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Physiology 2 > Muscle Physiology Midterm 1 > Flashcards

Muscle Physiology Midterm 1 Flashcards

1
Q

What are the 4 functions of muscles?

A

Generate force, fuel storage, temperature regulation, and force absorption.

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2
Q

2 examples of isotonic contractions

A

concentric and eccentric

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3
Q

Shortening contraction?

A

Concentric (fibres move closer to each other; up phase in a bicep curl)

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4
Q

Lengthening contraction?

A

Eccentric (fibres move away from each other; lowering phase in bicep curl)

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5
Q

Isometric contraction?

A

Muscle contracts, but muscle fibres are static/don’t move

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6
Q

What type of isotonic contraction generates more force?

A

Eccentric contraction generate more force…can lower much more weight than we can curl or squat

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7
Q

What type of muscle contraction causes the most damage?

A

Eccentric/lengthening…downhill running = muscles always shortening = painful

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8
Q

Percentage muscle makes up of total body mass?

A

30-40%…sometimes closer to 50

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9
Q

In order to maintain muscle mass, what must be equal?

A

The rate of protein synthesis and the rate of protein degradation

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10
Q

During muscular hypertrophy what is occurring?

A

Less protein breakdown and more protein synthesis (extracting more AA from diet to build more muscle/protein) results in NET muscle growth

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11
Q

What happens during muscular atrophy?

A

Protein degradation exceeds protein synthesis…AA used as a fuel source for other metabolic processes and to support other tissues

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12
Q

3 fuels in muscle

A

proteins, glycogen, lipid droplets

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13
Q

Why is it a good thing muscle protein is broken down for energy in times of need?

A

Muscles can still contract (just not with as much force) even at reduced protein levels, but my sacrificing itself, the muscle allows other systems/organs, like the kidney to continue working

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14
Q

Shivering thermogenesis?

A

Get cold, muscles contract. Overal mechanical efficiency is on about 20% with the balance of energy given off as heat.

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15
Q

Nonshivering thermogenesis?

A

UCP and SR Ca-ATPase

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16
Q

How does uncoupling proteins generate heat?

A

Dissipate the protein gradient in the inner mitchondrial membrane created by food stuffs, by allowing the H ions to flow back into the matrix without going through the ATP-synthase molecules, releasing the energy as heat instead

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17
Q

How do UCP increase BMR?

A

Food is being used to create gradient, but if no ATP is made from this gradient, more energy (food) must be used to create enough of a gradient to make ATP

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18
Q

How do muscles work as force absorbers?

A

Protect the skeleton and internal organs

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19
Q

What is muscle made of?

A

Approximately 20-30 thousand proteins

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20
Q

Is muscle homogeneous?

A

NO…heterogeneous

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21
Q

What makes a muscle heterogeneous?

A

Different proteins (pumps, channels, enzymes, etc), in different concentrations (more myosin than UCPs) and forms (different myosin isoforms,etc)

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22
Q

What determiens the specialized function and characteristics of a muscle cell?

A

Amount and patterns of expressions of various Protein isoforms

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23
Q

Are muscles homogeneous in structure/function?

A

YES! All have myosin, actin, Ca pumps, etc. Just in different amounts

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24
Q

Is muscle adaptable?

A

YES. Depends on stress placed on muscle. Example, 12-18 hours after a limb is casted, already there is an increase in protein breakdown and wasting and concentrations of proteins are already changing, like mitochondrial proteins

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25
Q

Contractile proteins?

A

Actin and myosin

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26
Q

Bulk of sacroplasm in muscle is made up of ?

A

Actin and myosin (2/3 dry mass)

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27
Q

Actomyosin ATPase does what?

A

Allws for interaction between actin and myosin. Myosin is an ATPase that uses ATP to chanfe shape of myosin molecule and allot connection with actin

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28
Q

Regulatory proteins?

A

Troponin and tropopmyosin

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29
Q

Role of regulatory proteins?

A

Regulate actin/myosin interactions (blocking function), so control contraction/relaxation cyle

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30
Q

Why is Ca2+ regulated?

A

If it wasn’t, contraction would be happening all the time.

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31
Q

Purpose of SR?

A

ER in other cells; storage, release and uptake of Ca2+; uses CA2+ ATPase to uptake CA into SR…used ATP because pumping Ca2+ against concentration gradient

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32
Q

What happens when calcium concentrations increase in the muscle fibre?

A

Ca binds to troponin, causing it to change shape and remove tropomyosin’s blocking action, allowing for strong actin-myosin interaction (increase in force)

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33
Q

How is muscle an excitable tissue?

A

Innervated by a motoneuron, which releases Ach onto motor endplate, causing a depolarization.

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34
Q

Purpose of t-tubules?

A

Propagation of APs into muscle cell

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35
Q

5 cellular systems of muscle

A
  1. Contractile system (myofibrils) 2. Ca2+ Regulation System 3. Excitation System–Electrical Potential 4. Metabolic/Energy System 5. Nucleus/multi-nucleation
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36
Q

The specific term used to refer to the ability of skeltal muscle to adapt to stress?

A

Plasticity

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37
Q

What is the function of SERCA?

A

UPTAKE of Ca2+

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38
Q

3 energy systems in muscle

A

PCr/High Energy Phosphate transfer system, Glycolytic system in cytosol of 11 reactions to form ATP from carbs, Oxidative Phosphorylation in mitochondria to make ATP from carbs, fats, AA

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39
Q

Broad term for enzymes that split ATP into ADP and Pi?

A

ATPase

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40
Q

Why are muscles multi-nucleated?

A

Need LOTS of proteins and also helps allow the cells to be elongated, which is better than many single nucleated cells working independently

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41
Q

Can muscle fibres regenerate?

A

NO, but can gain more nuclei, which allows for more proteins to be synthesized

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42
Q

% of ATP Actomyosin ATPase uses for crossbridge cycling?

A

70-80%

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43
Q

% ATP Ca2+ ATPase uses to pump calcium unto the SR?

A

20-30%

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44
Q

% ATP sarcolemma ATPase uses to maintain Na+/K+ gradient?

A

less then 10%

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45
Q

Purpose of t-tubules?

A

Allow AP to go into the muscle fibre, not just along the sarcolemma

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46
Q

Triad of the reticulum consists of?

A

2 terminal cisternae and tranverse tubule

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47
Q

2 types of mitchondria in muscle

A

SS mitochondria near the sarcolemma and IMF mitochondria between fibres

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48
Q

Purpose of triad of the reticulum?

A

Where AP is linked to calcium release…where electrical event is turned into chemical event

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49
Q

Does the sarcolemma cover the nuclei?

A

YES…want genetic information inside the cell

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50
Q

Skeletal muscle is composed of?

A

Connective tissues, muscle fasicles, blood vessels, nerves

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51
Q

Muscle fasicles are composed of?

A

individual muscle fibres/cells

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52
Q

Muscle fibres are composed of?

A

Sarcolemms, t-tubules, sarcoplasm, and multiple nuclei

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53
Q

Sarcoplasm consists of?

A

SR, myofibrils, mitochondria, gylcogen granules

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54
Q

Myofibrils are composed of?

A

Troponin, actin, tropomyosin, myosin, titin, nebulin

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55
Q

Thin filaments are composed of?

A

Actin, tropomyosin, troponin

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56
Q

Thick filaments are made of?

A

Myosin

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57
Q

Thin and thick filaments are organized into?

A

Sarcomeres

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58
Q

Cytoskeleton proteins?

A

Titin and nebulin

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59
Q

Purpose of cytoskeleton proteins?

A

Provide structure

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60
Q

What is the smallest function unit (can see length change) unit of a muscle?

A

Sarcomere…about 2.5 micrometres, but can change by stretching/shortening of sarcomeres

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61
Q

What is the most abundant molecule in skeletal muscle?

A

Myosin

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62
Q

Why is myosin considered a motor protein?

A

Converts chemical energy in ARP into the mechanical energy of movement

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63
Q

What does a certain myosin isoform determine?

A

Contractile speed (Vmax)

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64
Q

How many heavy chains does a myosin molecule have?

A

2 HC that intertwine to form a long coiled tail and a pair of heads that bind actin, forming cross bridges

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65
Q

How many reactive sites does myosin have and for what?

A

1 for actin and 1 for nucleotide (ATP) binding site

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66
Q

How many light chains are associated with the heavy change of each myosin head?

