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HUB3006F > Muscles > Flashcards

Muscles Flashcards

1
Q

What are the functions of skeletal muscle?

A
  1. Moves the skeleton.
    a. Muscle contracts which pulls on tendons which move the bones
  2. Maintain posture & body position.
  3. Supports soft tissues.
    a. Abdominal wall and floor of pelvic cavity has layer of skeletal muscles
  4. Guard entrances and exits.
    a. Sphincters
  5. Maintain body temperature.
    a. Contractions use energy
  6. Reservoir for protein storage
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2
Q

What are the properties of muscle cells?

A
  1. Contractility
    a. Ability of proteins within muscle cells to draw together
  2. Excitability
    a. Responsive in the presence of various stimuli
  3. Conductivity
    a. Electrical impulses are conducted along the entire length of the plasma membrane
  4. Extensibility
    a. Can be stretched up to 3 times their resting length without damage
  5. Elasticity
    a. Can return to original shape after being stretched
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3
Q

What are the 5 fascicle arrangements?

A
  • Circular
  • Convergent
  • Parallel
  • Fusiform
  • Pennate
    o Short fascicles attach obliquely to a central tendon
    o Unipennate = If fascicles insert into only one side of the tendon
    o Bipennate = if fascicles insert into opposite sides of the tendon
    o Multipennate = if fascicles insert from several different sides
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4
Q

What are the 8 muscle modes of action?

A 
1.	Extensor: 
	o	↑ angle at a joint
2.	Flexor: 
	o	↓ angle at a joint
3.	Abductor: 
	o	Moves limb away from midline of body
4.	Adductor
	o	: Moves limb towards midline of body
5.	Levator: 
	o	Moves insertion ↑
6.	Depressor:
	o	Moves insertion ↓
7.	Rotator: 
	o	Rotates bone along its axis
8.	Sphincter: 
	o	Constricts an opening
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5
Q

What are the levels of muscle architecture?

A
  1. Epimysium
    a. Covers each muscle
    b. Allows muscle to contract & move while maintaining structural integrity
    c. Separates individual muscles from each other
  2. Muscle
  3. Perimysium
    a. Covers each fascicle
  4. Muscle fascicle (bundle of muscle fibers)
  5. Endomysium
    a. Covers each muscle fiber forming the basement membrane
  6. Muscle Fiber (Cell)
  7. Myofibril
  8. Sarcomere
  9. Myofilaments
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6
Q

What are the types of Muscle Fibre?

A
  1. Type 1: Slow Twitch / Slow Oxidative (SO)
    i. O because primarily use oxidative pathways to reduce ATP
    ii. Have most mitochondria because primarily use oxidative pathways (krebbs, etc.)
  2. Type 2: Fast Twitchi. 2A-Fast Oxidative Glycolytic (FOG): slowest of T2’s
    ii. 2X-Fast Glycolytic (FG): intermediate
    iii. 2B: Fastest twitch – only found in specialized muscle

c. Twitch = simplest muscle contraction in response to a single stimulus

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7
Q

What are myofibrils?

A
  • Cylindrical organelles in the sarcoplasm of muscle cells
  • Bundles of specialized proteins organized into repeating contractile structures (sarcomeres)
  • Contains thick and thin myofilaments
    o Thick = Myosin
    o Thin = Actin
  • Also regulatory proteins (tropomyosin & troponin) and 2 giant accessory proteins (titin & nebulin)
  • Thick & Thin overlap = striated appearance
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8
Q

What is a sarcomere?

A
  • Repeating functional unit within myofibril

- Divided into the I band (2 halves), A band, H-zone, M line, Z line (bisects the I band, separates adjacent sarcomeres)

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9
Q

What is the I Band?

A
  • Light Band in sarcomere
  • Only thin (actin) filament
  • Shortens during contraction due to increasing overlap of actin & myosin
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10
Q

What is the A Band?

A
  • Dark Band in sarcomere
  • Both actin and myosin filaments
  • Middle region (H zone) contains only myosin
  • Remains the same size during contraction
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11
Q

What is the H Zone?

