Neuromechanics Flashcards

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1
Q

Overview of the neural circuitry

A
  • Electrical signals
  • for communication between periphery and brain
  • must be generated by a stimulus
  • must be propagated down an axon
  • must be transmitted to next cell in line
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2
Q

Afferent and efferent neurones

A

Afferent neurones- carry information from sensory receptors (skin) to the central nervous system (cell bodies located outside the spinal cord and along the axon)

Efferent neurones- carry motor information away from the central nervous system/brain to the muscles and glands to initiate an action. (Cell body is a the end, and inside spinal cord)

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3
Q

Reflex loop

A

Spinal cord makes a decision instead of the brain

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4
Q

Simple summary of nervous circuit

A
  • cerebral cortex initiates nervous command.
  • lower nervous centres process commands, interact with other areas and process Afferent (sensory) feedback.
  • feedback used to modulate and correct neural commands
  • a reflex does not require any thought input.
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5
Q

Inter-neurone (relay)

A

Relay neurones are found between sensory and motor neurones (in the brain and spinal cord) and allow sensory and motor neurones to communicate.

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6
Q

How signals flow

A
  • differences in electrical potential
  • high energy electrons and low energy electrons cause potential energy difference
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7
Q

Passive transport

A

Movement down the concentration gradient (chemical force)

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8
Q

Importance of myelin

A

The myelin sheath is a greatly extended and modified plasma membrane wrapped around the nerve axon in a spiral fashion. It allows electrical impulses to transmit quickly and efficiently along the nerve cells.

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9
Q

More of Ranvier

A

A periodic gap in the myelin sheath on the axon of certain neurones that serves to facilitate the rapid conduction of nerve impulses (recharge the action potential that runs along the axon)

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10
Q

Saltatory conduction

A

Describes the way an electrical impulse skips from node to node down the full length of an axon.

Myelin speeds up propagation:
- fatty sheath around axon
- not continuous (nodes of ranvier)
- multiple sclerosis
- axon diameter (larger faster)

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11
Q

Action potential signal phases

A
  • resting membrane potential, maintained by sodium-potassium pumps.
  • depolarisation, Na+ channels open for Na+ to move in (depolarising it)
  • overshoot. Na+ Channels close and K+ channels open to re-polarise the cell.
  • Re-polarisation. K+ moves out of the cell.
  • Afterhyperpolarisation. Additional K+ moves out of cell, hyperpolarising it.
  • cell returns to resting membrane potential.
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12
Q

Absolute refectory period

A
  • during depolarisation
  • neurone unable to respond to another stimulus
  • Na+ channels already open, can’t open more.
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13
Q

Relative refectory period

A
  • during re-polarisation
  • neuron responds only to a very strong stimulus
  • K+ channels open (Na+ closed could open again)
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14
Q

Muscle structure

A

Muscle fascicles- muscle fibres bundled as a unit.
Muscle fibres- consists of a single muscle cell.
Myofibril- muscle cell basic rod like unit (within fibre)
Filaments- within the myofibril
Proteins

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15
Q

3 types of muscular tissue

A

Skeletal muscle
Cardiac muscle
Smooth muscle

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16
Q

Skeletal muscle

A
  • striated
  • elongated cells
  • multinucleated cells
  • voluntary
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17
Q

Cardiac (heart) muscle

A
  • striated
  • branched cells
  • 1-3 central nuclei
  • involuntary
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18
Q

Smooth muscle

A
  • nonstriated
  • single central nucleus
  • involuntary
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19
Q

Angle of Pennation P-CSA VS A-CSA

A

P-CSA- area of the cross section of a muscle perpendicular to its fibres

A-CSA- area of the cross section of a muscle perpendicular to its longitudinal axis

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20
Q

Angle of pennation definition

A
  • the angle between the longitudinal axis of the whole muscle and it’s fibres
  • in some cases the aponeurosis runs nearly the whole length of the muscle
  • muscle fibres can be relatively short, but run at a large angle to the aponeurosis.
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21
Q

Effect of pennation

A
  • direction of force therefore is not the same as the direction of pull
  • this is offset by a larger physiological cross-sectional area
  • pennation angle alters the relationship between shortening of the fibres and the shortening of the whole muscle.
  • muscles with greater angles of pennation have more sarcomeres in parallel so can generate more force.
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22
Q

Epimysium

A
  • tough coat that covers the entire surface of the muscle belly.
  • separate muscles from surrounding tissues and organs.
  • connected to deep fascia
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23
Q

Perimysium

A
  • cover of the muscle bundle
  • loose connective tissue
  • intramuscular nerve branches
  • arterioles, venules
  • intramuscular nerve branches
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24
Q

Endomysium

A
  • surrounds individual muscle fibres
  • pathway ➡️ blood vessels and nerves
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25
Q

Z lines

A

Define the end of sarcomere

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26
Q

I zone

A

Where no overlap between filaments occur

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27
Q

A zone

A

Length of myosin filament

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28
Q

H zone

A

Gap between ends of actin filament

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29
Q

M Line

A

Centre of myosin filament

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30
Q

Actin and myosin

A

Actin filaments, usually in association with myosin, are responsible for many types of cell movements.
Myosin slides along actin to contract the muscle fibre in a process that requires atp
Actin also maintains cell shape and structure.

