Muscle Architecture Flashcards
Orientation of Muscles
epimysium -> perimysium -> endomysium -> sarcolemma -> sarcoplasmic reticulum
Epimysium
surrounds entire muscle; also known as fascia
Perimysium
surrounds fasciculi
Endomysium
surrounds myocytes (mus cells/mus fibers)
Sarcolema
muscle cell membrane; underlies the endomysium
Transverse (T-) Tubules
invaginations of sarcolemma
Transmit action potential into interior mus cell
closely apposed to SR
SR
membranous sac underlying the sarcolemma
responsible for Ca+ storage (release and uptake)
integral to mus contraction
Terminal Cisternae
bulbous enlargements of SR
store and release Ca
Sarcolemma
mus cell membrane;
contains sarcoplasm, cellular proteins, organelles, and myofibrils
Myofibrils
divided into individual contractile units (myosin and actin)
Thick Filaments
myosin
think filaments
actin
location of troponin and tropomyosin
actin filament
Zone of Sarcomere
from Z-disc to Z-disc
M Line
myofibril
H Zone
contains just myosin
I Band
contains just actin
Zone of Overlap
contains both myosin and actin
A Band
2 overlaps and H zone
Titin/Connectin
molecular blueprint
molecular spring
contribution to signal transduction
How is titin a molecular blueprint?
specifies and coordinates assembly of structural, regulatory and contractile proteins
How is titin a molecular spring?
links z-disk to M band
maintains relative position of actin and myosin
contributes ot mus extensibility and passive force development
Nebulin
molecular ruler
how is nebulin a molecular ruler?
incorporated into and co-extensive with actin
extens form z-disk to end of actin myofilament
precisely regulates actin length
Obscurin
intimately surrounds sarcomere, primarily at Z-disk and M-band regions
coordinates assembly and organization of SR with myofilament
Myosin Chains
2 heavy and 2 light polypeptides
2 heavy myosin chains
light meromyosin
heavy meromyosin
What does the light meromyosin do?
intertwine in double helix formation to form molecular backbone
what does the heavy meromyosin do?
project outward to form neck (S2) and globular head (S1)
what are the two light chain myosin polypeptides
1 essential and 1 regulatory chain for each S1/S2 complex
isoforms fine tune contraction velocity
Actin
thin
double helix
contains mysoin binding site
Tropomyosin
resides in groove along length of actin protein
what is the purpose of tropomyosin in the absence of Ca+?
blocks the myosin binding site
Troponin
spaced at regular intervals along length of actin protein 3 subunits (Ti, Tc, Tt)
what does troponin do in resting state
regulates position of tropomyosin relative to myosin binding site
What is the sequence of events for muscle contraction
1) action potential propogated along sarcolemma and into T-Tubes
2) Stim release of Ca+ from SR
3) Ca+ binds to Tc - conformation change that pulls tropomyosin away from myosin binding site
4*) hydrolysis of ATP cocks myosin head
5) cocked head binds to action and CONTRACTION OCCURS
6) hydrolysis of ATP detaches myosin head from actin
7) With action potential and thus Ca+ present, cycle keeps on
8) No AP and No Ca+ –> toponin and tropomyosin return and block binding site
Slow Twitch Fibers
low myosin-ATPase activity associates with lower max contraction and longer time to peak tension
Fast Twitch Fibers
high myosin-ATPase activity associates with higher max contraction and shorter time to peak tension
Type I Fibers
slow oxidative
Type IIa Fibers
fast oxidative-glycolytic
Type IIb (or IIx) Fibers
fast glycolytic
Myoplasticity
changes in use and environment can generate alterations in structural and enzymatic protein content
what predomenately changes fibers according to myoplasticity?
gene expression
Levels: structure, type, metabolism, energy storage, cap den, fxn
What causes myoplastic adaptations in endurance training?
delayed onset of metabolic acidosis
increased fatigue resistance
increased O2 consumption
What are the adaptations in endurance training?
- increased oxidative capacity
- increased mitochondrial density
- increased expression of type I
- decreased expression type IIa (takes years)
- decreased expression type IIb (takes days)
What causes myoplasitc adaptations in resistance training?
increase contractibility
improved elasticity
improved neuromotor recruitment
What are the adaptations in resistance training?
- increased CSA in all fibers
- increased nuclei/cell
- decreased mitochondria density
- decreased type I
- decreased type IIb
- increased type IIa
- little cap change
DMD
dystrophin ~5% of cytoskeletal membrane
X-linked recessive
inability to produce dystrophin
DMD intervention
emphasis on mobility
develop large mus groups and improve strength and increase endurance
avoid joint contractures - rom, stretching, braces
strengthen - resistance, pool