A

2…phoshphorylatable light chain and alkali light chain

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67
Q

Isoforms of the alkali light chain?

A

2 isoforms (LC1 and LC3)

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68
Q

Purpose of the alkali light chain?

A

Provides structural stability to cross bridge and regulates myosin ATPase activity (dependent on if it is LC1 or LC3)

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69
Q

Alkali light train is also known as?

A

The ESSENTIAL light chain

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70
Q

Phosphorylatable light chain is also known as?

A

The REGULATORY light chain (LC2)

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71
Q

Purpose of phosphorylatable light chain?

A

As Ca2+ is released during muscle activation, some of the Ca2+ can activate myosin light chain kinase, resulting in the phosphorylation of the P light chain, which can increase force and rate of force development

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72
Q

How many myosin molecule makes up a thick filament?

A

250 molecules, each thick filament arranged so bipolar myosin heads clustered at the ends and contral region is a bundle of myosin tails (H zone)

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73
Q

2nd most abundant protein in muscle

A

actin

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74
Q

Actin is composed of?

A

Small globular units (G action) that form long strands of fibrous actin (F actin)

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75
Q

Actin filament is formed by?

A

2 strands of F actin in coiled coil

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76
Q

How many active sites and for what does a G actin molecule have?

A

2 active site to which myosin heads will bind during contraction

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77
Q

Shape of tropomyosin?

A

long, rod-shaped, double-stranded, helical protein that is wrapped about the long axis of the actin backbone

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78
Q

Purpsoe of tropomyosin?

A

Serves to block the active site on actin, thereby inhibiting action and myosin from binding under resting conditions (Steric Blocking Model)…muscle contraction cannot occur

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79
Q

Troponin is a complex of how many polypeptides/subunits?

A

3

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80
Q

3 types of troponin?

A

Tropomyosin binding (T), inhibitory binding (I), and calcium-binding (C)

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81
Q

Job of T troponin?

A

Positions the 3 subunit complex of troponin on thin filament

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82
Q

Job of troponin I>

A

Binds to actin and inhibits interaction of actin and myosin

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83
Q

Job of troponin C?

A

Binds up to 4 Ca2+ and with Ca2+ bound, relieves inhibition of myosin binding to action by sliding troponin I out of the way, what moves tropomyosin and frees up the active site to allow strong cross bridges between actin and myosin

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84
Q

How many troponin complexes for every actin monomer?

A

7 troponin complexes for every 7 actin monomers

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85
Q

How many thin filaments surround each thick filament?

A

6

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86
Q

How many thick filaments surround each thin filament?

A

3

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87
Q

I-band consists of?

A

Thin filaments only

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88
Q

A band consists of?

A

Thin and thick filaments

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89
Q

H-zone consists of?

A

Tails of myosin/thick filaments only

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90
Q

Purpose of M line?

A

Keeps thick filaments in position and proper spacing. Also holds them in a regular hexagonal lattice

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91
Q

Purpose of A disk?

A

Keeps thin filaments in position

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92
Q

Purpose of alpha actinin?

A

Actin cross-linking protein in Z-disk region that anchors thin (actin) filaments, 2 isoforms

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93
Q

Purpose of desmin?

A

Conect 2 sarcomeres from adjacent myofibrils

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94
Q

Purpose of nebulin?

A

An ineleastic (rigid) giant protein that lies alongside think filaments and attaches to Z-dosk…helps align the actin filaments of the sarcomere, which stops them from being “floppy”

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95
Q

Purpose of titin?

A

Huge elastic molecule that stretched from 1 Z-disk to next M-line (1/2 a sarcomere), stabilizes position of contractile filaments (keeps thick filaments in middle between 2 z-lines for optimal length to generate force), and its elasticity returns stretched muscles to resting length

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96
Q

3rd most abundant protein in muscle?

A

TITIN

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97
Q

Major protein damaged during eccentric loading?

A

TITIN…actually breaks, which causes some sarcomeres not to return to optimal resting spot, so not optimum amount of myosin.actin interaction, so not enough force

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98
Q

Proteins at the M-line?

A

M protein and myomesin

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99
Q

Purpose of dystrophin?

A

Flexible, elongated actin-binding protein that anchors superficial myofibrils to sarcolemms, which allows for even distribution of force across the sarcolemms to avoid tearing of the membrane

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100
Q

Largest protein in body?

A

TITIN

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101
Q

Largest gene in the body codes for?

A

Dystrophin

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102
Q

Scientist that discovered sliding filament theory?

A

Huxley inn 1954

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103
Q

Basis of sliding filament theory?

A

Overlapping muscle filaments of fized lengths (thick and thin filaments slide past each other in an energy-requiring process, resulting in muscle contraction

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104
Q

During muscle contraction what shortens in the sarcomere?

A

H-zone nad I-band shorten, as z disks come closer together

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105
Q

What remains constant during muscle contraction?

A

A band

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106
Q

A band represents the length of?

A

Thick filaments (250 myosin molecules put together)

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107
Q

Myosin molecule consists of?

A

2 heavy chains intertwined to form a long coiled tail and a pair of heads that bind actin, forming cross bridges. Each head has 2 binding sites and 2 light chains associated with it.

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108
Q

2 thin filaments consist of?

A

2 strands of F-actin molecules in a coil with troponin subunits every 7 actin and tropomyosin wrapped about the long axis of the actin backbone

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109
Q

Excitation-Contraction coupling?

A

The sequence of events by which an action potential at the sarcolemms (an electrical event) initiates the sliding of the myofilaments, resulting in contraction (a mechanical event)

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110
Q

Steps on excitation-contraction coupling?

A

AP generated in MN, which releases ACh at NMJ, starting depolrization of sarcolemms. AP conducted along sarcolemma and into t-tubules. AP triggers Ca2+ release from the SR. Ca2+ binds to Troponin C, relieving troponin C, allowing tropomyosin to move from the actin active site. Strong cross bridges between actin and myosin. The power stroke of myosin moves actin filaments past it and the muscle contraction

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111
Q

Relaxation in muscle?

A

Excitation (neural input) stops and Ca2+ is pumped back into SR by SERCA. Decrease in cystolic Ca2+ causes Troponin ! to go back to original spot, placing tropomyosin back to covering actin binding site. Binding site is blcoked so the actin and myosin dissociate and the muscle relaxes

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112
Q

Can a muscle contract without an AP?

A

Yes, just needs calcium

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113
Q

The Steric Blocking Model?

A

States that the regulatory protein, tropomyosin, exerts a blocking function between actin and myosin effectively preventing their interaction. Essentially, there’s NO actin-myosin interaction possible at low Ca2+ levels and role of calcium is simply to control the movement of TM in and out of blocking position

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114
Q

Kinetic studies show what contradictory evidence against the Steric Blocking Model>

A

Myosin can bind actin in 2 steps…an initial weak bound state (even at low Ca2+) and a strongly bond or rigor-like state in the presence of high Ca2+

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115
Q

TM movement into grovve of teh F-actin helix results in?

A

An increase in the number of myosin heads attached to actin

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116
Q

Calcium regulates both what and what?

A

Both the attachment of myosin ot actin and the transition from weak to strong binding states

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117
Q

The Kinetic Model?

A

Is based on the observation that actin-myosin can combine in weak binding at low Ca2+, and therefore the steric blocking mod is not entirely valid, although, there can still be some steric blocking. Rather, a KINETIC STEP in actin-myosin is involved, working through ATPase activity but results in transition from weak to strong binding

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118
Q

In An intact muscle, the initial event that is needed to begin contraction (not force generation) is?

A

Generation of an AP

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119
Q

What is responsible for the transition from weak to strong binding?

A

Increase in cystolic Ca2+ results In Myosin releasing Pi, allowing for strong attachment betwee actin and myosin because tropomyosin is out of blocking position

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120
Q

Steps on the Kinetic Model?

A

Myosin can bind to TN-TM-Actin both in the presence and absence of activating calcium levels, but activating calcium levels enhance interaction. Binding of Ca2+ to TN-C overcomes the inhibition of TN-I. TM filament moves. Activation of TN-TM-Actin (open binding site on actin). M-ADP-Pi binding to TN-TM-Actin* overcomes the rate limiting step of myosin ATP hydrolysis with release of Pi molecule. M-ADP binds the thin filament with a higher affinity and muscle contraction proceeds

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121
Q

What is the cross-bridging cycle?

