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PT 509 Physiology > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

Myogenesis

A

Formation of muscle tissues in the embryo

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2
Q

What develop along the length of the embryo out of somites on spine?

A

Skeletal Muscles

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3
Q

What are somites?

A

Small clusters of myogenic precursor cells, tells body to start myogenesis

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4
Q

What are satellite cells?

A

Inactivated throughout growth until there’s muscle damage and we need repair due to exercise or injury

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5
Q

What structure let’s us know that myogenesis is complete?

A

When the nucleus moves form the center to the side

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6
Q

Prenatal: Week 5

A

Primary myotubes

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7
Q

Prenatal: Week 7

A

Secondary myotubes

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8
Q

Prenatal: Week 20

A

Myofibers

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9
Q

Can babies move before week 20?

A

Yes

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10
Q

When are fiber types determined?

A

At birth, but you can SLIGHTLY modify with training adaptations

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11
Q

Prenatal: Week 8

A

Formation of neuromuscular junction

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12
Q

Prenatal: Week 16-35

A

Elimination of extra connections

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13
Q

Infancy to Adolescence: 1st year

A

Increase # and size of fibers

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14
Q

Infancy to Adolescence: Birth

A

Type 1, 28-41%

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15
Q

When does strength increase linearly?

A

Age 12-13

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16
Q

Adolescence to Adulthood:

A 
Mass before strength
Sex differences
Peak strength: 20-30s
Declines in 50s (sarcopenia)
Fiber type, functional demands
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17
Q

Skeletal Muscle Anatomy

A 
Muscle
Muscle fasciculus
Muscle fiber
Myofibril
Sacromere (Z-Z)
H, Z, A, I bands
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18
Q

Muscle fibers

A

single cells
multinucleated
surrounded by sarcolemma

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19
Q

myofibrils

A 
contractile elements (actin, myosin, titan)
surrounded by sarcoplasm
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20
Q

cellular organelles lie…

A

between myofibrils (mitochondria, sarcoplasmic reticulum)

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21
Q

Sarcomere zone

A

Z to Z

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22
Q

A band

A

H zone inside also Actin overlap with Myosin

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23
Q

Titan is for…

A

structural support on ends of Z disc

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24
Q

Z is for…

A

maintaining overlap (if overlaps too much) force cannot happen… (missing Titan is critical!!)

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25
Q

H zone is…

A

M line

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26
Q

I band…

A

Only actin! No overlap!

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27
Q

Is there more overlap when a muscle is relaxed?

A

NO, when it is more contracted!

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28
Q

Which band stays the same width?

A

A band

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29
Q

Which zones/bands become shorter?

A

H & Sarcomere zone, I band

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30
Q

F-actin

A

doublestranded helix
active sites
myosin heads to bind to active sites

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31
Q

Tropomyosin

A

covers active sites

prevents interaction with myosin

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32
Q

Troponin

A

binds actin
binds tropomyosin
binds Ca

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33
Q

Muscle contraction can happen without Calcium? T/F

A

FALSE, we need Ca to bind to troponin in order for contractions to occur!! We rely on Ca heavily!!

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34
Q

How does Ca create contraction?

A

Pulls active sites on actin away so myosin can bind and power stroke can happen

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35
Q

Troponin is bound to what?

A

Tropomyosin!

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36
Q

What is blocking myosin from actin?

A

Tropomyosin!

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37
Q

Myosin is composed of…

A

TWO heavy chains
FOUR light chains
“head” region - site for ATPase

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38
Q

What is ATPase on myosin head used for?

A

Breakdown ATP to help power stroke and excitation contraction!

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39
Q

How are the myosin placed?

A

Tail to Tail with heads near Z disc

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40
Q

Mechanism of Muscle Contraction THEORY:

A

Binding of Ca to troponin results in a conformational change in tropomyosin that uncovers the active sites on the actin molecule, allowing for myosin to bind.

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41
Q

An increase of cross bridging causes a high or low force?

A

HIGH

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42
Q

Cross bridging steps:

A

1) Binding, myosin cross bridge binds to actin molecules
2) Power stroke, cross bridge bends, pulls actin inward
3) Detachment, cross bridge detaches at end of power stroke and returns to original conformation
4) Binding, cross bridge binds to more distal actin molecule, REPEATS!