A
  • Central region of A band in sarcomere
  • Only thick myosin filaments
  • Shortens during contraction due to increasing overlap of actin & Myosin filaments
  • No longer visible when muscle is fully contracted
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12
Q

What are Z discs?

A
  • Middle of the I band in the sarcomere

- Narrow, plate-shaped regions of dense material that separate one sarcomere from the next

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13
Q

What are the 3 regions of a Myosin molecule?

A
  1. Long thin fibrous rigid tail
  2. Hinge region
  3. 2 heads
    a. Contain actin binding domain (blue dot), and…
    b. An ATPase site (purple dot)
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14
Q

Structure of a Myosin molecule

A
  • Myosin = Large protein that forms thin rod-like molecule when bound to other M’s
  • Myosin mol Is a hexamer of 2 identical myosin heavy chains (Green) & 2 non-identical myosin light chains (brown)
-	3 regions:
	o	Long thin fibrous rigid tail
	o	Hinge region
	o	2 heads
		1.	Contain actin binding domain (blue dot), and…
		2.	An ATPase site (purple dot)
  • Middle of thick filament attached to M line
    o Tails of mols all point to M line
    o Heads all point to Z-discs = clusters of heads on either end of filament
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15
Q

What is the structure of the thin filament?

A 
-	Made of 3 proteins:
	o	Actin (structural)
	o	Tropomyosin (regulatory)
	o	Troponin (regulatory) – 1 of its subunits binds Ca2+
  • Actin monomers form a double stranded filament = backbone
  • Each monomer has myosin binding site
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16
Q

What is the thin filament doing in the relaxed state?

A

Tropomyosin physically covers myosin binding site

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17
Q

What is the thin filament doing the the contracted state?

A

o Ca2+ binds reversibly to troponin
o Troponin-Ca2+ pulls tropomyosin away from myosin-binding sites
o Allows Myosin heads to bind

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18
Q

What is the purpose of Titin & Nebulin in the sarcomere?

A

They ensure proper alignment of filaments within a sarcomere

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19
Q

Titin

A

o Huge elastic mol
o Largest known protein
o From 1 Z disc to neighbouring M line
o 2 functions: stabilizes the position of contractile filaments & its elasticity returns stretched muscles to their resting length

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20
Q

Nebulin

A

o Inelastic giant protein
o Lies alongside thin filaments & attaches to Z disc
o Helps align the actin filaments

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21
Q

Sarcoplasmic Reticulum

A
  • Is a modified ER
  • Consists of interconnected sacs & tubes that surround each myofibril
  • Terminal cisternae = expanded portion at end of each DR (2x per SR)
  • Stores Ca2+ used for muscle contraction – most in terminal cisternae
  • [Ca2+] ↑in SR than cytoplasm
  • SR membrane has Ca2+ release channels = Ryanodine Receptors
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22
Q

What are Ryanodine Receptors?

A

Ca2+ Release channels in the sarcoplasmic reticulum membrane

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23
Q

What are Transverse Tubules?

A
  • Extensions of the sarcolemma that enter the cell
  • Fill the narrow gap between adjacent SR’s terminal cisternae
  • Contain extra-cellular fluid
  • Contain voltage-gated Ca2+ channels (DHP receptors)
  • Allow action potentials to move into interior of the muscle cell
  • Triad = structure where a T-tubule meets the 2 terminal cisternae
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24
Q

How does an action potential move down the sarcoplasmic reticulum?

A

o Depolarization starts at motor end plate
o Action Potential (AP) transmitted along sarcolemma
o Descends into fibre via T-tubules
o Depolarization of T-tubule membrane
o Ca2+ channels open into the SR cisternae
o Rapid release of Ca2+ from SR

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25
Q

What is the Sliding Filament Theory?

A
  • Thin filaments slide over the thick filaments resulting in shortening of sarcomere & muscle
  • Head of myosin filament can bind to thin filament at Myosin binding domains
  • When heads bind they bend 45° towards middle of sarcomere pulling thin filament towards the M line
  • Heads then detach move back and are able to re attach to the thin filament and repeat
  • Thick and thin filaments don’t change length – sarcomeres shorten
  • Requires ATP hydrolysis & Ca2+
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26
Q

What is a myosin cross bridge?