A

The cyclic events that are necessary for the generation of force within the myosin heads during muscle contraction

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122
Q

Event responsible for the power stroke?

A

Release of ADP

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123
Q

Cross bridge cycling biochemical events?

A

Ca2+ activates Thin Filament, which alters ATPase to release Pi. Release of Pi is responsible for transition from weak to strong binding. Release of ADP responsible for power stroke,. ATP binding results in detachment from actin and/or weak binding

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124
Q

Sarcolemma?

A

Outer surface of plasma membrane that surrounds the entire cell

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125
Q

T-tubules?

A

Invaginations of the sarcolemma into the fibers interior along a line vertical to the fibre axis. Lumen of the t-tubule system is continuous with the extracellular space

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126
Q

Where are t-tubules located in sarcomere?

A

Near border of A-I junction in sarcomere and connects with Z-line of the myofibrils via intermediate filaments called desmin

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127
Q

Composition of sarcolemma and t-tubules?

A

Phospholipid bilayer with a variety of specialized proteins (channels, pumps, transporters, receptors, etc)

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128
Q

How is Ca2+ released from SR?

A

AP travels down t-tubules trips off DHPR, which is physically connected to RyR on the SR, causing them to open ad release Ca2+ into cytosol

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129
Q

What is resting membrane potential difference?

A

An electrical gradient between the extracellular fluid and the intracellular fluid

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130
Q

For sarcolemms and the T-tubules’ membrane potentials are determined essentially by what 3 ions?

A

Na+, K+, and Cl-

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131
Q

What 2 factors contribute to the net membrane potential?

A

Concentration gradient across the membrane (how many ions are where) and membrane permeability (more permeable to some ions than others, can change permeability by opening/closing ion channels)

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132
Q

Extracellular, intracellular concentrations of Na+?

A

150 Extracellular mM and 15 Intracellular mM

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133
Q

What is the extracellular and intracellular concentrations of K+?

A

5 mM Extracellular and 150 mM intracellular

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134
Q

What is the extracellular and intracellular concentrations of Cl-?

A

123 mM Extracellularly and 4.2 mM Intracellularly

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135
Q

What is equilibrium potential?

A

The embrane potential difference that exactly opposes the concentration gradient of the ion

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136
Q

What is the equilibrium of K+?

A

-90 mV

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137
Q

Equilibrium potential of Na+?

A

+60 mV

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138
Q

What is the RESTING membrane potential of muscle?

A

-70 mV

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139
Q

Why is the resting MP of muscle -70 mV?

A

Muscle cells are about 40x more permeable to K+ that to Na+, and as a result, a cells resting MP is closer to the Ek of -90 mV than to the ENa of +60 mV

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140
Q

What determines membrane permeability to a particular ion?

A

Opening and closing of ion channels

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141
Q

What causes changes in MP (i.e. the AP)?

A

Changes in membrane permeability to Na+ and K+ (i.e. opening of Na+ or K+ channels)

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142
Q

Steps in an AP

A
  1. Resting MP -70 mV 2. Depolarizing stimulus (ACh onto motor end plate) 3. Membrane depolarizes to threshold. Voltage-gated Na+ channels open and Na+ enters cell. Voltage-gated K+ channels begin to open slowly 4. Rapid Na+ entry depolarizes cell 5. Na+ channels close and sower K+ channels open 6. K+ moves from cell to ECF 7. K+ channels remain open and additional K+ leaves cell, hyperpolarizing it 8. Voltage-gated K+ channels close, some K+ enters cell through leaky channels 9. Cell returns to resting ion permeability and resting MP
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143
Q

What does the Na+ - K+ - ATPase do?

A

Carries 3 Na+ out of the cell at the same time as 2 K+ are moved into the cell. This action requires 1 ATP for every 3 Na+ and 2K+ pumped across.

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144
Q

Why is the ratio of Na+ pumped out of the cell and K+ pumped into the cell in a 3:2 ratio?

A

Want to have more positive charges leaving than coming in, in order to maintain negative MP

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145
Q

Function of Na+-K+-ATPase?

A

Insure the primary control of cell volume and maintenance of Na+ and K+ gradients across the cell membrane

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146
Q

Structure of the Na+-K+-ATPase?

A

Sarcolemmal enzyme; functional dimer (alpha and beta subunits…both must be present for pump to work)

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147
Q

Capacity of Na+-K+-ATPase determined by?

A

Concentration of pumps (how many pumps there are) and the activity of the pumps (how fast/slow they are working)

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148
Q

Alpha subunit of Na+/K+ ATPase has binding sites for?

A

ATP and Na+/K+

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149
Q

Beta subunits in the Na+-K+-ATPase serve what purpose?

A

Involved in proper insertion of alpha subunit into the plasma membrane and required for proper enzymatic activity

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150
Q

Isoforms of alpha subunits in Na+/K+ ATPase?

A

Alpha 1 and alpha 2

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151
Q

Isoforms of Beta subunits in Na+-K+-ATPase?

A

Beta 1, Beta 2, and Beta 3

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152
Q

What happens to the NA+/K+ ATPase during exercise?

A

E/NE bind to beta2-adrenoreceptors, activate adenylate cyclase and increase cAMP levels. This second messenger activates protein kinase A, which increases Na+-K+-ATPase activity. Alsom alpha-beta subunits are translocated from the SR to the sarcolemma.

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153
Q

What is the SR?

A

Extensive membrane system surrounding each myofibril within muscle cells that plays a critical role in skeletal muscle to regulate intracellular free calcium, and to store Ca2+, release it, and uptake Ca2+ upon relaxation

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154
Q

Two parts of the SR?

A

Terminal Cisternae/Junctional SR and Longitudinal SR

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155
Q

Purpose of terminal cisternae/junctional SR?

A

Forms junction with T-Tubule called triad membrane (10-20 nm gap), contains Ca2+ release channel (Ryanodine Receptor), most Ca2+ is found bound to calsequestrin, and its major function is Ca2+ release

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156
Q

Purpose of longitudinal SR?

A

Contain the Ca2+-ATPase pumps (SERCA), and its major function is Ca2+ UPTAKE

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157
Q

Function of calsequestrin?

A

Found in the SR and has a high capacity Ca2+ binding (storage) in the lumen of SR

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158
Q

Phospholamban (PLN)?

A

Found in SR and regulates SERCA activity; expression is fibre type and species dependent

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159
Q

Sarcolipin (SLN)?

A

PLN homologue that regulates SERCA activity; expression is fibre and species dependent

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160
Q

Triadin/Junctin?

A

2 junctional SR proteins that form complex with CRC and CSQ to regulate CRC function

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161
Q

How many Ca2+ can SERCA bring into cell, and for what metabolic cost?

A

2 Ca2+ per 1 ATP

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162
Q

What do PLN and SLN do to the efficiency of SERCA?

A

Decrease efficiency…but increase BMR

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163
Q

Where is the ATP binding site on SERCA?

A

in the cytosol

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164
Q

What is the purpose of the phosphorylation domain in SERCA?

A

Influences activity and confirmation

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165
Q

How transmembrane helices does SERCA have?

A

10

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166
Q

How many binding sites does SERCA have for calcium?

A

2

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167
Q

Elementary steps of Ca2+ translocation?

A
  1. Binding of 2 Ca2+ to the enzyme in a strong binding confirmation towards the cytoplasm (2Ca2+:E1) 2. ATP binds to the enzyme (2CA2+:E1:ATP) 3. ATP is hydrolyzed and a phosphorylated intermediate is formed (2Ca2+:E1~P) 4. Change in the enzyme configuration from the E1 to E2 state with translocation of Ca2+ to the lumen (2Ca2+:E2~P) 5. Release of Ca2+ to the lumen of the SR. Affinity of Ca2+ binding sites reduced by 3-fold (E2~P) 6. Mg2+ dependent hydrolysis of the E2~P intermediate (E2~Pi) 7. Release of inorganic phosphate (E2) 8. Change in enzyme confirmation from E2 to E1 state (E1)
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168
Q

RYR1 gene is for expression of ryanodine receptors for what?

A

Skeletal muscle

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169
Q

RYR2 gene is for expression of ryanodine receptors for what?

A

Cardiac and smooth muscle

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170
Q

Malignant hyperthermia?