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31
Q

Sarcoplasmic reticulum

A
  • each myofibril is enveloped in a membranous bag known as the sarcoplasmic reticulum.
  • it’s function is the storage and release of calcium for muscle contraction
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32
Q

T-Tubules

A

Transverse tubules run into the sarcomere at two points: the level of the A and I bands
Contain large number of calcium channels to pump calcium from sarcoplasmic reticulum in and out of sarcomere

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33
Q

Motor unit

A
  • a motor neuron and all of its muscle fibres it innervates
  • each muscle fibre is innervated by a single axon branch
  • single impulse travelling down the motor neurone passes down the axon branch and stimulates all the muscle fibres at the same moment.
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34
Q

Muscle fibres 3 category’s

A
  • large, fast and fatiguable
  • medium, moderate speed and fatiguability
  • small, slow and fatigue resistant
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35
Q

Synapse

A

Where neurons connect and communicate with each other via chemical messengers
Whole area is the neuromuscular junction

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36
Q

Neuromuscular junction phases

A
  • it’s the synapse between a motor neuron and a muscle fibre
  • synaptic boutons can release neurotransmitters, situated over the end plate of the muscle fibre
  • separated by the synaptic cleft
  • junctional folds in end plate contain ligand-gated ion channel receptors for the neurotransmitter acetylcholine.
  • when action potential travels down a motor neurone, causes release of acetylcholine in the synaptic cleft.
  • acetylcholine binds to the receptors on the junctional folds.
  • causes ion channels to open allowing positive sodium ions to flow into the postsynaptic cell.
  • produces depolarisation (executory post synaptic potential) leading to opening of voltage gated sodium channels, causing endplate potential to lead to an action potential.
  • causes contraction.
  • acetylcholineesterase breaks down acetylcholine terminating it’s effects on the muscle fibre.
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37
Q

How do thick and thin filaments interact (cross bridge cycling)

A
  • cross bridge formation- phosphorylated myosin head attaches to actin.
  • the power stroke
  • adp and pi released from myosin head
  • myosin head changes to bend, low energy state
  • shape change pulls actin towards the m line
  • atp attaches to myosin, breaking the cross bridge
  • attached adp hydrolysed by myosin atpase to adp and pi bringing it back to high energy state.
38
Q

High intensity exercise/heavy weight lifting induce what neural adaptations

A
  • fibre type shift to IIa
  • inter muscular coordination
  • motor unit recruitment
  • nerve conduction velocity
  • ## reflexive responses
39
Q

Neural and structural adaptations in response to long term resistance training

A
  • motor unit recruitment
  • improved synchronisation of motor units
  • rate coding/firing frequency
  • reflex sensitivity
  • inter muscular coordination
    Larger pennation angle
  • larger muscle cross sectional area
40
Q

Excitation contraction coupling

A
  • nerve impulse triggers release of acetylcholine from the synaptic knob into synaptic cleft.
  • acetylcholine binds to acetylcholine receptors in motor end plate of neuromuscular junction.
  • initiates a muscle impulse in sarcolemma which of muscle fibre.
  • as muscle impulse spreads quickly from sarcolemma along t tubules, calcium ions released from terminal cisternae into the sarcoplasm.
  • causes post synaptic depolarisation
41
Q

What is a cross bridge

A

Globular head of a myosin molecule that projects from a myosin filament in muscle and in the sliding filament hypothesis of muscle contraction is held to attach temporarily to ah adjacent actin filament and draw it into the a band of a sarcomere

42
Q

Cross bridge cycle (fuel required)

A
  • myosin cross bridge attaches to the actin myofilament.
  • working stroke. Myosin head pivots and bends as it pulls on the actin filament, sliding towards the m line.
  • as new atp attaches to the myosin head the cross bridge detaches
  • as atp is split to adp and pi cocking of the myosin head occurs.
43
Q

Summary of events of excitation contraction coupling

A
  • action potential moves along sarcolemma to the t tubules
  • calcium ions are released from sr
  • calcium ions then bind to Troponin
  • tropomyosin moves away from the myosin binding sights on actin
  • when nervous stimulation ceases, Ca is pumped back into the sr and contraction ends.
44
Q

Titin function

A

To provide structure, flexibility and stability to those cell structures.
Provides a passive force, stability of myosin filaments and stability of sarcomeres
Molecular spring- passive elasticity
Maintain A band in the centre