A
  • ↑Ca2+ levels in cytosol initiates the power stroke (when heads swivel pushing actin towards centre)
  • Ca2+ binds to troponin
  • Troponin-Ca2+ complex pulls tropomyosin away from myosin-binding site
  • Myosin binds strongly with actin and completes power stroke
  • Energy required comes from hydrolysis of ATP by the ATPase in the myosin head
    o Energy released is trapped by myosin & stored as potential E in the angle between the myosin head and the long axis of myosin filament
    o PE becomes kinetic E as power stroke moves Actin
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27
Q

What is the process of a myosin cross bridge power stroke?

A
  1. Resting sarcomere
  2. Contraction cycle begins – arrival of Ca2+
  3. Active sites exposed – Ca2+ + troponin move tropomyosin exposing Myosin-binding sites
  4. Cross-bridges form – energized heads bind to actin
  5. Myosin-heads pivot – E that was stored in resting state is released (Power stroke)
  6. ATP binds to head, allowing them to release actin - Cross-bridges detach
  7. Myosin reactivates when free myosin head hydrolyses ATP into ADP & P
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28
Q

What is a motor unit?

A

Smallest functional unit of neural control over muscle contraction

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29
Q

What does a motor unit consist of?

A
  • Cell Body
  • Outgrowing alpha motor neurone
  • Muscle fibres it innervates
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30
Q

What is the innervation ratio?

A

The number of muscle cells in a single motor unit

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31
Q

What is an action potential?

A
  • Wave of depolarisation that moves along the membrane of nerve or muscle
  • Due to sudden change in resting membrane potential - inside of cell becomes + charged relative to the outside
  • This is caused by a sudden transient ↑in permeability of the membrane to Na+
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32
Q

What is a Neuromuscular Junction?

A
  • Specialised structure consisting of the terminal branches of the axon of an alpha motor neuron & target muscle cells that these terminal branches make contact with
  • (Motor End Plate)
33
Q

What is the synaptic cleft?

A

The space between the membranes of nerves & muscle cells

34
Q

Where in a muscle fibre is the neuromscular junction found?

A

Near the middle

35
Q

What is the process of Acetylcholine crossing the synaptic cleft as a result of an action potential?

A
  1. Action Potential arrives at presynaptic terminal of the neuromuscular junction, Ca2+ channels open allowing calcium to flow into terminal.
  2. ↑[Ca2+] results in vesicles migrating to membrane of nerve, membranes fuse releasing acetylcholine
  3. [Acetylcholine] ↑at nerve end of cleft than muscle, so it diffuses across the cleft. Binds to receptor mols within the sarcolemma resulting in opening of Na channels
  4. Influx of Na into cell initiates secondary AP which is propagated in all directions
36
Q

What is Excitation-Contraction coupling?

A

The process where electrical stimulus triggers release of Ca2+ from sarcoplasmic reticulum - initiating sarcomere shortening

37
Q

What is the process of excitation-contraction coupling?

A
  1. Action Potential arrives at presynaptic terminal of neuromuscular junction, Ca2+ channels open allowing calcium to flow into terminal.
  2. ↑[Ca2+] results in vesicles migrating to membrane of nerve, membranes fuse releasing acetylcholine
  3. [Acetylcholine] ↑at nerve end of cleft than muscle, so it diffuses across the cleft. Binds to receptor mols within the sarcolemma resulting in opening of Na channels
  4. Influx of Na into cell initiates secondary AP which is propagated in all directions along the sarcolemma and down the T-tubules,
  5. Triggers Ca2+ release from the SR,
  6. Ca2+ binds to troponin which undergoes a conformational change, removing the blocking action of tropomyosin,
  7. Contraction occurs,
  8. Ca2+ is actively removed into the SR when the action potential ends,
  9. Tropomyosin blockage is restored, and the muscle relaxes.
38
Q

What is an isometric contraction?