A

Defect in ryanodine receptor. Anesthetics or stress lead to prolonged release of Ca2+ and prolonged contraction and damage

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171
Q

SR proteins involved in altering efficiency of SERCA?

A

Phospholamban and sarcolipon

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172
Q

Transition of the E1 to the E2 is important in SERCA because?

A

Decreases affinity for Ca2+ binding to SERCA and the Ca2+ binding site is now facing the lumen

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173
Q

Muscle fibers are classified by?

A

Contractile characteristics, myofibrillar organization, E-C coupling, metabolism, phosphorylation state, membrane transporters, histochemistry, and morphological features

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174
Q

2 primary factors that differentiate muscle fibre types?

A

Rate of speed of contraction (Vmax) and fatigue characteristics

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175
Q

Which had faster Vmax type 1 or 2?

A

Type 2

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176
Q

The rate of speed of contraction is directly related to?

A

Actomyosin ATPase activity, which is determined by the MHC isoform

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177
Q

Order fastest to slowest muscle fibre types?

A

HC2B HC2x(d) HC2a HC1

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178
Q

Do humans express HC2b fibers?

A

No!!! Only rodents

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179
Q

At pH 4.6, M-ATPase of type 1 fibers stain?

A

Dark

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180
Q

At pH 4.6, M-ATPase of type 2a fibers stain?

A

Light

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181
Q

At pH 4.6, M-ATPase of type 2b/x fibers stain?

A

Medium

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182
Q

Type 1 fibers are acid what? Alkali what?

A

Acid stable, alkali labile

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183
Q

Type 2 fibers are acid what? Alkali what?

A

Acid labile, alkali stable

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184
Q

Index of fatigue?

A

Final tension/initial tension x 100

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185
Q

Shape of slow, fast resistant, and fast fatigue muscle fatigability graph?

A

Almost straight line, some what steep, super curved

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186
Q

The maximal rate of muscle shortening is influenced by?

A

Myosin heavy chain expression, which determines which myosin ATPase isoform is present

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187
Q

At pH of 7, which fibre type in rats would have the highest ATPase activity?

A

MHCIIb

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188
Q

At a pH of 7 what fibre type in humans would have the highest ATPase activity?

A

MHCIIx

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189
Q

What does SAG refer to?

A

The time it takes to observe a reduction in force output

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190
Q

How is SAG determined?

A

Using a protocol of continuous tetanic stimulations (muscle contraction) for a period of time (until force begins to drop)

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191
Q

Based on metabolic characteristics, fibres are classified as?

A

Fast-Glycolytic, Fast-Oxidative-Glycolytic, or Slow-Oxidative

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192
Q

For an an oxidative test, SO fibres will stain?

A

Dark

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193
Q

For an oxidative test, FOG (IIa) fibres will stain?

A

Medium

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194
Q

For an oxidative test, FG (IIx/d) will stain?

A

Medium-light

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195
Q

For a glycolytic test a SO (I) fibre will stain>

A

Light

196
Q

For a glycolytic test a FOG (IIa) fibre will stain?

A

Med/Med-light

197
Q

For a glycolytic test FG (IIx/d) will stain?

A

Medium

198
Q

Histochemical stains for metabolic characteristics are only what type of measures?

A

QUALITATIVE measures of aerobic/anaerobic potential

199
Q

Can metabolic properties be used to determine a fibre type?

A

NO!! Due to the diversity found within individual fibre types (as determined by myosin ATPase activity)

200
Q

Oxidative potential from least oxidative to most oxidative?

A

Type IIb (IIdx), Type IIa, Type I

201
Q

Glycolytic potential from least to most glycolytic?

A

Type I, Type IIa, Type IIb (IIdx)

202
Q

Phosphorylation Potential for ATP from least to most?

A

Type I = Type IIa = Type IIx (IIdx)

203
Q

Phosphorylation potential for PCr form least to most?

A

Type I, Type II

204
Q

Fibre type classification schemes?

A

Type I = Slow-Oxidative = Slow Fatigue
Type IIa = Fast-Oxidative-Glycolytic = Fatigue Resistant
Type IIb = Fast-Glycolytic = Fast Fatigue

205
Q

Morphological characteristics of muscle fibre types?

A

Muscle fibre diameter (size), capillary density (muscle blood flow), and myoglobin content (cellular O2 transport)

206
Q

Size of human muscle fibres from smallest to biggest?

A

Type I, Type IIa, Type IIx

207
Q

Size in rat muscle size from smallest to biggest?

A

Type IIa, Type I, Type IIb

208
Q

Least oxidative to most oxidative fibres in rats?

A

Type IIb, Type I, Type IIa

209
Q

Capillaries/area from least to most?

A

Type IIx, Type IIa, Type IIax, Type I

210
Q

SDH concentration from least to most?

A

Type IIx, Type IIax, Type IIa, Type I

211
Q

What is the purpose of hybrid fibres (Type IIax)?

A

Contains MHC a and MHC x, allows the muscle to be “in the middle,” allows for diversity and a continuum of properties

212
Q

The maximal rate of muscle shortening is influenced by?

A

Myosin heavy chain expression, which determines which myosin ATPase isoform is present

213
Q

At pH of 7, which fibre type in rats would have the highest ATPase activity?

A

MHCIIb

214
Q

At a pH of 7 what fibre type in humans would have the highest ATPase activity?

A

MHCIIx

215
Q

What does SAG refer to?

A

The time it takes to observe a reduction in force output

216
Q

How is SAG determined?

A

Using a protocol of continuous tetanic stimulations (muscle contraction) for a period of time (until force begins to drop)

217
Q

Based on metabolic characteristics, fibres are classified as?

A

Fast-Glycolytic, Fast-Oxidative-Glycolytic, or Slow-Oxidative

218
Q

For an an oxidative test, SO fibres will stain?

A

Dark

219
Q

For an oxidative test, FOG (IIa) fibres will stain?

A

Medium

220
Q

For an oxidative test, FG (IIx/d) will stain?

A

Medium-light

221
Q

For a glycolytic test a SO (I) fibre will stain>

A

Light

222
Q

For a glycolytic test a FOG (IIa) fibre will stain?

A

Med/Med-light

223
Q

For a glycolytic test FG (IIx/d) will stain?

A

Medium

224
Q

Histochemical stains for metabolic characteristics are only what type of measures?

A

QUALITATIVE measures of aerobic/anaerobic potential

225
Q

Can metabolic properties be used to determine a fibre type?

A

NO!! Due to the diversity found within individual fibre types (as determined by myosin ATPase activity)

226
Q

Oxidative potential from least oxidative to most oxidative?

A

Type IIb (IIdx), Type IIa, Type I

227
Q

Glycolytic potential from least to most glycolytic?

A

Type I, Type IIa, Type IIb (IIdx)

228
Q

Phosphorylation Potential for ATP from least to most?

A

Type I = Type IIa = Type IIx (IIdx)

229
Q

Phosphorylation potential for PCr form least to most?

A

Type I, Type II

230
Q

Fibre type classification schemes?

A

Type I = Slow-Oxidative = Slow Fatigue
Type IIa = Fast-Oxidative-Glycolytic = Fatigue Resistant
Type IIb = Fast-Glycolytic = Fast Fatigue

231
Q

Morphological characteristics of muscle fibre types?

A

Muscle fibre diameter (size), capillary density (muscle blood flow), and myoglobin content (cellular O2 transport)

232
Q

Size of human muscle fibres from smallest to biggest?

A

Type I, Type IIa, Type IIx

233
Q

Size in rat muscle size from smallest to biggest?

A

Type IIa, Type I, Type IIb

234
Q

Least oxidative to most oxidative fibres in rats?

A

Type IIb, Type I, Type IIa

235
Q

Capillaries/area from least to most?

A

Type IIx, Type IIa, Type IIax, Type I

236
Q

SDH concentration from least to most?

A

Type IIx, Type IIax, Type IIa, Type I

237
Q

What is the purpose of hybrid fibres (Type IIax)?

A

Contains MHC a and MHC x, allows the muscle to be “in the middle,” allows for diversity and a continuum of properties

238
Q

Name 2 factors that can influence SDH levels

A

Fibre type (higher in Type I than Type II) and training status (endurance training increased SDH by increasing mitochondria levels)

239
Q

What are the definitive ways to determine a fibre type?

A

Immunofluroescence and pre-incubation to determine the MHC isoform/myosin ATPase

240
Q

What is the purpose of myoglobin?