45
Q

Nebulin

A
  • Large protein
  • alpha helical structure
  • entire length of the thin filament
  • molecular protein ruler
  • interaction- tropomyosin, troponin
  • regulation of muscle contraction
46
Q

Tension velocity relationship

A
  • weak (low force) at high velocity
  • strong (high force) at low velocity
47
Q

What determines muscle force production

A
  • muscle fibre phenotypes and size
  • pennation angle
  • hennemann’s size principle
  • rate coding
  • length tension relationship
  • force velocity curve
  • stretch shortening cycle
  • muscle spindles and Golgi tendon organs
48
Q

Contractile mechanisms

A

Potentiation- active stretch increases force generating capacity. Removal of slack from passive tissue.

Coupling time- increased time for cross-bridge coupling. Constitutes to active stiffness.

Pre load- catch like mechanism. High frequency burst of impulses.

49
Q

Why counter movement jump is higher

A
  • greater activation intensity in time
  • greater joint moments at the start of push off
  • muscles build a high level of active state and force before shortening
  • so can produce more work over the first part of their shortening distance.
50
Q

Muscle spindles

A
  • found deep in muscle belly in intrafusal fibres contained within a collagenous capsule
  • two types of intrafusal fibre (large contain cluster of nuclei, small contain a chain of nuclei)
  • fibres run parallel to extrafusal fibres.
51
Q

Inhibition: Golgi tendon organs

A
  • situated at the musculotendonous junction and attach end to end.
  • ends of large myelinated axons called Afferent fibres.
  • detect rapid changes in muscular force
  • discharge increases via an inhibitory motoneuron.
52
Q

Voluntary force production

A
  • main function of skeletal muscle is to produce force and act on the bone to which the muscle is attached to either stabilise joint complexes and thereby protect bony structures, maintain posture or joint position and enable movement.
53
Q

Muscle activation- excitation contraction coupling

A

As the final common pathway from the nervous system to muscle, the motor unit transmits an activation signal generated by the nervous system to engage the contractile proteins and produce the muscle forces needed for reflex responses, automatic behaviours and voluntary actions.

54
Q

Neural aspects of muscle force production

A
  • motor unit recruitment and firing frequency are pretty similar mechanisms of force regulation at the whole muscle level.
  • motor units recruited in a systematic order during voluntary contractions of increasing magnitude according to the size principle.
  • motor unit firing frequency represents rate of neural impulses delivered from the motor neurone to the muscle fibres.
55
Q

Methods of measuring neural activation

A
  • electromyography (EMG, intra muscular and surface)
  • the interpolated twitch technique
  • mechanomyograms
  • trans cranial magnetic stimulation
  • MRI
  • measurement of V and H waves
56
Q

What is strength

A

Strength is defined as the ability of the neuromuscular system to produce force.
Influenced by bio mechanical, neural and morphological factors.
Contributions of each depend on the strength task.

57
Q

Biomechanical factors affecting strength

A
  • force
  • length
  • velocity
  • power
  • time available
  • time required to sustain force
58
Q

Neural factors affecting strength

A
  • voluntary agonist activation. (Recruitment and amplitude firing frequency, synchronisation)
  • antagonist activation
  • stabiliser activation
  • synergist activation
59
Q

Morphological factors affecting strength

A
  • muscle size
  • architecture (fascicle length/angle of pennation)
  • tendon stiffness
  • muscle contractile properties
  • muscle fibre type
60
Q

Agonist

A
  • muscle generally termed agonists when contracting concentrically they cause joint motion through a specified plane of motion
61
Q

Antagonist

A
  • muscle usually located opposite of the joint from the agonists and have the opposite concentric action, and work in tandem with agonist muscles as a pair
62
Q

Stabilisers

A

Surround the joint or body part and contract to fixate or stabilise the area to enable another limb or body part segment to exert force and move.

63
Q

Synergists

A

Assist the action of the agonist muscles, but are not prime movers of the action and are known as guiding muscles.

64
Q

Why is in Vivo measurement more complicated

A
  • muscles contain mixed fibre types
  • have different architectural characteristics
  • can be influenced by the level of voluntary neuromuscular activation.
65
Q

What is explosive strength/rate force development

A

Explosive for is a measure of the capability to increase force from a low or resting level as quickly as possible
RFD considered even more important than maximal strength during sports like sprinting or jumping etc

66
Q

Evidence for neural adaptations

A
  • improvement in neural function, increasing strength following RT indicated neural function pre training was sub optimal.
  • increases in maximal contraction force and RFD occur also due to changes in the nervous system
67
Q

Indirect evidence for neural adaptations

A
  • disproportionally larger increase in strength than muscle size with resistance training
  • specificity of training phenomenon
  • cross over training effect
  • imagined contractions
68
Q