A

The muscle contracts but doesn’t shorten

39
Q

What is an eccentric contraction?

A
  • The muscle lengthens while trying to contract

- The force produced < the opposing force

40
Q

What is a concentric contraction?

A
  • The muscle visibly shortens

- The force produced by the muscle > the opposing force

41
Q

What is a muscle twitch?

A

o Simplest muscle contraction – performed in vitro

o Latent phase, Contraction phase, Relaxation phase

42
Q

What is Summation?

A

If the muscle is stimulated before it fully relaxes, the force produced by the second twitch will be greater than the first

43
Q

What is incomplete tetanus?

A

Increased frequency of stimulation leads to the relaxation time between successive twitches getting shorter and shorter as the strength of contraction increases in amplitude.

44
Q

What is complete tetanus?

A

A stimulation frequency is eventually reached where there is no visible relaxation between successive twitches. The contraction becomes smooth and sustained.

o Power produced = 4-5X bigger than single twitch

45
Q

What do Muscle Proprioceptors do?

A
  • Determine position of limb in space from:
    o Joint angle
    o Muscle length
    o Muscle tension
46
Q

What is a muscle spindle?

A
  • Connective tissue capsules (receptors) found in the perimysium
  • Contain specialized fibres with afferent & efferent nerve supplies
  • Provide sensory info about the:
    o Absolute length of the muscle
    o Rate of change in length
  • Spindles monitor muscle movement
  • Gamma motor neurons cause contraction of spindle muscle fibres to take up the slack during muscle contraction
47
Q

What is the Golgi Tendon Organ?

A
  • Receptors
  • Respond to tension rather than length
  • When tension gets dangerously high, sends stim signals to activate the antagonist and inhibitory signals for the agonist
48
Q

Describe the Patellar Reflex Arc

A
  • Patellar tendon is tapped
  • Spindle receptors in the quadriceps are stretched
  • Impulse sent to the spinal cord along the sensory neuron
  • Direct synapse with the motor neuron (monosynaptic reflex)
  • Action potential is generated in the motor neuron
  • Contraction of quadriceps muscle
  • Raises the leg
  • Involuntary reaction
49
Q

What is Plasticity?

A

The capacity for adaptive change

50
Q

What is Myoplasticity?

A

The capacity of skeletal muscle for adaptive change

51
Q

How is anaerobic training characterised?

A

Characterised by high-intensity intermittent bouts of exercise & requires ATP to be regenerate faster than the aerobic exercise system is capable of

52
Q

How is increased neural drive thought to occur as a result of anaerobic training?

A

o ↑agonist (maj muscles involved In a specific movement/exercise) muscle recruitment
o Improved neural firing rates
o ↑synchronization in timing of neural discharge during high intensity muscular contraction
o ↓inhibitory mechanisms

53
Q

Do neural or structural changes typically occur first in muscles as a result of training?

A

Neural

54
Q

What are the central neural adaptations to training?

A
  • The intent to produce maximal force & power causes an ↑ in Motor cortex activity, resulting in ↑motor unit activitation
  • As the level of force developed increases or when a new exercise or movement is being learned -> primary motor cortex activity ↑to support enhanced need for neuromuscular function.
  • Adaptations reflected by substantial neural changes in the spinal cord.
    o Post anaerobic training, recruitment of fast-twitch motor units ↑ as a means to support ↑levels of force expression.
  • Research has shown that only 71% of muscle tissue is activated during maximal efforts in untrained populations
55
Q

What are the Motor Unit Adaptations to training?

A
  • Change in firing rate/frequency of motor unit affects ability to generate force
    o Reflects summation of successive muscle contractions
  • Gains in max strength/power of agonist muscles generally associated with:
    o ↑recruitment
    o ↑rate of firing
    o ↑synchronization of neural discharge
  • Size principle:
  • Selective recruitment:
  • Change in level of tissue activation resulting from chronic resistance training
    o ↑muscle size doesn’t require as much neural activation to lift a given load
    o Highlights importance of progressive overloading during resistance training
  • Changes in rate & sequence of firing
    o + relationship between magnitude of force produced and rate of firing
    o ↑in firing rate dependent on muscle size; small muscles rely on increased firing rate to enhance force production while large muscles depend more on recruitment
56
Q

What is the Size Principle (Motor Unit Adaptations)?

