Lecture 5 Flashcards
(107 cards)
1
Q
Myogenesis
A
Formation of muscle tissues in the embryo
2
Q
What develop along the length of the embryo out of somites on spine?
A
Skeletal Muscles
3
Q
What are somites?
A
Small clusters of myogenic precursor cells, tells body to start myogenesis
4
Q
What are satellite cells?
A
Inactivated throughout growth until there’s muscle damage and we need repair due to exercise or injury
5
Q
What structure let’s us know that myogenesis is complete?
A
When the nucleus moves form the center to the side
6
Q
Prenatal: Week 5
A
Primary myotubes
7
Q
Prenatal: Week 7
A
Secondary myotubes
8
Q
Prenatal: Week 20
A
Myofibers
9
Q
Can babies move before week 20?
A
Yes
10
Q
When are fiber types determined?
A
At birth, but you can SLIGHTLY modify with training adaptations
11
Q
Prenatal: Week 8
A
Formation of neuromuscular junction
12
Q
Prenatal: Week 16-35
A
Elimination of extra connections
13
Q
Infancy to Adolescence: 1st year
A
Increase # and size of fibers
14
Q
Infancy to Adolescence: Birth
A
Type 1, 28-41%
15
Q
When does strength increase linearly?
A
Age 12-13
16
Q
Adolescence to Adulthood:
A
Mass before strength Sex differences Peak strength: 20-30s Declines in 50s (sarcopenia) Fiber type, functional demands
17
Q
Skeletal Muscle Anatomy
A
Muscle Muscle fasciculus Muscle fiber Myofibril Sacromere (Z-Z) H, Z, A, I bands
18
Q
Muscle fibers
A
single cells
multinucleated
surrounded by sarcolemma
19
Q
myofibrils
A
contractile elements (actin, myosin, titan) surrounded by sarcoplasm
20
Q
cellular organelles lie…
A
between myofibrils (mitochondria, sarcoplasmic reticulum)
21
Q
Sarcomere zone
A
Z to Z
22
Q
A band
A
H zone inside also Actin overlap with Myosin
23
Q
Titan is for…
A
structural support on ends of Z disc
24
Q
Z is for…
A
maintaining overlap (if overlaps too much) force cannot happen… (missing Titan is critical!!)
25
H zone is...
M line
26
I band...
Only actin! No overlap!
27
Is there more overlap when a muscle is relaxed?
NO, when it is more contracted!
28
Which band stays the same width?
A band
29
Which zones/bands become shorter?
H & Sarcomere zone, I band
30
F-actin
doublestranded helix
active sites
myosin heads to bind to active sites
31
Tropomyosin
covers active sites
| prevents interaction with myosin
32
Troponin
binds actin
binds tropomyosin
binds Ca
33
Muscle contraction can happen without Calcium? T/F
FALSE, we need Ca to bind to troponin in order for contractions to occur!! We rely on Ca heavily!!
34
How does Ca create contraction?
Pulls active sites on actin away so myosin can bind and power stroke can happen
35
Troponin is bound to what?
Tropomyosin!
36
What is blocking myosin from actin?
Tropomyosin!
37
Myosin is composed of...
TWO heavy chains
FOUR light chains
"head" region - site for ATPase
38
What is ATPase on myosin head used for?
Breakdown ATP to help power stroke and excitation contraction!
39
How are the myosin placed?
Tail to Tail with heads near Z disc
40
Mechanism of Muscle Contraction THEORY:
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.
41
An increase of cross bridging causes a high or low force?
HIGH
42
Cross bridging steps:
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!
43
Does the actin or myosin move inwards?
Actin! Myosin does not move!
44
Role of Ca in Cross Bridge: Relaxation
no excitation
no cross-bridge
muscle fiber relaxed
45
Role of Ca in Cross Bridge: Excitation
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
Where does calcium comes from?
Sarcoplasmic reticulum (lateral sacs)
47
How does the calcium get released?
By an AP (Excitation-Contraction Coupling)!
48
What happens to the Ca after AP stops?
Goes back in the SR
49
Nueromuscular Transmission
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
Neuromuscular Junction
Synaptic trough: synaptic vesicles that has ACh
Synaptic cleft: AcetylASE (AChe)
Synaptic subneural clefts: contains ACh gated channels, voltage gated Na channel
51
Role of Na Channel on motor neuron...