Direct evidence for neural adaptation

A
  • increased surface EMG following resistance training
  • assessment of completeness of activation using tetanic contractions and inter polated twitch technique
  • evidence is controversial
  • methodological issues
69
Q

Hypothesised their training elicits changes in the following:

A

Increased motor unit recruitment
Preferential recruitment of high threshold MUs
Lowering thresholds of MU recruitment

70
Q

Sites of adaptation

A

Upper motor neurones
Cerebrum
Brain stem, mid brain, pons, medulla
Spinal cord
Lower motor neurones

71
Q

What does the h reflex do

A

Measures the efficiency of synaptic transmission

72
Q

Autogenic inhibition

A
  • normal intrinsic inhibitory mechanisms are the Golgi tendon organs which inhibit muscle contraction if tension is too high.
  • prevents damage to bones and tendon
  • training can decrease inhibitory response
  • muscle can generate more force.
73
Q

What is fatigue

A
  • the reduced ability to produce muscle force (task failure)
  • intense prolonged excitation of muscle leads to a reversible decline in its force generating capacity and rate of contraction, commonly known as fatigue
  • fatigue can also be defined as a decrease in the match/baseline psychological and physiological function of the athlete.
74
Q

What is exhaustion (task failure)

A
  • the limit of human endurance during constant power exercise, that is, the point at which a participant is unwilling or unable to continue a physical task, has been referred to as the point of exhaustion.
75
Q

3 types of fatigue

A

Acute/high intensity fatigue

Cumulative/prolonged or low intensity fatigue

Chronic fatigue

76
Q

Acute or high intensity fatigue

A

Typically arises from acute periods of anaerobic activity during match play

77
Q

Cumulative/prolonged or low intensity fatigue

A

A decline in function over the course of match play/ long duration fatigue

78
Q

Chronic fatigue

A

Cumulative fatigue over the course of multiple training sessions or matches that could heighten athletes risk of injury

79
Q

Power duration relationship

A

The duration that exercise can be maintained decreases as the power requirements increase.

80
Q

Types of fatigue

A

Extreme- task failure before vo2 max attained.

Severe- above cp that can be maintained until vo2 max

Heavy- between Lt and cp

Moderate- below Lt

81
Q

Dehydration as a football fatigue mechanism

A
  • negative fluid balance common after football
  • dehydration level depends on climate and atmospheric conditions
  • moderate fluid loss doesn’t impair anaerobic, cognitive or technical performance but can impair aerobic performance.
  • main factors influencing recovery are fluid consumption
  • rehydration crucial for recovery
82
Q

Glycogen depletion

A
  • in football muscle glycogen is very important for energy production
  • glycogen stores deplete over the course of a match
83
Q

Muscle damage

A
  • during football, explosive actions like sprinting, decelerating, jumping etc are performed
  • involves the stretch shortening cycle and intense eccentric actions and can cause muscle damage
  • could be micro tears or whole muscle damage
84
Q

Symptoms of muscle damage

A
  • disruption if intracellular muscle structure, sarcolemma and extra cellular matrix
  • prolonged impairment of muscle function
  • delayed onset of muscle soreness (stiffness and swelling)
85
Q

Main markers to study muscle damage

A
  • maximal voluntary contraction strength
  • blood markers such as creatine kinase and myoglobin concentrations
  • muscle pain, joint ROM and swelling
86
Q

DOMS

A
  • following unaccustomed exercise, discomfort in the skeletal muscle might be experienced
  • intensity increases for 24 hours and eventually disappears 5-7 days post exercise
  • doms is a type 1 muscle strain (tenderness)
87
Q

Mechanisms of DOMS

A
  • lactic acid
  • muscle spasm
  • connective tissue damage
  • inflammation
  • enzyme efflux theories and other models.
88
Q

Mental fatigue

A
  • football match play evokes psychological stress due to: sustained concentration, perceptual skills, decision making under pressure.
  • players must read environmental cues and make appropriate decisions
  • working cognitively is a demanding task
  • intense periods mean athlete can’t fully recover psychologically, affecting motivation and causing mental burnout.
  • travel can disrupt circadian rhythms and increase stress
89
Q

Acute neuromuscular fatigue

A
  • featigue can be defined as a reduction in muscle performance following muscle contractions, which largely recovers after a period of rest
  • actuate changes that occur with muscle fatigue negatively affect muscle performance
  • risk factor of sports related injured and negatively associated with explosive sporting actions
90
Q

Peripheral fatigue

A

Peripheral fatigue is defined as the loss of force caused by processes occurring distal to the neuromuscular junction and is thought to be the main contributor to muscle fatigue during high intensity exercise

91
Q

Central fatigue

A

There is often sustained central component to fatigue defined as the progressive exercise induced reduction in voluntary activation or neural drive to the muscle