A

o Represents the relationship between motor unit twitch force & recruitment threshold

o Governs recruitment & derecruitment of motor units in an orderly manner

o Motor units recruited in an ascending order according to their recruitment thresholds & firing rates -> motor units high in the recruitment order are only used for high force/speed/power outputs.

57
Q

What is Selective Recruitment (Motor Unit Adaptations)?

A

o Ability of an athelete in some cases to inhibit low-threshold units & activate high-threshold units.

o Critical when force production is required at high speeds

o Appears to be a beneficial intrinsic neural mechanisms favoring explosive exercise

o Specific training methods may enhance selective recruitment

58
Q

What are the Neuromuscular Junction Adaptations to training?

A
  • Post high & low intensity running – ↑NMJ total area
  • High-intensity training -> disperse, irregular-shaped synapses and greater total length of nerve terminal branching
  • Resistance training -> ↑end plate perimeter length and area, & ↑dispersion of acetylcholine receptors within endplate region
  • All of these are beneficial changes in response to training
59
Q

What is Cross-Education?

A

Cross-Education = ↑strength & neural activity in contralateral resting muscle in response to unilateral resistance training. Neural mechanisms a factor

60
Q

What is Bilateral deficit?

A

The force produced when both limbs contract together is less than the sum of forces they produce when contracting unilaterally. Neural mechanisms are a factor

61
Q

What is Bilateral Facilitation?

A

Increase in voluntary activation of agonist muscle group

62
Q

What are the muscular adaptations to training?

A
  • Structural & functional changes encompassing:
    o ↑size
    o Fibre type transitions
    o Enhanced biochem and ultrastructural components
  • Muscle hypertrophy (growth)
  • Role of satellite cells in resistance training-induced hypertrophy:
    o Located between basal lamina and sarcolemma
    o Training -> satellites activated & divide -> ↑number of myonuclei in fibre
    o In theory this should enhance fibres ability to synthesize proteins -. assists in muscle growth
  • Hyperplasia
  • Fibre type transitions:
    o Proportions of each type of fibre are genetically determined, changes within each subtype can occur following anaerobic training
    o Transitions from types 2X -> 2A
  • Structural & architectural changes:
    o Pennation angle = affects force production capabilities as well as the range of motion of a muscle. Larger angles also accommodate greater protein deposition
    o Resistance training -> ↑angle of pennation
-	Other:
	o	↑myofibrillar volume
	o	↑cytoplasmic density
	o	↑sarcoplasmic reticulum and T-tubule density
	o	↑Na-K ATPase activity
63
Q

What is Muscle Hypertrophy?

A

o Term given to enlargement of muscle fibre cross-sectional area following training
o + relationship between hypertrophy & muscular strength
o Involves ↑net accretion (↑synthesis, reduction in degradation) of actin & myosin, and ↑number of myofibrils in fibre
o Protein synthesis ↑rapidly following single resistance training session
o Molecular signals that stimulate muscle protein synthesis following a bout of resistance exercise:
1. Muscle contraction during resistance exercise activate a mechanoreceptor on the sarcolemma that stims the enzymes responsible for synthesising of PA (phosphatidic acid)
2. Results in PA mols binding to mTOR (protein kinase B-mammalian target of rapamycin) -> mTOR activation
3. Contraction-induced activation of mechanoreceptors also activates an enzyme (Erk) that phosphorylates and inhibits TSC2
4. Exercise-induced activation of Erk blocks TSC2/s ability to inhibit Rheb leaving it free to activate mTOR (primary activator of protein synthesis).

64
Q

What are satellite cells?

A

Satellite cells = undifferentiated, predicted to play key role in growth & repair

65
Q

What is hyperplasia?

A

o ↑in number of muscle fibres via longitudinal fibre splitting in response to high-intensity resistance training

o Doesn’t appear to be a maj strat for muscle tissue adaptation to resistance training

66
Q

What are the 6 stages of development in the Long Term Athlete Development Model?

