to relax = withdraw limb away from stimulus
132
Q

Steps in crossed extensor reflex

A
  1. Painful stimulus activates sensory neurons = sends impulses to spinal cord
  2. Branches of afferent nerve fibers cross to opposite side of spinal cord
  3. Synapse with interneurons in spinal cord
  4. Excite/inhibit motor neurons in the muscles of opposite limb
  5. Contract/relax muscles to support the body’s weight

E.g. step on a nail = the leg that steps on the nail will pull away & other leg will extend to support your weight.

HSC1007 A&P (8 decks)

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