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HES 305 > module 1 > Flashcards

module 1 Flashcards

1
Q

what is the skeletal neuromuscular system key for

A
  • facilitation of energy to action
  • fine to gross motor movement
  • high plasticity
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2
Q

what is the structure of the muscle unit

A
  1. skeletal muscle
  2. muscle fascicle
  3. muscle fiber
  4. myofibril
  5. myofilaments
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3
Q

what is the smallest functional unit of muscle structure

A

sarcomere

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4
Q

what is the band with only thin filaments

A

I band

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5
Q

what is the center of H zone also known as

A

M line

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6
Q

what holds the M disc of thick filament to the Z disc

A

titan

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7
Q

what is the connection between thick and thin filaments called

A

cross bridge cycle

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8
Q

define satellite cells

A

located within the sarcolemma (between plasma and basement membrane)
- helps regenerative cell growth

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9
Q

what occurs with age for satellite cells

A

proliferation declines with aging

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10
Q

what happens when you stress muscle and role of satellite cells

A
  1. proliferation (mitosis)
  2. some cells activate to differentiate and become part of muscle
  3. important when you have atrophy because they help rehabi
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11
Q

explain the myogenic pathway

A
  1. mitosis into additional satellite cells
    2.formation of myotube
  2. translocation of myotube across sarcolemma
  3. fusion of myotube with existing myofibrill
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12
Q

what are the contractile properties of muscle

A
  1. thick filaments
    -6 subunit myosin protein
    -2 heavy chains
    -2 light chains
  2. thin filaments
    -2 twisted strings of spherical actin molecules
    -tropomyosin on actin
    -troponin
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13
Q

explain the contractile contractile mechanism for thick filament

A
  1. before binding to actin, myosin must be activated by hydrolysis of ATP
  2. ATP hydrolysis –> myosin head 45 deg -> 90 deg
  3. aftering binding to actin, Pi+energy released from myosin -ATP binding site=> myosin head rotate swing back (bound to actin)
    4, ADP then released from myosin head binding site
  4. myosin stays attached until another ATP binds
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14
Q

explain the contractile mechanism for thin filaments

A
  1. at rest, tropomyosin provides steric block on actin-binding sites
  2. to initiate contraction:
    i)Ca2+ released from SR, binds to troponin C sites
    ii) troponin makes conformational change, move tropomyosin from actin binding
    iii) allows myosin-actin cross-bridging to occur
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15
Q

explain how calcium is released from SR (contraction)

A
  1. t-tubules progate electrical depolarization resulting from AP from motor neurons
  2. DHP and RyR convert to chemical signals to terminal cisternae
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16
Q

what does speed of relaxation depend on

A

muscle tissue ans fibre type

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17
Q

how is calcium handled during relaxation

A
  • decrease Ca2+ requires ATP
  • SERCA responsible for reuptake Ca2+
    -ability to release ans resequester Ca2+ MAY CONTRIBUTE TO EXERCISE INDUCED FATIGUE
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18
Q

what are the 3 charateritisc of nerve action potentials

A

-large axons
-myelinated
-inside resting neuron is approx -70mV (membrane ATPase pump works to keep gradient

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19
Q

what are the two factors that influence neural speed

A

-axon size (thicker = faster)
-myelinated (causes faster speed conduction through insulated properties)

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20
Q

name 4 piece of protein that create the muscle architecture

A
  1. desmin: connects z-discs of sarcomeres from 2 myofibrils
  2. nebulin: binds actin, nonelastic
  3. titin: connects m-line to z-discs. a molecular spring
  4. a-acinin: forms z-discs
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21
Q

what are the 5 steps of nerve action potential

A

1.membrane is completely polarized
2. AP is initiated, region of membrane depolarizes, resulting in adjacent regions becoming depolarized.
3. when an adjacent region is depolarized to its threshold, AP starts there
4. repolarization occurs due to K+ outflow. The depolarization spreads forward, triggering AP
5. depolarization spreads forward, repeating the process

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22
Q

why is the refractory period important in a-motor neurons and heart cells.

