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51 Cards in this Set

  • Front
  • Back
Epimysium is made of what kind of CT?

What vasculature lies in epimysium?
Dense CT


Bld vessels, nerves
What vasculature lies in perimysium?
Bld vessels, nerves
Muscle spindles
What vasculature lies in endomysium?
Capillaries
Purpose of satellite cells
Stem cells

Remain in basal lamina

Can divide & fuse with myofibers to create large myofibers
Characteristics of Myofibers
1. Multinucleated, along perimenter
2. Striated
3. Basal lamina made by myoblast
4. Angular-looking cells
5. Cannot divide
(take on more nucleus by fusing with satellite cells)
Difference between Pennate & Strap
Pennate can undergo greater changes in tension

Strap capable of greater changes in length
Is there more stress at the ends(musculotendinous jxn) of myofibers or midsection?
-The ends have larger SA
-When F develops-->transmitted to tendon and because of large SA less stress at jxn. More stress at the midsection.
Golgi Tendon organ
-Force
-lie at the jxn btw myofibers & tendons/aponeurosis
-axon embedded in collagen
-Upon contraction-->distorts axon endings-->AP
Muscle spindles
-Lie within the perimysium
-Stretch reflex
-Upon stretching-->spindles activated-->depolarization
Trophism
Neurons secrete tropic factors which bind to receptors on myofibers causing altered cellular activity.
Embryonic development of skeletal m?
Mesoderm
Embroyonic devopment of myofibers
Mesenchymal cells-->myoblast-->myotube-->myofiber
Why would a myofiber need additional nuclei?
Large myofibers need to maintain protein synthesis for fiber growth
Sarcoplasmic reticulum
Another name for the ER

Storage area for calcium, released with an action potential in T-tubule
Sarcolemma
-PM of muscles
-has voltage-gated Na/K channels
Invaginations of the sarcolemma is called?
T-tubules that allows AP conduction interior
Thin filaments are linked where?
Z-line
thick filaments are anchored to?
M-line
What does contraction do?
Thin filaments slide towards M-line

Pulls Z-disc towards center
Tropomyosin
Regulatory proteins that blocks binding of thick filaments
What happens with Ca++ present with tropomyosin
Ca binds to Troponin-->binds to to tropomyosin-->exposes myosin binding sites
What are the 3 subunits of Troponin?
1. Tn-T: where tropomyosin binds
2. Tn-C: where Ca binds
3. Tn-I: inhibition
Myosin head has what important feature?
It has ATPase
A band
Where thick & thin filaments overlap
I-band
Thin filaments only
Titin
extends from z-line to m-line

limits stretch
Desmin
-Not in smooth
-links Z-line of one myofibril to adjacent myofibril
-genetic errors result in weak muscle bc no coordination
Dystrophin
achors actinof cell on inside to glycoproteins of the CM

genetic error, change in length no transmitted to glycoproteins externally
Duchenne muscular dystrophy
No dystrophin

No structural stability linking contractile proteins to CM

death of muscle fibers, look large bc filled with fat
Hypertrophy
Inc. in cell size, NOT #

Stretch signal-->Inc. protein synthesis-->inc. cell size-->recruitment of satellite cells
Stimulant of satellite cells
IGF-1-->hypertrophy
Inhibitor of satellite cell proliferation
Myostatin

No inhibition of satellite cell proliferation
Hyperplasia
Increase cell #, NOT size
Atrophy
Dec. in myofiber # or size

Caused by loss of innervation
What happens to motor neurons that lose innervation and then motor neurons grow back
New motor units larger than normal, will not be in normal mosaic pattern
What happens in aging
Atrophy-->loss of myofibers-->replaced by fat cells

Satellite pool dec-->limits repair ability-->loss of myofiber

Dec. in # of motor units
Attachment (rigor)
-Crossbridge formation
-High affinity for ATP
Release
ATP binds to myosin-->conformational change in head-->dec. myosin affinity for actin-->release crossbridge
Hydrolysis/Bending
-ATP hydrolyzed
changes shape of myosin head-->moves towards Z-line

Resting state (low Ca++)-->tropomyosin & troponin block myosin on actin
Power stroke
-release of ADP + pi-->inc. affnity for myosine & actin-->pull of myosin towards sarcomere-->shortening
Postsynaptic terminal for skeletal muscule
-Junctional folds
-Ach binds to nicotinic cholinergic receptors
Role of Ca++
Depolarization-->Voltage sensing DHSR change conformation-->signals RyR-->opens Ca++ channels in SR
How does relaxation occur involving Ca++?
Ca ++ ATPase on SR moves Ca++ back into SR

Ca++ ATPase has a higher affinity for Ca++ than troponin does.
If we administer Lidocaine (blocks AP) what would happen?
everything downstream will be blocked
If we block or dec. Ach receptors what would happen?
End plate potential dec.
If we block or dec. SR Ca++ ATPase what would happen?
dec. in sarcomere Ca++ reuptake

inc. duration of cross bridge cycling

inc. myofiber shortening or force
Defect in dystrophia (muscle weakening & atrophy)
dec. myofiber shortening or force
Blocking AchE
Inc. end plate potential, myofiber AP, sarcomere Ca++ release, sarcomere Ca++ reuptake, cross bridge cycling, dec. myofiber shortening for force
What records electrical activity of the motor unit
EMG (electromyologram)
Spontaneous contraction of myofiber (independent of motor neuron)
Fibrillation
Spontaneous firing of a motor unit
Fasciculation