A

Intracellular oxygen buffer and facilitates oxygen delivery to mitochondria

241
Q

What type of fibres have the most myoglobin?

A

Type I

242
Q

What type of fibres have the highest Na+/K+ ATPase activity?

A

Type I because they are used more throughout the day, so there MP is disturbed more, making the Na+/K+ ATPase work more

243
Q

Subunits of Na+/K+ ATPase found in Type I fibres?

A

Alpha 1 and Beta 1

244
Q

Na+/K+ ATPase isoform found in Type II fibres?

A

Alpha 2 and Beta 2

245
Q

SERCA isoform in Type I fibres?

A

SERCA2

246
Q

SERCA isoform in Type II fibres?

A

SERCA1

247
Q

RYR Isoform in Type I fibres?

A

RYR1-Slow

248
Q

RYR Isoform in Type II fibres?

A

RYR1-Fast

249
Q

What fibres have the highest Ca2+-ATPase activity?

A

Type II

250
Q

Fibre type that has the fastest Ca2+ uptake?

A

Type II

251
Q

Which fibre has the fastest Ca2+ release and most number of RYR channels?

A

Type II

252
Q

Isoforms of tropomyosin?

A

alpha, beta, and gamma

253
Q

Predominant isoform in Type II fibres?

A

Alpha subunit

254
Q

Predominant isoform in Type I fibres?

A

Beta subunit

255
Q

What does the beta subunit do to cross-bridge development?

A

Slows the rate of cross-bridge development, causes a slower rate of force development, and decreases steady-state level of force

256
Q

How do different troponin isoforms influence contraction?

A

The different isoforms respond different to Ca2+ and how it acts with tropomyosin

257
Q

Z-disk width in fibres from least to greatest?

A

FG, FOG, and SO

258
Q

Lipid droplets in fibres from least to most?

A

FG, FOG, and SO

259
Q

Glycogen granules in fibre types from least to greatest?

A

SO, FOG, and FG

260
Q

What is a motor unit?

A

A set of muscle fibres innervated by a single motor neuron that have: 1. a certain capacity for producing tension 2. A particular contraction speed 3. A characteristic range of firing rate 4. A specific susceptibility to neuromuscular and contractile fatigue 5. A distinctive hitsochemical profile 6. Well-defind morphological properties

261
Q

The characteristics of moto units are matched to the activity of the?

A

Motoneurons. EXAMPLE, a motor unit that is constantly stimulated will be different than one that isn’t stimulated as much, even if they are the same fibre type makes up the motor unit

262
Q

Are all muscle fibres in a motor unit the same fibre type?

A

YES! And, they share other properties, like oxidative capacity, etc.

263
Q

Smallest amount of muscle that can be activated voluntarily?

A

The motor unit

264
Q

How do you increase force in muscle?

A

Recruit more motor units and increase the frequency of stimulation

265
Q

Once a motor unit is recruited, how many fibres within the unit will contract?

A

ALL OF THEM!!

266
Q

Graduation od force in skeletal muscle is coordinated largely by?

A

The nervous system

267
Q

What motor units are recruited first?

A

Slow-oxidative followed by FOG, and finally SO

268
Q

Which of the following would influence absolutre force generation and/or contraction in a fibre?

A

Myosin isoform, tropomyosin isoform, troponin isoform

269
Q

What motor units have the most fibres per unit? The least?

A

Fast fatiguable have the most fibres per motor unit, and slow have the least amount of fibres

270
Q

What kind of muscles have the fewest numbers and sizes of motor units?

A

Muscles that require strict control over the amount of force produced, such as the eye muscles.

271
Q

Motor neuron for Type I fibres?

A

Alpha 2

272
Q

Motor neuron for FOG fibres?

A

Alpha 1

273
Q

Motor neuron for FG fibres?

A

Alpha 2

274
Q

Neuron size of Type 1 fibres?

A

Small

275
Q

Neuron size of fast fibres?

A

Large

276
Q

Conduction velocity of slow fibres?

A

Slow

277
Q

Conduction velocity of fast fibres?

A

Fast

278
Q

Recruitment threshold of slow fibres?

A

Low

279
Q

Recruitment threshold of fast fibres?

A

High

280
Q

Can MHC isoform change in response to the activity of the motorneuron?

A

YES!!! MN signal dictates property of fibres

281
Q

Power athletes have majority of what type of fibres?

A

Fast fibres

282
Q

Endurance athletes have majority of what type of fibres?

A

Slow fibres

283
Q

Non-athletes and weightlifters have majority of what type of fibre?

A

Have about 50% slow and 50% fast

284
Q

Is fibre type the most important thing in determining what makes an elite athlete?

A

NO! Abilitiy to recruit, metabolic properties, biomechanics, etc. are more important

285
Q

Most malleable tissue in body?

A

Skeletal muscle

286
Q

At 25% of pool recruited how many slow fibres are activated?

A

ALL OF THEM

287
Q

At 50% of pool recruitment, how many type IIa fibres are activated?

A

ALL OF THEM

288
Q

Name 2 experimental models that show it’s possible to change a Type II into a Type I fibre

A

Chronic low frequency stimulation and surgically switching the MN

289
Q

What light chain isoform increases Vmax?

A

LC 3 (alkali light chain)

290
Q

All fibres must have what light chain?

A

LC2 (regulatory/phosphorylatable)

291
Q

What do the varying isoforms of the light chain do?

A

They can change the Vmax independent of the heavy chain

292
Q

Reasons to assess muscle/group of muscles ability to generate force?

A
  1. To evaluate effects of any acute perturbation on muscle function (exercise, hypoxia, etc) 2. To evaluate muscle adaptations to exercise training or chronic exposure to different environments 3. To determine the effects of different chemical stimuli (drugs) on muscle function 4. To determine role of different genes in muscle function **Use a Pre-Test vs. Post-Test
293
Q

Isotonic contraction?

A

Contraction at near constant tension

294
Q

Primary function of muscle?

A

To generate force

295
Q

Isokinetic?

A

Contraction near a constant velocity

296
Q

Power = ?

A

Force x Velocity

297
Q

At maximal velocity of contraction what is the theoretical force produced?

A

0

298
Q

At the maximal isometric force what is the velocity?

A

0

299
Q

The force-velocity curve is defined by what equation?

A

Hill Equation Velocity = (max isometric force - Force/load on muscle) / Force on muscle V = (Po-P)/P

300
Q

In a concetric contraction, as velocity increases, what happens to force?

A

Decreases

301
Q

What fibre type can produce more power?

A

Type II x

302
Q

What fibre type can produce more force at a particular speed?

A

Type II x

303
Q

Max power in most muscles occurs at a velocity between?

A

200-300 degrees per second

304
Q

What is maximal isometric strength defined as?

A

The maximal force that can be generated with a maximal voluntary contraction in a given muscle or muscle group under a given set of conditions (i.e. fixed length or joint angle)

305
Q

Force is greatest during what type of contraction?

A

Eccentric

306
Q

Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?

A

(HCIIb)(HCIIb) and (LC3F)2(LC2F)2

Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2

307
Q

2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?

A

Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))

308
Q

Mechanical output in muscles depends on?

A

Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command

309
Q

Fatigue?

A

A decrement in force or power output

310
Q

Central fatigue?

A

A failure to maximally activate the muscle

311
Q

Peripheral fatigue>

A

Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)

312
Q

Central fatigue happens above where?

A

Above the sarcolemma

313
Q

Latent period?

A

Time it takes for stimulus (electrical) to travel to and cause changes in the muscle

314
Q

Contraction time?

A

Time it takes to generate Pt starting from the point in time when force first begins to increase

315
Q

+dF/dt ?

A

Maximal RATE of force development…slope of twitch curve

316
Q

-dF/dt?

A

Maximal rate of force decline…RELAXATION from max force to 0 force

317
Q

1/2 RT?

A

Time it takes for force to decline to 50% of Pt during relaxation

318
Q

Twitch response is determined by?

A

Both the contractile and series elastic elements

319
Q

Parallel Elastic Elements?

A

Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.

320
Q

Series Elastic Elements?

A

Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force

321
Q

Force development with shortening contraction only occurs after slack in what is taken up?

A

SEE

322
Q

How does increasing frequency of stimulation increase force output?

A

Summation. Stimuli that are closer together do not allow muscle to fully relax.

323
Q

What does repetitive stimulation do to force production?