A

-a-alpha MN=shorter because of fast contractions
-heart cells=ventricles need time to fill with blood

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23
Q

what happens at the neuromuscular junction

A
  1. AP arrives at an axon terminal (sends electric signal along surface)
  2. voltage gated calcium channels open and calcium enters the motor neuron
  3. calcium entry causes a release of ACh into synaptic cleft (vesicles undergo exocytosis)
  4. release neurotransmitters across synaptic cleft
  5. neurotransmitters bind to receptors on postsynaptic neuron
  6. acetylcholinesterase degrades ACh where reuptake by the presynaptic neuron and diffusion occurs (closing channels)
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24
Q

what happens when AChE is removed

A

channel stays open, CA2+ keeps coming in and causing depolarization resulting in symptoms such as spasm

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25
Q

how does a cell stay at rest

A

thru hyperpolziation
- excitatory postsynaptic potentials
-inhibitory postsynaptic potentials
(determine whether nerve reaches “all or nothing” threshold

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26
Q

how does botulism affect Ach

A

prevents release of ACh into the NMJ. Causes paralysis (extreme)
-no Ca2+ gets released from SR
-Gates close stopping AP

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27
Q

what are nicotinic receptors

A

ligand gated ions channels

28
Q

describe a muscle AP

A

transmission of nerve impulse by neurotransmitte across synaptic cleft to postsynaptic motor end plate
–opens voltage gate Na2+ channels = MAP

29
Q

fine movement

A

low ratio
-ie. 1 muscle fibre/motor neuron (occulur movement)

30
Q

gross movement

A

high ratio
-ie. 100 fibres. motorneuron (quads)

31
Q

what is a limiting factor in generating muscle power

A

energy producing capacity of the muscle protein filaments

32
Q

how do smaller animals have a bigger advantage in physical activities

A

endurance (mito: smaller > larger)
-speed and power (smaller > larger)
ie. running uphil

33
Q

what percent of slow twitch fibres do athletes carry

A

45-55%

34
Q

twitch

A

contractile response of a muscle fibre to a single MAP

35
Q

define response to meural firing

A

the brief contrcation of all muscles fibres in a MU in response to a single action potential

36
Q

what are the four periods during an Action potential

A
  1. latent period: delay between arrival of AP and initiation of contraction
  2. contraction period: when ca2+ binds to troponin and the actin-myosin cross bridges are formed
  3. relaxation period: when Ca2+ is actively pumped back into the SR, myosin heads detach from actin and muscle tension decreases
  4. refractory period: the period when the muscle tissue is unable to respond to a subsequent AP
37
Q

define summation

A

when a second AP trigger muscle contration before the first contraction has finished result: stronger contraction

38
Q

tetanus

A

very frequent wave summations

39
Q

what are the 2 types of wave summation and define

A

unfused (incomplete) tetanus: - occurs when muscle fibers are stimulated at a rate where it is an incomplete relax between stimuli
fused (complete) tetanus
- occurs when muscle fibers are stimulated at a rate where there is no relax between stimuli

40
Q

what is hennemans size principle

A

smaller (fatigue resistent) to larger - slow twitch fibers are activated first

41
Q

why is the size principle important

A
  • allows for smooth movement
  • we do not always need maximal force
    -save energy(type 1 MF have more mitochondria to resist fatigue)
42
Q

what is the definition of fatigue and the two types

A

fatigue: inability to meet force/energy demand
-peripheral fatigue: brain send a signal but the muscle is not responding
-central fatigue: brain cannot send signal

43
Q

motor unit rotation

A

-some MU’s deactivate and others become active, maintaining contraction strength
-occurs in postural muscle groups and others

basically rotation the muscle fibres so you can sustain the demand for longer

44
Q

what are proprioceptors and how do they send information

A
  • proprioceptors: send info to CNS about changes in length, tension ans joint angles
    1. muscle spindle: detect change in length
    2. GTO: resong th force and tension ans inhibit agonist muscles
45
Q

explain muscle length and passive tension

A

as muscle hit critical length, they “load” passive components of sarcomere
- titin/tendon will load up like a spring creating tension
- as we extend we load potential force which creates tension

46
Q

describe passive force (length tension relationship)

A

force produced by contractile mechanism

47
Q

describe active force (LT)

A

force produced by contractile mechanism

48
Q

describe optimum length

A

maximum active force
- optimal overlap of actin - mysion XB produce greatest tension develop

