Transcript Slide 1

3 types:
1) skeletal-pulls on bones to
cause movement
2) cardiac-pumps blood thru
circulatory system
3) smooth-pushes fluids &
solids thru body, regulates
blood vessel diameter
Skeletal Muscle:
Functions:
a) Produce skeletal
movements
-contract & tendons pull
on bones
b) Maintain posture &
position
-constant tension keeps
head in position &
body over feet
c) Soft tissue support
-muscles lining abdominopelvic cavity support
weight of organs & offer
protection
d) Guard entrances & exits
-closes openings in
digestive & urinary
tracts
e) Produce heat
-contractions require
energy that is
converted into heat to
maintain temp.
f) Nutrient reserve storage
-proteins in muscles are
broken down to
provide amino acids
for enzymes & energy
Organization
-3 connective tissue layers
1) Epimysium:
-surrounds entire
muscle
-separates muscle
from other
tissues/organs
2) Perimysium:
-divides muscle into
compartments
-each contains a fasciclebundle of muscle
fibers
-each receives a branch
of blood vessels &
nerves
3) Endomysium:
-surrounds individual
muscle fibers (cells)
Collagen fibers from each
layer join to form a tendon
(connects muscle to
bone) or aponeurosis
(broad sheet that
connects muscle to bone)
Microscopic structure
-cells can be 30 cm long &
100 µm (.1 mm)diameter
-very large compared to most
cells
-multinucleate
-may be 100’s/cell
-lie just below membrane
-Sarcolemma-plasma
membrane of muscle fiber
-Sarcoplasm-cytoplasm
-Transverse (T) tubulesnarrow tubes, continuous
w/ sarcolemma that
extend thru sarcoplasm
-fluid-filled
-contain same electrical
charge as sarcolemma
-send impulse to entire
fiber so it all contract
together
-Myofibrils- cylindrical structures
that run the length of a fiber
-made of myofilaments: thin
strands/filaments of
protein
-2 types
1)Thin filaments-actin
2)Thick filaments-myosin
-can shorten & are
responsible for muscle
contracting
-anchored to ends of
sarcolemma which
eventually becomes a
tendon which pulls on
bone
-space filled w/ mitochondria &
glycogen
-Sarcoplasmic reticulummembrane complexs, similar
to smooth ER
-surround each myofibril
between T-tubules
-terminal cisternaeexpanded, fused
chambers where SR
meets T-tubule
-triad-2 terminal cisternae & a
T-tubule
-cells pump CA2+ ions out of
cells, they also transport
them into the terminal
cisternae
-may have 1000x higher
concentration of free
2+
Ca
-calsequestrin (protein)
binds Ca2+
2+
-total Ca may be
40,000x greater
-contractions begin when
2+
Ca ions are released
into sarcoplasm
-Sarcomere- repeating,
individual contractile units in
myofibrils
-1 myofibril can have 10,000
-4 components:
1) Thick filaments-myosin
w/ associated titin
(elastic filaments)
2) Think filaments-actin
3) Stabilizing proteins
4) Regulating proteins
-create banded/striated
appearance
I-band-light band (only actin)
A-band-dark (myosin & actin)
H-zone- only myosin
M-line-proteins that stabilize
position of thick bands
Zone of overlap-thin filaments
between thick
-6 thin surround a thick
-3 thick surround a thin
p. 289
Z-line-boundary between
sarcomeres
-proteins that connect thin
filaments
-titin proteins extend from
thick filaments & attach to
Z-line
-helps filament alignment
-Surrounded by 2 T-tubules &
triads located at zones of
overlap
-Thin filaments:
-each contains 4 proteins
-active site: area where
myosin can bind
-covered by troponintropomyosin complex
when a muscle is
relaxed
-in resting muscle,
2+
intracellular Ca
concentrations are very
low & binding site is
empty
-Troponin-tropomyosin
complex must move in
order for contraction to
occur
-calcium triggers process
-Thick filaments
-contain 300 twisted myosin
molecules
-tail-where molecules are
bound to each other
-head-projects toward actin
-made of 2 globular
protein subunits
-interact w/ active site to
form cross-bridges
-hinge that allows head to
pivot freely
-arranged so tails point
toward M-line
-core contains titin that
extends past fiber &
attaches to Z-line
Contraction
Events:
1)H-zones & I-bands get
smaller
2)Zones of Overlap get larger
3)Z-lines get closer together
4)A-band width stays
constant
Sliding Filament Theory-thin
filaments slide toward M-line
moving across thick
filaments, causing sarcomere
to shorten & muscles to
contract
-When muscles contract they