A

Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.

324
Q

Force is greatest during what type of contraction?

A

Eccentric

325
Q

Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?

A

(HCIIb)(HCIIb) and (LC3F)2(LC2F)2

Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2

326
Q

2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?

A

Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))

327
Q

Mechanical output in muscles depends on?

A

Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command

328
Q

Fatigue?

A

A decrement in force or power output

329
Q

Central fatigue?

A

A failure to maximally activate the muscle

330
Q

Peripheral fatigue>

A

Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)

331
Q

Central fatigue happens above where?

A

Above the sarcolemma

332
Q

Latent period?

A

Time it takes for stimulus (electrical) to travel to and cause changes in the muscle

333
Q

Contraction time?

A

Time it takes to generate Pt starting from the point in time when force first begins to increase

334
Q

+dF/dt ?

A

Maximal RATE of force development…slope of twitch curve

335
Q

-dF/dt?

A

Maximal rate of force decline…RELAXATION from max force to 0 force

336
Q

1/2 RT?

A

Time it takes for force to decline to 50% of Pt during relaxation

337
Q

Twitch response is determined by?

A

Both the contractile and series elastic elements

338
Q

Parallel Elastic Elements?

A

Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.

339
Q

Series Elastic Elements?

A

Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force

340
Q

Force development with shortening contraction only occurs after slack in what is taken up?

A

SEE

341
Q

How does increasing frequency of stimulation increase force output?

A

Summation. Stimuli that are closer together do not allow muscle to fully relax.

342
Q

What does repetitive stimulation do to force production?

A

Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.

343
Q

Force is greatest during what type of contraction?

A

Eccentric

344
Q

Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?

A

(HCIIb)(HCIIb) and (LC3F)2(LC2F)2

Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2

345
Q

2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?

A

Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))

346
Q

Mechanical output in muscles depends on?

A

Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command

347
Q

Fatigue?

A

A decrement in force or power output

348
Q

Central fatigue?

A

A failure to maximally activate the muscle

349
Q

Peripheral fatigue>

A

Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)

350
Q

Central fatigue happens above where?

A

Above the sarcolemma

351
Q

Latent period?

A

Time it takes for stimulus (electrical) to travel to and cause changes in the muscle

352
Q

Contraction time?

A

Time it takes to generate Pt starting from the point in time when force first begins to increase

353
Q

+dF/dt ?

A

Maximal RATE of force development…slope of twitch curve

354
Q

-dF/dt?

A

Maximal rate of force decline…RELAXATION from max force to 0 force

355
Q

1/2 RT?

A

Time it takes for force to decline to 50% of Pt during relaxation

356
Q

Twitch response is determined by?

A

Both the contractile and series elastic elements

357
Q

Parallel Elastic Elements?

A

Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.

358
Q

Series Elastic Elements?

A

Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force

359
Q

Force development with shortening contraction only occurs after slack in what is taken up?

A

SEE

360
Q

How does increasing frequency of stimulation increase force output?

A

Summation. Stimuli that are closer together do not allow muscle to fully relax.

361
Q

What does repetitive stimulation do to force production?

A

Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.

362
Q

Force is greatest during what type of contraction?

A

Eccentric

363
Q

Considering only myosin heavy chain and light chain, what fibre type would have the highest Vmax?

A

(HCIIb)(HCIIb) and (LC3F)2(LC2F)2

Humans: (HCIIx)(HCIIx) and (LC3F)2(LC2F)2

364
Q

2 ways mechanical properties of specific muscles or muscle groups can be measured voluntarily?

A

Performance based on tasks involving maximal efforts: isometric (maximal voluntary contraction) and dynamic (maximal POWER output at constant velocity (isokinetic) or constant force (isotonic))

365
Q

Mechanical output in muscles depends on?

A

Both the neural commands to the muscle (activation) and the muscle itself (response) to neural command

366
Q

Fatigue?

A

A decrement in force or power output

367
Q

Central fatigue?

A

A failure to maximally activate the muscle

368
Q

Peripheral fatigue>

A

Failure at the level of the muscle itself (muscle not able to appropriately respond to the neural stimulus)

369
Q

Central fatigue happens above where?

A

Above the sarcolemma

370
Q

Latent period?

A

Time it takes for stimulus (electrical) to travel to and cause changes in the muscle

371
Q

Contraction time?

A

Time it takes to generate Pt starting from the point in time when force first begins to increase

372
Q

+dF/dt ?

A

Maximal RATE of force development…slope of twitch curve

373
Q

-dF/dt?

A

Maximal rate of force decline…RELAXATION from max force to 0 force

374
Q

1/2 RT?

A

Time it takes for force to decline to 50% of Pt during relaxation

375
Q

Twitch response is determined by?

A

Both the contractile and series elastic elements

376
Q

Parallel Elastic Elements?

A

Elastic elements in parallel with contractile elements. Epimysium, perimysium, endomysium, sarcolemma, SR, capillaries, and titin. Responsible for the passive tension in muscle. Run ALONG myofibrils.

377
Q

Series Elastic Elements?

A

Elastic elements in series with contractile elements. Z-line and tendon. Helps smooth out the rapid changes in tension for gradual transition in force

378
Q

Force development with shortening contraction only occurs after slack in what is taken up?

A

SEE

379
Q

How does increasing frequency of stimulation increase force output?

A

Summation. Stimuli that are closer together do not allow muscle to fully relax.

380
Q

What does repetitive stimulation do to force production?

A

Causes saturating levels of cytoplasmic Ca2+, leading to tetanus.

381
Q

List and explain 3 factors that would influence force and/or power in muscle in which all fibres are fully activated and not fatigued.

A
  1. Velocity of movement…Power is a function of FxV, and therefore, is usually maximal around 200-300 degrees per second 2. Muscle length…optimal length will produce the most force 3. Fibre type composition…For a given velocity, both force and power are higher in Type II compared to Type I 3.Fibre size…bigger = more force
382
Q

In mammailian muscle, the twitch force is what percent of the tetanic force?

A

10-20% Important because it allows for gradual, controlled increases in force.

383
Q

Why do slow twitch fibres generate more force at lower frequency stimulation than fast twitch fibres?

A

They exhibit slower relaxation rates, so fused tetanus occurs at lower frequency of stimulation.

384
Q

Why do Type II fibres need higher frequency of stimulation to reach tetanus than a Type I fibre?

A

SERCA 1, found in Type II fibres, can uptake Ca2+ faster, meaning it can relax faster than Type I. So, a high frequency is needed to reach saturating sarcoplasmic levels

385
Q

What is weakness?

A

Persistent loss of force (extended time)

386
Q

What fibre type shows greater decreased in velocity and power when fatigued?

A

Type II

387
Q

Why do Type II fibres fatigue faster?

A

Inherent biochemical properties

388
Q

The duty cycle?

A

Tc/(Tc+Tr) The higher the duty cycle the faster you fatigue or shorter you can produce desired force

389
Q

Tension Time Index (TTI)?

A

(F/MVC) x Tc/(Tc+Tr) …determines fatigue. If TTI > 0.15 or 15%, fatigue will occur

390
Q

Sites of fatigue for central fatigue in a voluntary activity?

A

Failure within nervous system, reduced central drive (motor unit recruitment, firing frequency), and feedback from muscle to inhibit activation (i.e. the muscle spindle)

391
Q

Sites of fatigue in voluntary or involuntary activity for peripheral fatigue?

A

Excitation: sarcolemms, t-tubule, SR, or something with increasing Ca2+ levels
Contraction: regulatory proteins (TN-C) or hte cross-bridge cycle (actin and myosin)

392
Q

Perihperal sites of fatigue divided into what 2 kinds?

A

Excitation and Contraction

393
Q

What is an interpolated twitch?

A

A single supramaximal stimulus is superimposed on a MVC

394
Q

If an interpolated twitch it applied during an MVC and there is no measurable increase in force, what does this mean?

A

Maximal activation is believed to occur (no central fatigue)

395
Q

MVC depends on what in the individual?

A

MOTIVATION to recruit all motor units…last 5% of motor units are very difficult to recruit

396
Q

What are 2 properties of the isometric twitch that can be measured to assess muscle relaxation?

A

1/2 RT and -dF/dt

397
Q

4 things that affect central fatigue?