49
Q

during a length tension relationship why doesn’t the muscle show a plateau

A

none of the bare zone are happening at the same time
-helps make movement smooth

50
Q

why might concentric force decrease the more velocity is given

A
  • it takes time to create CB to attach and detach
    -atp needed to hydrolyze with myosin atpase
    -myosin head cant detatch fast enough, therefore, drag effect is created causing decrease in force
51
Q

why does force increase during fast eccentric contraction

A

the greater the strain placed on myosin heads, facilitates the attachment of the second myosin heads more frequently
- z disc more away from each other we generate less force than demanded - we mechanical pull apart the myosin heads which myosin heads bind back creating a mini power stroke which needs less ATP

52
Q

how can improvements in max power output be caused

A

through increasing max force we can more/and increasing our movement velocity

53
Q

what is the force velocity and power velocity relationship dependent on?

A

the number of attached cross bridges
-force production decreases as the velocity of the contraction increases

54
Q

what are 2 main factors that the force and power velocity relationship are affected by

A

muscle fibre type
- typeIa and IIx generated 2-4x the peak power (compared to type I)
-type IIx have fastest velocities (5.6 fiber length/s)
- type IIa have 3.5 fibers
- type I contract at 0.8fib/s

55
Q

describe the characteristics of resistance training

A
  • train close to current force generating capacity
  • overload (beyond current capacity)
    -dynamic and static (iso) training to increase strength
  • all ages if safe practices followed
56
Q

describe the difference between isokinetic and isometric

A

-isometric: help isolate angles of strength, remove pain points
-isokinetics: maximize force through ROM

57
Q

what are the benefits of understanding where peak force occurs

A
  • inform rehabiiation, strengthing and performance
58
Q

what are benefits of graphs showing abnormal strength

A

-detect injuries, efficiency concerns and return to play
-injury site, pain, compensations

59
Q

what are factors affecting fatiguability

A

-F-V & P-V relationships (ECC exhibits greater absolute but less relative decrease in force)
-fibre-type distribution (type I less fatigue)
-training (delay fatigue, increase absolute intensities and relative intensities)

60
Q

what are some mechanisms for neuromuscular fatigue

A

decrease in XB formation/function
-# of cycling XB
-force per XB
-rate of activation & deactivation of XB
-rate of XB cycling

61
Q

what decreases during fatigue in the brain

A

-decrease in excitation and firing rates of MN
-failure of volitional drive to motor cortex

62
Q

what decreases during fatigue in the spine

A

decrease in excitability of MN, spindles support, reflex inhibition, MU firing rates

63
Q

what decreases during fatigue in the NMJ

A

neuromuscular junction failure– muscle fibers drop out

64
Q

what decreases during fatigue in the muscle

A
  • decrease excitability of sarcolemma (decrease in MAP size)
    -impaired t tubules SR function - ECC failure
65
Q

summarize the 4 neural mechanisms of fatigue failure

A
  1. decrease activation from higher centres (motor cortex signals)
  2. altered reflex inputs to MN (reflex inhibition, muscle spindles)
  3. decrease MN excitability
  4. failure neuromuscular transmission (decrease in neurotransmitter release, sarcolemma propagation)
66
Q

name the 9 steps in Excitation contraction coupling (ECC)

A
  1. MAP along sarcolemma
  2. MAP down t-t
  3. MAP excites voltage-sensing protein in t-t
  4. voltage sensing protein excites SR Ca2+ release channels to open
  5. Ca2+ release from SR
  6. Ca2+ binds to troponin on actin filament
  7. CB cycling
  8. SR Ca2+ reuptake
  9. CB cycling stops
67
Q

name the two main muscle mechanisms to fatigue

A

1.impaired ECC
-decrease in Ca2+ released per MAP
-increase K+ intracellular = repeated MAPs would decrease amplitude of MAP along sarcolemma
-Ca2+ uptake by SERCA pumps
2. metabolic factors
-decrease ATP and PCr in hi-intensites exercise (decrease # of XB’s)
-increase ADO leads to decrease Vmax
-increase Pi leads to decrease in Ca2+ sensitivity of myofibers

HES 305 (1 decks)

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