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types of muscle tissue
skeletal, cardiac, smooth
skeletal muscle
attaches to bone = movement
voluntary control
muscle fibers → striated and multiple nuclei
cardiac muscles
found on wall of heart
involuntary control
striations 1-2 nuclei
smooth muscle
found on walls of hollow organs
involuntary
one nucleus no striations
spindle shaped
characteristics of muscle tissue
excitable, contractable, extensible, elastic
function of skeletal muscle
movement, stabilize joints, maintain posture and position, heat generation
skeletal muscle connective tissue
epimysium, perimysium, endomysium
epimysium
dense irregular CT surrounds WHOLE muscle
perimysium
fibrous CT surrounds fascicles
endomysium
fine areolar connective tissue; surrounds individual muscle fiber
where does skeletal muscle attach to bone
extension of epimysium that is continuous with tendons
skeletal muscle type of attachements
direct and indirect
direct attachment
epimysium fuses with periosteum of bone or pericardium of cartilage
indirect attachement
connective tissue wrappings gather and extend beyond muscle as ropelike (tendon) or sheetlike (aponeurosis)

aponeurosis
sarcolemma
plasma membrane of muscle fibers
sarcoplasm
cytoplasm of muscle fibers
myofibrils
for contraction; modified organelles gives muscle striated appearance
sarcoplasmic reticulum
smooth ER for Ca2+ storage
smooth ER surrounding myofibrils
T-tubules
extension of sarcolemma
allows for transmission of electrical nerve impulses to travel to interior
myofilaments
allows for contraction to occur; consists of thick and thin filaments
make up sarcomeres
thick filaments
composed of myosin
thin filaments
composed of actin and regulatory proteins tropomyosin and troponin
myosin
contains 2 heavy and 4 light polypeptide chains
bind and unbind to form contraction
tropomyosin and troponin
regulatory proteins controlling thin filament binding sites
sarcomere
smallest contractile unit in muscle fiber
made of thick and thin filaments

sarcomere regions
A bands → dark regions (thick and thin)
H zone → light region in middle of A band
M line → middle of H zone
I bands → lighter region (thin)
z disc → coin shaped

filaments and proteins within sacromere
elastic filament, dystrophin protein, nebulin, myosin, C proteins
dystrophin
links thin filament to proteins on sarcolemma
nebulin, myosin and c proteins
bind filaments/sacromere together and maintain alignment of sacromere
elastic filament
titin protein → holds thick filament in place; helps recoil after stretch
Duchenne muscular dystrophy (DMD)
caused by defective dystrophin gene = sarcolemma of patients tear easily = entry of excess Ca = contractile fibre dmg
triads
formed by t tubule surrounded by terminal cistern of SR on either side
important in transmission of electrical signals and release of Ca
neuromuscular junction
end of axon → splits into many branches that interact with fiber
axon terminal
where axon meets sarcolemma
synaptic cleft
gap between axon terminal and sarcolemma
steps needed for muscle contraction
nerve stimulation
action potential
propagation across sarcolemma
Ca release
steps occurring at neuromuscular junction
nerve stimulation and action potential generation
ACh
neurotransmitter that carries signal along axon to innervate skeletal muscle
ligand gated channels
chemical messengers bind to receptors to open the channels
voltage gated channels
changes in voltage open or close channels
propagation of signal at NMJ
AP arrives at terminal
VGCC on axon terminal opens = Ca flows into axon terminal
Ca influx = ACh released
ACh diffuses across and binds to ligand gated receptors on sarcolemma
channel opens = Na flow into muscle fiber
acetocholinesterase degrades ACh and channel closes
end plate potential
when Na flows into muscle fiber and membrane potential becomes positive
how does end plate potential lead to action potential
membrane change causes wave of depolarization to spread away from motor end plate to rest of sarcolemma where VGC exist
causes Na channels to open and K channels to close
travels down to t tubules
RMP of skeletal muscle
90 mV
excitation contraction coupling
at rest → myosin binding sites on actin are closed = covered by tropomyosin
Ca levels rise → bind to troponin
troponin pulls tropomyosin off binding sites → myosin binds to form cross bridge
sliding filament model
thick and thin myofilaments don’t change in length
thin slides against thick = more overlap (shortens)
cross bridge cycling
ATP hydrolyzed = energy allows myosin head to bind to actin
ADP and Pi released = creates energy → myosin head bends and pulls actin filament to M line
ATP binds to myosin head → cross bridge breaks
ATP is hydrolyzed → myosin head returns to ready position
motor nerve stimulation summation
successive stimuli added together
produces stronger muscle contraction each time
tetanus
fusion of contractions produces continuous contraction
factors increasing force generation
increased frequency of stimuli
recruitment of more muscle fibers
large muscle fibers and type
length of overlap of myofilaments
isotonic contraction
change in muscle length in response to given load
types of isotonic contractions
eccentric and concentric
concentric contraction
muscle contract and shorten
eccentric contraction
muscle contract and lengthens
isometric contractions
muscle length remains constant as it contracts
type 1 muscle fibers
slow contraction
low force generated
high mitochondria and capillaries
high fatigue resistance
type II A fibers
intermediate contraction speed
medium force generated
some mitochondria medium capillary density
30 mins of use before fatigue
type II B
fast speed of contraction
high force generated
few mitochondria and capillaries
fast fatigue
myoglobin
hemoglobin but in muscle
aids with oxygen delivery to skeletal muscle tissue
metabolic pathways
direct, anaerobic, aerobic pathways
direct pathways
creatine phosphate quickly turned into ATP via creatine kinase; limited
anaerobic pathways
glycolysis → no oxygen; inefficient and produces lactic acid
for high intensity short duration
aerobic pathway
for long duration exercise (day to day)
large gain of ATP
produces lots of CO2
smooth muscle structure
connective tissue covering similar to skeletal muscle
only covers groups of cells (not whole muscle)
smooth vs skeletal
less sarcoplasmic reticulum
have gap junctions
involuntary control
excited or inhibited
slow contraction
mainly aerobic
shorter myosin no sarcomeres
thick and thin arranged diagonally
calmodulin
replaces troponin in smooth muscle
controls binding
smooth muscle contraction
caveolae have VGCC → opens during depolarization
Ca entering cell leads to release of Ca from SR
phases of muscle healing
destruction, repair, remodeling
muscle injury - destruction
myofiber rupture (necrosis)
hematoma → capillaries rupture, bruising
inflammatory response
muscle injury repair
macrophage cleans debris
myofibrils begin to regenerate
angiogenesis
muscle injury remodeling
myofibers mature
scar tissue reorganized to regain functional capacity
rhabdomyolysis
rapid breakdown of muscle fibers → leads to buildup in kidney (harmful)