A
  1. Motivation…TMS increases force generation in participants experiencing fatigue, and serious athletes show less fatigue 2. Perceived Pain…distraction helps maintain force 3. Brain activity…decreased neural activity in the brain motor cortex during and following exhaustive exercise 3. Neurotransmitters….Decreased ACh release following repeated stimulation and HIGH serotonin levels are associated with fatigue and lethargic behaviour
398
Q

2 components of metabolic peripheral fatigue?

A
  1. Reduced energy supply (ATP, PCr) 2. Build-up of metabolic by-products (ADP, Pi, H+)
399
Q

Non-metabolic peripheral fatigue?

A

Due to structural alterations to proteins and/or membranes involved in excitation and contraction processes (i.e. damage due to mechanical disruption) from eccentric exercise, free radicals, or proteolytic enzymes that increase activity during exercise

400
Q

What is low-frequency fatigue?

A

Failure to generate the same force at low frequencies of stimulation (10, 20 Hz)

401
Q

What causes low frequency fatigue?

A

Failure to activate the muscle despite adequate excitation…Ca2+ sensitivity or Ca2+ release

402
Q

Is low frequency fatigue long or short lasting?

A

Long lasting…may take several hours to days to regain original force

403
Q

What helps overcome low frequency fatigue?

A

Caffeine…open RyR channels and keep them open

404
Q

High frequency fatigue?

A

Failure to generate the same force at high frequencies of stimulation (50, 100 Hz)

405
Q

What causes high-frequency fatigue?

A

Likely due to failure of the APs along the sarcolemma or T-tubular system, which could be due to the accumulation of K+ in the T-tubules (T-tubular block)

406
Q

Is high frequency fatigue short or long lived?

A

Short lived because gradients are restored very rapidly following exercise

407
Q

How is calcium related to peripheral fatigue?

A

It may also be due to reduced Ca2+ sensitivity or responsiveness of regulatory proteins (TN-C)

408
Q

Force-pCa relationship?

A

At low frequency, a decline in pCa will cause a big decrease in force, since the TN-C is not saturated with Ca2+. At high frequency, though, a decline in Ca2+ there is no decline in force output when pCa2+ declines because TN-C is already saturated.

409
Q

List and explain 3 factors that would influence force and/or power in muscle in which all fibres are fully activated and not fatigued.

A
  1. Velocity of movement…Power is a function of FxV, and therefore, is usually maximal around 200-300 degrees per second 2. Muscle length…optimal length will produce the most force 3. Fibre type composition…For a given velocity, both force and power are higher in Type II compared to Type I 3.Fibre size…bigger = more force
410
Q

In mammailian muscle, the twitch force is what percent of the tetanic force?

A

10-20% Important because it allows for gradual, controlled increases in force.

411
Q

Why do slow twitch fibres generate more force at lower frequency stimulation than fast twitch fibres?

A

They exhibit slower relaxation rates, so fused tetanus occurs at lower frequency of stimulation.

412
Q

Why do Type II fibres need higher frequency of stimulation to reach tetanus than a Type I fibre?

A

SERCA 1, found in Type II fibres, can uptake Ca2+ faster, meaning it can relax faster than Type I. So, a high frequency is needed to reach saturating sarcoplasmic levels

413
Q

What is weakness?

A

Persistent loss of force (extended time)

414
Q

What fibre type shows greater decreased in velocity and power when fatigued?

A

Type II

415
Q

Why do Type II fibres fatigue faster?

A

Inherent biochemical properties

416
Q

The duty cycle?

A

Tc/(Tc+Tr) The higher the duty cycle the faster you fatigue or shorter you can produce desired force

417
Q

Tension Time Index (TTI)?

A

(F/MVC) x Tc/(Tc+Tr) …determines fatigue. If TTI > 0.15 or 15%, fatigue will occur

418
Q

Sites of fatigue for central fatigue in a voluntary activity?

A

Failure within nervous system, reduced central drive (motor unit recruitment, firing frequency), and feedback from muscle to inhibit activation (i.e. the muscle spindle)

419
Q

Sites of fatigue in voluntary or involuntary activity for peripheral fatigue?

A

Excitation: sarcolemms, t-tubule, SR, or something with increasing Ca2+ levels
Contraction: regulatory proteins (TN-C) or hte cross-bridge cycle (actin and myosin)

420
Q

Perihperal sites of fatigue divided into what 2 kinds?

A

Excitation and Contraction

421
Q

What is an interpolated twitch?

A

A single supramaximal stimulus is superimposed on a MVC

422
Q

If an interpolated twitch it applied during an MVC and there is no measurable increase in force, what does this mean?

A

Maximal activation is believed to occur (no central fatigue)

423
Q

MVC depends on what in the individual?

A

MOTIVATION to recruit all motor units…last 5% of motor units are very difficult to recruit

424
Q

What are 2 properties of the isometric twitch that can be measured to assess muscle relaxation?

A

1/2 RT and -dF/dt

425
Q

4 things that affect central fatigue?

A
  1. Motivation…TMS increases force generation in participants experiencing fatigue, and serious athletes show less fatigue 2. Perceived Pain…distraction helps maintain force 3. Brain activity…decreased neural activity in the brain motor cortex during and following exhaustive exercise 3. Neurotransmitters….Decreased ACh release following repeated stimulation and HIGH serotonin levels are associated with fatigue and lethargic behaviour
426
Q

2 components of metabolic peripheral fatigue?

A
  1. Reduced energy supply (ATP, PCr) 2. Build-up of metabolic by-products (ADP, Pi, H+)
427
Q

Non-metabolic peripheral fatigue?

A

Due to structural alterations to proteins and/or membranes involved in excitation and contraction processes (i.e. damage due to mechanical disruption) from eccentric exercise, free radicals, or proteolytic enzymes that increase activity during exercise

428
Q

What is low-frequency fatigue?

A

Failure to generate the same force at low frequencies of stimulation (10, 20 Hz)

429
Q

What causes low frequency fatigue?

A

Failure to activate the muscle despite adequate excitation…Ca2+ sensitivity or Ca2+ release

430
Q

Is low frequency fatigue long or short lasting?

A

Long lasting…may take several hours to days to regain original force

431
Q

What helps overcome low frequency fatigue?

A

Caffeine…open RyR channels and keep them open

432
Q

High frequency fatigue?

A

Failure to generate the same force at high frequencies of stimulation (50, 100 Hz)

433
Q

What causes high-frequency fatigue?

A

Likely due to failure of the APs along the sarcolemma or T-tubular system, which could be due to the accumulation of K+ in the T-tubules (T-tubular block)

434
Q

Is high frequency fatigue short or long lived?

A

Short lived because gradients are restored very rapidly following exercise

435
Q

How is calcium related to peripheral fatigue?

A

It may also be due to reduced Ca2+ sensitivity or responsiveness of regulatory proteins (TN-C)

436
Q

Force-pCa relationship?

A

At low frequency, a decline in pCa will cause a big decrease in force, since the TN-C is not saturated with Ca2+. At high frequency, though, a decline in Ca2+ there is no decline in force output when pCa2+ declines because TN-C is already saturated.

437
Q

List and explain 3 factors that would influence force and/or power in muscle in which all fibres are fully activated and not fatigued.

A
  1. Velocity of movement…Power is a function of FxV, and therefore, is usually maximal around 200-300 degrees per second 2. Muscle length…optimal length will produce the most force 3. Fibre type composition…For a given velocity, both force and power are higher in Type II compared to Type I 3.Fibre size…bigger = more force
438
Q

In mammailian muscle, the twitch force is what percent of the tetanic force?

A

10-20% Important because it allows for gradual, controlled increases in force.

439
Q

Why do slow twitch fibres generate more force at lower frequency stimulation than fast twitch fibres?

A

They exhibit slower relaxation rates, so fused tetanus occurs at lower frequency of stimulation.

440
Q

Why do Type II fibres need higher frequency of stimulation to reach tetanus than a Type I fibre?

A

SERCA 1, found in Type II fibres, can uptake Ca2+ faster, meaning it can relax faster than Type I. So, a high frequency is needed to reach saturating sarcoplasmic levels

441
Q

What is weakness?

A

Persistent loss of force (extended time)

442
Q

What fibre type shows greater decreased in velocity and power when fatigued?

A

Type II

443
Q

Why do Type II fibres fatigue faster?

A

Inherent biochemical properties

444
Q

The duty cycle?

A

Tc/(Tc+Tr) The higher the duty cycle the faster you fatigue or shorter you can produce desired force

445
Q

Tension Time Index (TTI)?