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43
Q

Does the actin or myosin move inwards?

A

Actin! Myosin does not move!

44
Q

Role of Ca in Cross Bridge: Relaxation

A

no excitation
no cross-bridge
muscle fiber relaxed

45
Q

Role of Ca in Cross Bridge: Excitation

A

Muscle fiber is excited and Ca is released
Ca binds to troponin, pulling troponin-tropomyosin complex aside to expose binding site
Cross-bridging bind occurs
Binding of actin/myosin cross bridge triggers power stroke that pulls actin inward (contraction)

46
Q

Where does calcium comes from?

A

Sarcoplasmic reticulum (lateral sacs)

47
Q

How does the calcium get released?

A

By an AP (Excitation-Contraction Coupling)!

48
Q

What happens to the Ca after AP stops?

A

Goes back in the SR

49
Q

Nueromuscular Transmission

A

specialized synapse between motorneuron and muscle fiber

occurs at a structure on the muscle fiber called the motor end plate (usually only one per fiber)

50
Q

Neuromuscular Junction

A

Synaptic trough: synaptic vesicles that has ACh
Synaptic cleft: AcetylASE (AChe)
Synaptic subneural clefts: contains ACh gated channels, voltage gated Na channel

51
Q

Role of Na Channel on motor neuron…

A

helps release neurotransmitter, releases ACh, ACh moves outer membrane and undergoes fusion/exocitosis… influx Ca in…allows stim of vesicles to fuse with membrane… At fuse into cleft

52
Q

ACh has binding sites to

A

open channels and stir Na influx… allows change of gradient in muscle to swim Na channels to set AP throughout muscle

53
Q

ACh is going to be…** (know this)

A

released, and is what carries signal of AP into muscle via stimulation of channels on receiving ends of the other skeletal muscle to transmit AP

54
Q

Myasthenia Gravis

A

autoimmune disease that target ACh receptors
body produces anti-bodies to target ACh
blocks/destroys ACh (receptor) from binding
results in muscle weakness due to loss of contraction
face/upper regions

**muscle activation inhibited

55
Q

Excitation-Contraction Coupling: T-tubules

A

invaginations of sarcolemma filled with extracellular fluid
penetrate the muscle fiber, branch and form networks
transmit APs deep into the muscle fiber

56
Q

Excitation-Contraction Coupling: SR

A

terminal cistenae form junction adjacent to T-tubule membrane
storage of Ca

57
Q

How is Ca released?

A

T-tubule has DHP (sensitive to AP), stimulates…
SR, lateral has own receptor , Ryanodine
Rayonne joins together to release Ca
Ca released from SR

**via voltage one one to open gates…

58
Q

ECC process!

A 
ACh released at NMJ
Na comes in and ACh starts AP
AP in T-tubule alters DHP receptor
DHP opens Ca release in SR, Ca enters cytoplasm
Ca binds to troponon, actin/myosin binds
Myosin heads power stroke
Actin slides inwards of sarcomere
59
Q

Relaxation

A

depends on reuptake Ca into SR
AChASE breaks down ACh at NMJ
muscle fiber AP potential stops
Ca going back to SR

60
Q

ATP Involvement

A

1) ATP is split into ADP and P, the myosin head is energized
2) Myosin head attaches to actin, cross bridge
3) Pi generated in previous contraction is released, power stroke happens, Myosin pivots and pulls actin toward M line. ADP released
4) NEW ATP attaches to myosin head, bridge weakens and detaches
REPEAT

61
Q

Passive

A

ability to generate tension before contraction takes place, due to additional contractile related proteins (Titan)

Eccentric

62
Q

Active

A

Concentric

63
Q

Speed of contraction depends on…

A

our ability to hydrolyze/breakdown ATP

64
Q

High Vmax, fast/white

A

rapid cross bridge cycling

rapid rate of shortening

65
Q

Low Vmax, slow/red

A

slow cross bridge cycling

slow rate of shortening

66
Q

Type 1, slow fibers

A 
Oxydative
small diameter
high myoglobin
many mitochondria
low glycolytic enzyme
67
Q

Type 2, fast fibers

A 
Glycolytic
large diameter
low myoglobin content
low capillary density
few mitochondria
high glycolytic enzyme
68
Q