put tension on attached
tendons
Control of Muscle Activity
-nerves from central nervous
system (brain & spinal cord)
control contractions
-Neuromuscular junction: area
where nerve connects/
communicates w/ muscle
fiber
-1/fiber
-ends w/ synaptic terminal
-filled with acetylcholine
(Ach)-a
neurotransmitter that
is released by the
neuron from the
synaptic terminal,
attaches to muscle
fiber & alters the
permeability of the
sarcolemma
-Synaptic cleft: space
between synaptic terminal &
muscle sarcolemma
-Motor end plate: sarcolemma
opposite synaptic terminal
that houses receptors
where Ach binds
-folded to  surface area
-Acetylcholinesterase:
(AChE)-enzymes that
breaks down ACh, found
in synaptic cleft &
sarcolemma
-Steps of Stimulation
1) Action potential: (electrical
impulse to signal release
of ACh) reaches synaptic
terminal
2) ACh is released thru
exocytosis into synaptic
cleft
3) ACh binds to motor end
plate receptors & changes
+
permeability to Na ions,
which move into
sarcoplasm until AChE
removes ACh from
receptor sites
4)
+
Na
movement creates an
action potential in
sarcolemma, moves
inward thru T-tubules
5) ACh broken down by
AChE & system is ready
for another action
potential
Excitation-Contraction Coupling:
process that uses the stimulus
from an action potential to
create a muscle contraction
-occurs at triads
-action potential causes
cisternae to release Ca2+ ions
into sarcoplasm at a
sarcomere’s zone of overlap
-normally troponin (enzyme)
covers the active site of actin
strands, Ca2+ causes
troponin to release & allow
for myosin heads to bond
-begins the contraction cycle
Contraction cycle:
1) Troponin removed & active
sites available
2) Myosin head binds to active
site forming a cross-bridge
(requires 1 ATP)
3) Myosin heads pivot from
being pointed away from the
M-line to being pointed
towards it (power stroke)
4) Cross-bridges detach
(myosin head lets go of
active site)
5) Another ATP is split to reenergize free myosin head
which causes it to pivot back
to its original position
-Cycle begins again as long as
Ca2+ is present & ATP is
available
-Each power stroke shortens
the sarcomere by 1%
-Length of contraction depends
on:
1) Length of stimulation at
neuromuscular junction
2) Availability of free Ca2+
ions in sarcoplasm
3) Availability of ATP
-ACh binding occurs only
briefly, so action potentials
must continue to be applied
in rapid succession to
maintain a contraction
-Once action potential ends,
sarcoplasmic reticulum
permeability changes &
absorbs Ca2+, active site is
recovered
-sarcomere slowly returns to
original length
-at death, no more nutrients/
2+
oxygen cycles, Ca enters
sarcoplasm which triggers
contraction. Cross-bridges
can’t detach because there’s
no ATP-causes rigor mortisconstant contraction of skeletal
muscles at death, lasts 15-25
hours until autolytic enzymes
break down Z-lines & titin
Tension:
-amount of tension depends on
number of pivoting crossbridges
-level at muscle fibers depends
on:
a) resting length & size of
zone of overlap
b) frequency of stimulation
-sarcomere length must be
optimal for good tension
-allows for max. # of crossbridges to form & pull on
fibers
-extreme stretching/
compression is prevented
by muscle arrangement,
connective tissue, & bones
-titin fibers also help prevent
extreme stretching
-stimulation frequency
-single contraction lasts 7100 milliseconds
-this can be extended by
repeated stimulation &
sustained contractions
which  tension
-Twitch: single stimuluscontraction-relaxation
sequence in a muscle fiber
-time varies
-3 phases
1) Latent period: action
potential releases ACh &
SR releases Ca2+
-no tension produced (2
msec)
2) Contraction phase: tension
rises to a peak, Ca2+
binds to troponin, active
sites exposed, crossbridges form (2-15 msec)
2+
Ca
3) Relaxation phase:
levels fall, active sites
covered w/ tropomyosin &
cross-bridges decrease,
tension falls (15-40 msec)
-Treppe: second stimulation is
applied immediately after
relaxation period ends,
tension increases w/ each
stimulus until max. tension is
reached (after 30-50
stimulations)
-results from gradual  in
Ca2+ because SR can’t
reabsorb all
-Wave summation: second
stimulus begins before
relaxation phase ends
-create more powerful
contractions
-tension will rise to 4x treppe
max.