A

(F/MVC) x Tc/(Tc+Tr) …determines fatigue. If TTI > 0.15 or 15%, fatigue will occur

446
Q

Sites of fatigue for central fatigue in a voluntary activity?

A

Failure within nervous system, reduced central drive (motor unit recruitment, firing frequency), and feedback from muscle to inhibit activation (i.e. the muscle spindle)

447
Q

Sites of fatigue in voluntary or involuntary activity for peripheral fatigue?

A

Excitation: sarcolemms, t-tubule, SR, or something with increasing Ca2+ levels
Contraction: regulatory proteins (TN-C) or hte cross-bridge cycle (actin and myosin)

448
Q

Perihperal sites of fatigue divided into what 2 kinds?

A

Excitation and Contraction

449
Q

What is an interpolated twitch?

A

A single supramaximal stimulus is superimposed on a MVC

450
Q

If an interpolated twitch it applied during an MVC and there is no measurable increase in force, what does this mean?

A

Maximal activation is believed to occur (no central fatigue)

451
Q

MVC depends on what in the individual?

A

MOTIVATION to recruit all motor units…last 5% of motor units are very difficult to recruit

452
Q

What are 2 properties of the isometric twitch that can be measured to assess muscle relaxation?

A

1/2 RT and -dF/dt

453
Q

4 things that affect central fatigue?

A
  1. Motivation…TMS increases force generation in participants experiencing fatigue, and serious athletes show less fatigue 2. Perceived Pain…distraction helps maintain force 3. Brain activity…decreased neural activity in the brain motor cortex during and following exhaustive exercise 3. Neurotransmitters….Decreased ACh release following repeated stimulation and HIGH serotonin levels are associated with fatigue and lethargic behaviour
454
Q

2 components of metabolic peripheral fatigue?

A
  1. Reduced energy supply (ATP, PCr) 2. Build-up of metabolic by-products (ADP, Pi, H+)
455
Q

Non-metabolic peripheral fatigue?

A

Due to structural alterations to proteins and/or membranes involved in excitation and contraction processes (i.e. damage due to mechanical disruption) from eccentric exercise, free radicals, or proteolytic enzymes that increase activity during exercise

456
Q

What is low-frequency fatigue?

A

Failure to generate the same force at low frequencies of stimulation (10, 20 Hz)

457
Q

What causes low frequency fatigue?

A

Failure to activate the muscle despite adequate excitation…Ca2+ sensitivity or Ca2+ release

458
Q

Is low frequency fatigue long or short lasting?

A

Long lasting…may take several hours to days to regain original force

459
Q

What helps overcome low frequency fatigue?

A

Caffeine…open RyR channels and keep them open

460
Q

High frequency fatigue?

A

Failure to generate the same force at high frequencies of stimulation (50, 100 Hz)

461
Q

What causes high-frequency fatigue?

A

Likely due to failure of the APs along the sarcolemma or T-tubular system, which could be due to the accumulation of K+ in the T-tubules (T-tubular block)

462
Q

Is high frequency fatigue short or long lived?

A

Short lived because gradients are restored very rapidly following exercise

463
Q

How is calcium related to peripheral fatigue?

A

It may also be due to reduced Ca2+ sensitivity or responsiveness of regulatory proteins (TN-C)

464
Q

Force-pCa relationship?

A

At low frequency, a decline in pCa will cause a big decrease in force, since the TN-C is not saturated with Ca2+. At high frequency, though, a decline in Ca2+ there is no decline in force output when pCa2+ declines because TN-C is already saturated.

465
Q

What happens to force production when there is a rundown of Na+ and K+ gradients due to repetitive muscle activation?

A

Action potential propagation in sarcolemma and in t-tubules impaired or abolished. Reduced Ca2+ release from SR. Reduced tension development.

466
Q

Role of the SR in fatigue is due to?

A

Activation failure (reduced Ca2+ release) and Impaired relaxation (reduced Ca2+ uptake)

467
Q

Metabolic fatigue in the SR is due to?

A

Decreasd ATP can reduce SERCA activity, AMP/IMP/Mg2+ directly inactivate Ca2+ release channel, and Pi can enter SR, interact with Ca2+ and cause Ca2+ precipitation (Ca2+ cannot be released so less force production)

468
Q

Is the metabolic contribution to reduced Ca2+ from SR fatigue recovered quickly or slowly?

A

Quickly upon the cessation of exercise. Although, Ca2+ free concentration and force (low-frequency) can be depressed for greater than 24 hours (long lasting fatigue), which must involve non-metabolic mechanisms

469
Q

Non-metabolic fatigue in the SR is due to?

A

O2 free radicals and proteolytic enzymes can cause damage to SERCA and RyR. NOTE: These same non-metabolic mechanism may also effect fatigue independent of the SR, since they can also damage other pumps and contractile proteins

470
Q

Changes in muscle twitch due to fatigue?

A

Decreased peak tension, decreased +dF/dr and -dF/dt, and increaed CT and 1/2 RT

471
Q

Where does post-tetanic potentiation occur?

A

In FAST TWTICH fibres only at LOW frequencies of stimulation

472
Q

What does post-tetanic potentiation do to the muscle twitch?

A

Increased Pt and Increased rate of contration

473
Q

What causes post-tetanic potentiation?

A

Increased Ca2+ in sarcoplasm bind to calmoudlin, which activated MLCK. MLCK phosphorylates LC2. Myosin filament is pushed away from backbone because the negative charge on phosphate repels it. The myosin head is now closer to actin, meaning the probability of crossbridge formation increases and hte rate of force development is increased because myosin is now closer to actin.

474
Q

Why doesn’t post-tetanic potentiation happen in slow twitch fibres?

A

Myosin Light Chain Phosphatase works to fast, so Ca2+ is removed before repulsion has a chance to occur

475
Q

Metabolic fatigue can be due to?

A

Decreased ATP availability and the buildup of ATP breakdown products

476
Q

What happens to force production when there is a rundown of Na+ and K+ gradients due to repetitive muscle activation?

A

Action potential propagation in sarcolemma and in t-tubules impaired or abolished. Reduced Ca2+ release from SR. Reduced tension development.

477
Q

Role of the SR in fatigue is due to?

A

Activation failure (reduced Ca2+ release) and Impaired relaxation (reduced Ca2+ uptake)

478
Q

Metabolic fatigue in the SR is due to?

A

Decreasd ATP can reduce SERCA activity, AMP/IMP/Mg2+ directly inactivate Ca2+ release channel, and Pi can enter SR, interact with Ca2+ and cause Ca2+ precipitation (Ca2+ cannot be released so less force production)

479
Q

Is the metabolic contribution to reduced Ca2+ from SR fatigue recovered quickly or slowly?

A

Quickly upon the cessation of exercise. Although, Ca2+ free concentration and force (low-frequency) can be depressed for greater than 24 hours (long lasting fatigue), which must involve non-metabolic mechanisms

480
Q

Non-metabolic fatigue in the SR is due to?

A

O2 free radicals and proteolytic enzymes can cause damage to SERCA and RyR. NOTE: These same non-metabolic mechanism may also effect fatigue independent of the SR, since they can also damage other pumps and contractile proteins

481
Q

Changes in muscle twitch due to fatigue?

A

Decreased peak tension, decreased +dF/dr and -dF/dt, and increaed CT and 1/2 RT

482
Q

Where does post-tetanic potentiation occur?

A

In FAST TWTICH fibres only at LOW frequencies of stimulation

483
Q

What does post-tetanic potentiation do to the muscle twitch?

A

Increased Pt and Increased rate of contration

484
Q

What causes post-tetanic potentiation?

A

Increased Ca2+ in sarcoplasm bind to calmoudlin, which activated MLCK. MLCK phosphorylates LC2. Myosin filament is pushed away from backbone because the negative charge on phosphate repels it. The myosin head is now closer to actin, meaning the probability of crossbridge formation increases and hte rate of force development is increased because myosin is now closer to actin.

485
Q

Why doesn’t post-tetanic potentiation happen in slow twitch fibres?

A

Myosin Light Chain Phosphatase works to fast, so Ca2+ is removed before repulsion has a chance to occur

486
Q

Metabolic fatigue can be due to?

A

Decreased ATP availability and the buildup of ATP breakdown products

Physiology 2 (16 decks)

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