A
  1. Active start
  2. FUNdamentals
  3. Learning to train
  4. Training to Train:
  5. Training to compete:
  6. Training to win:
  7. Active for life: any age
67
Q

Name some Sporting Development Models

A
  1. Long Term Athlete Development Model
  2. Developmental Model for Sport Participation
  3. Psycho-behavioural Model
  4. Bio-psycho-social approach & 3-World Continuum
68
Q

Long Term Athlete Development Model

A
  • 6 stages of development
  • Windows of Trainability:
    o Stamina
    o Strength
    o Speed
    o Skill
    o Suppleness
  • Are concerns around the lack of empirical evidence to support such a model.
69
Q

How does the 3-World Continuum classify the motives and objectives of an individual?

A
  1. Participation for personal well-being (PPW) – taking part in physical activity to satisfy needs other than personal progression
  2. Personal referenced excellence (PRE) – excellence in the form of participation and personal performance
  3. Elite referenced excellence (ERE) – Excellence in the form of high-level sporting performance and achievement
70
Q

What is Training Load?

A

The burden as a stimulus that is applied to a human biological system

71
Q

What is an External Training Load?

A

Any external stimulus applied to the athlete that is measured independently of their internal characteristics

72
Q

What is an internal Training Load?

A

A load measurable by assessing internal response factors within the biological system, which may be physiological, psychological or other

73
Q

What is Periodization?

A
  • Many definitions
  • Best thought of as a flexible concept – a systematic attempt to gain control of the adaptive responses to training in preparation for competition
74
Q

What does a periodised training program look like?

A
  • The training program is designed according to the main performance goal for the season.
  • Training loads are increased progressively and cyclically.
  • The training phases follow a logical sequence.
  • The training process is supported by a structured program of scientific monitoring.
  • Recovery or regenerative techniques are used intensively throughout the training program.
  • Emphasis on skill development and refinement is maintained throughout the training program.
75
Q

What is General Adaptation Syndrome (GAG)?

A

Assumes 3 distinct phases during stress (like an exercise session):

1. Alarm phase: recognition & initial response
2. Resistance phase: Body returned to either pre-exercisie homeostasis or new adapted higher state
3. Exhaustion phase: If accumulation of stress is too great. Synonymous with overtraining.
76
Q

What is the Stimulus-Fatigue-Recovery-Adaptation Theory?

A

o Extension of GAG
o Suggests that training stimuli -> general response that’s influenced by overall magnitude of training stressor.
o Greater overall magnitude of workload – greater the fatigue accumulation – longer delay before complete recovery and adaption can occur.
o This AND GAG share assumption that fitness & fatigue share a cause & effect relationship

77
Q

What is the fatigue-fatigue paradigm?

A

o Athlete preparedness may be evaluated based on the principle after-effects of training – fatigue and fitness.
o Suggests that fitness-fatigue demonstrate an inverse relationship.
o Implies that strats to maximise fitness and min fatigue will have greatest potential to optimize athlete preparedness

78
Q

What is the Allostasis approach to periodized training?

A

o Proposes that efficient regulation requires anticipating needs and preparing to satisfy them before they arise.
- As opposed to homeostasis in which the goal is a steady state

o Suggests organisms maintain physiological stability by anticipating needs before they arise

79
Q

What are the 6 principles of training?

A
  1. Principle of Individuality:
    o Each individual will respond differently
  2. Principle of Specificity:
    o Training adaptations will occur specifically to the muscle groups trained, the intensity of the exercise, the metabolic demands of the exercise and or specific
  3. Principle of Overload:
    o Body must be stressed by working against a stimulus or load that is greater than that to which it is accustomed
  4. Principle of Progression:
    o Training stimulus must gradually and constantly increase
  5. Principle of Diminishing Returns:
    o Performance gains are related to the level of training of each individual. Diminishes the further you get.
  6. Principle of Reversibility:
    o When training stimulus is taken away from an athlete they won’t be able to maintain a certain level of performance.

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