Motor unit

A

collection of muscle fibers innervated by a single moto neuron

69
Q

Motor unit: small

A

as few as 10 fibers/unit
precise control
rapid reacting

70
Q

Motor unit: large

A

as many as 1000 fibers/unit
coarse control
slower reacting

71
Q

Repetition

A

One complete movement of an exercise

72
Q

Set

A

A group of repetitions performed continuously without stopping

73
Q

Intensity

A

Absolute load (weight) that a contracting muscle experiences

74
Q

Training volume

A

Measure of the total amount of work performed

RepsxSetsxIntensity

75
Q

Strength

A

generate max force

76
Q

Power

A

generate submaximal force at high velocity

77
Q

Endurance

A

generate submaximal force for an extended time

ability to resist fatigue

78
Q

Rep Max

A

max number of reps per set that can be performed at given resistance with proper technique

79
Q

Strength

A

ability to exert muscular force

1) CSA of muscle fibers to generate force
2) intensity of recruitment

genetic fibers
joint angles/muscle length-tension/lever arm

80
Q

Power =

A

Force x Velocity

ability to exert force as rapidly as possible

81
Q

1RM =

A

100%

82
Q

6RM=

A

85%

83
Q

12RM=

A

70%

84
Q

Power/Strength

A

1RM 100% - 4RM 90%

85
Q

Hypertrophy

A

6RM 85% - 12 RM 70%

86
Q

Endurance

A

> 12RM 70%

87
Q

Periodization

A

varying periods of training volume, training adaptations

88
Q

Progressive overload

A

practice of continually increasing the stress placed on the muscle as it becomes capable of producing greater force or has more endurance

89
Q

Rest periods

A

Strength: 2-5 mins
Hypertrophy: 30 sec-1.5 min
Endurance

90
Q

Novice

A

2-3 days

91
Q

Interm.

A

3-4 days

92
Q

Advanced

A

4-7 days

93
Q

Outcomes…

A

nonathletes will see faster strength change than athletes

94
Q

Short term training, 8 weeks

A

neural factors

95
Q

Long term training, more than 8 weeks

A

hypertrophic factors

96
Q

Healthy adults

A

2-4x week (novice/intermediate)
N: 50-70%; 8-12RM
T: 70-85%; 6-12RM
Major muscles groups

97
Q

Older adults

A

2x/week
5-8/10RPE; 8-12RM
1-2 sets mod volume
8-10 exercises major muscle groups

98
Q

Ages 6-18

A 
2-3x/week
50-85%; 6-15RM; 1-3 sets
technique training
dyanmic warm up
back/abs
5-10% progression
99
Q

Goals

A

Systems
Muscular
Physical Function

100
Q

Sarcopenia

A

60-70,80+ years
50-60 years testosterone…

muscle loss
decrease contractile proteins/hormones
motor unit efficiency
type 2 atrophy

101
Q

DMD

A 
lordotic age 2
gower's/tren gait age 4
orthotics age 9
wheelchair age 11
bronchitis hospital age 16
102
Q

DMD Pathogenesis

A

abnormality in protein: dystrophin
…transfers/generate/move force from contraction to C.T.
support protein, connects plasma membrane to contractile proteins
BIG STABILIZER protein
allow muscle to contract under force

103
Q

Dystrophin

A

normally: strengthens muscle fibers and protects them from injury during contraction and relaxation
structural. ..
compromised: prone to injury and won’t be able to contract that well…

effects skeletal then eventually cardiac

104
Q

Dystrophin deficiency:

A

abnormal cell membrane with increased transient local membrane disruptions and inflows of Ca

activates enzyme: protease, breaks down protein that we do need…

alters Ca channel activity and increase Ca inflow

impaired Ca homeostasis causes

apoptosis (program cell death) and necrosis (not enough nutrients)

DMD is missing dystrophin…

105
Q

Clinical Manifestations DMD

A 
shoulders arms held back
sway back
weak glutes
knee flexed to take weight
thick LE (fat)
tight heel cord
toe walker
belly sticks out
thin
poor balance
weak front muscles
foot drop
106
Q

Tension is changed due to

A

length of sarcomere

107
Q

Optimal overlap for greatest amount of tension

A

max force can be done… at rest

PT 509 Physiology (9 decks)

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