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
ACh has binding sites to
open channels and stir Na influx... allows change of gradient in muscle to swim Na channels to set AP throughout muscle
53
ACh is going to be...**** (know this)
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
Myasthenia Gravis
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
Excitation-Contraction Coupling: T-tubules
invaginations of sarcolemma filled with extracellular fluid
penetrate the muscle fiber, branch and form networks
transmit APs deep into the muscle fiber
56
Excitation-Contraction Coupling: SR
terminal cistenae form junction adjacent to T-tubule membrane
storage of Ca
57
How is Ca released?
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
ECC process!
```
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
Relaxation
depends on reuptake Ca into SR
AChASE breaks down ACh at NMJ
muscle fiber AP potential stops
Ca going back to SR
60
ATP Involvement
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
Passive
ability to generate tension before contraction takes place, due to additional contractile related proteins (Titan)
Eccentric
62
Active
Concentric
63
Speed of contraction depends on...
our ability to hydrolyze/breakdown ATP
64
High Vmax, fast/white
rapid cross bridge cycling
| rapid rate of shortening
65
Low Vmax, slow/red
slow cross bridge cycling
| slow rate of shortening
66
Type 1, slow fibers
```
Oxydative
small diameter
high myoglobin
many mitochondria
low glycolytic enzyme
```
67
Type 2, fast fibers
```
Glycolytic
large diameter
low myoglobin content
low capillary density
few mitochondria
high glycolytic enzyme
```
68
Motor unit
collection of muscle fibers innervated by a single moto neuron
69
Motor unit: small
as few as 10 fibers/unit
precise control
rapid reacting
70
Motor unit: large
as many as 1000 fibers/unit
coarse control
slower reacting
71
Repetition
One complete movement of an exercise
72
Set
A group of repetitions performed continuously without stopping
73
Intensity
Absolute load (weight) that a contracting muscle experiences
74
Training volume
Measure of the total amount of work performed
| RepsxSetsxIntensity
75
Strength
generate max force
76
Power
generate submaximal force at high velocity
77
Endurance
generate submaximal force for an extended time
| ability to resist fatigue
78
Rep Max
max number of reps per set that can be performed at given resistance with proper technique
79
Strength
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
Power =
Force x Velocity
ability to exert force as rapidly as possible
81
1RM =
100%
82
6RM=
85%
83
12RM=
70%
84
Power/Strength
1RM 100% - 4RM 90%
85
Hypertrophy
6RM 85% - 12 RM 70%
86
Endurance
>12RM 70%
87
Periodization
varying periods of training volume, training adaptations
88
Progressive overload
practice of continually increasing the stress placed on the muscle as it becomes capable of producing greater force or has more endurance
89
Rest periods
Strength: 2-5 mins
Hypertrophy: 30 sec-1.5 min
Endurance
90
Novice
2-3 days
91
Interm.
3-4 days
92
Advanced
4-7 days
93
Outcomes...
nonathletes will see faster strength change than athletes
94
Short term training, 8 weeks
neural factors
95
Long term training, more than 8 weeks
hypertrophic factors
96
Healthy adults
2-4x week (novice/intermediate)
N: 50-70%; 8-12RM
T: 70-85%; 6-12RM
Major muscles groups
97
Older adults
2x/week
5-8/10RPE; 8-12RM
1-2 sets mod volume
8-10 exercises major muscle groups
98
Ages 6-18
```
2-3x/week
50-85%; 6-15RM; 1-3 sets
technique training
dyanmic warm up
back/abs
5-10% progression
```
99
Goals
Systems
Muscular
Physical Function
100
Sarcopenia
60-70,80+ years
50-60 years testosterone...
muscle loss
decrease contractile proteins/hormones
motor unit efficiency
type 2 atrophy
101
DMD
```
lordotic age 2
gower's/tren gait age 4
orthotics age 9
wheelchair age 11
bronchitis hospital age 16
```
102
DMD Pathogenesis
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
Dystrophin
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
Dystrophin deficiency:
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
Clinical Manifestations DMD
```
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
Tension is changed due to
length of sarcomere
107
Optimal overlap for greatest amount of tension
max force can be done... at rest