-rapid cycles that maintain max.
level during wave
summation-incomplete
tetanus
-Complete tetanus: faster
stimulations eliminates
relaxation phase
-SR can’t reabsorb Ca2+
-creates continuous,
strong contraction
Tension in Whole Muscle
-dependent on tension in fibers
& # of fibers contracting
-twitch is ineffective for useful
movement, treppe, or tetanus
is used
-Motor unit: all muscle fibers
controlled by a single motor
neuron
-fine motor areas have less
fibers/neuron than gross
motor
-smallest motor units are
activated first during a
contraction, larger units
create faster more
powerful movement
-recruitment: increasing # of
motor units contracting
based on movement
-all motor units contracting in
complete tetanus creates
peak tension can’t be
sustained because ATP
reserves run out
-units usually take turns
contracting so some have
time to recover
-asynchronous motor unit
summation
-Muscle tone: resting tension in
skeletal muscles
-don’t cause motion
-little tone=limp/flaccid
muscle
-motor units take turns
contracting
-stabilizes & maintains body
position, prevents sudden
motions, & allows
muscles to absorb sudden
shock
Contraction classifications
1) Isotonic contraction: tension
rises & length of muscle
changes
2 types:
a) Concentric contractions:
muscle tension exceeds
resistance & muscle
shortens
-e.g. flexion of elbow
b) Eccentric contraction: peak
tension is less than load &
muscle elongates due to
pull of another muscle or
gravity
-e.g. controlled extension
of elbow
2) Isometric contraction:
contraction where muscle
doesn’t change length
because tension never
exceeds resistance
-fibers shorten, but
connective tissue
stretches
-after contraction, fibers return
to original length because of
elastic forces, opposing
muscle contractions, &
gravity
Fiber Types:
1. Fast Fibers: large fibers that contract
quickly & forcefully
-fatigue rapidly
-”white meat”
2. Slow Fibers: smaller fibers that take
longer to reach peak tension
-more blood & myoglobin
-difficult to fatigue
-”red/dark meat”
Organization of the muscular
system
-muscle fibers in fascicle are
parallel, but fascicle
organization varies
Types
1. Parallel muscles: fascicles
parallel to long axis
-includes most skeletal muscles
-e.g. sartorius
-spindle-shaped w/ central
body (belly) are called
fusiform (e.g. biceps brachii)
2. Convergent muscle: fascicles
extend over a broad area &
converge at a common
attachment site
-shaped like fan or triangle w/
tendon at apex
-e.g. pectoralis & trapezius
3. Pennate muscle: fascicles form a
common angle w/ the tendon
a. unipennate-muscle fibers on
same side of tendon
b. bipennate-fibers on both sides
of tendon
c. multipennate-tendon branches
w/in pennate
-e.g. deltoid
4. Circular muscle/sphincter:
fascicles are concentrically
arranged around opening
-contraction decreases
diameter
-e.g. orbicular oris
Levers: rigid structure that
moves on a fixed point
(fulcrum)
-moves when an applied force
(AF) can overcome a
resistance (R)
-bone is lever, joint is fulcrum,
& muscle is AF
-can change
a. direction of applied force
b. distance/speed of
movement produced by
AF
c. effective strength of AF
Classes of Levers
1. 1st class: seesaw
-few in body
-e.g.-extension
of neck
nd
2
2.
class:
-small force can move
a larger weight
-e.g. ankle extension
(plantarflexion)
rd
3
3.
class:
-most common in
body
-speed/distance ↑
at expense of
effective force
Terminology
Origin: place where fixed end of muscle
attaches
Insertion: site where movable end
attaches to another structure
Action: specific movement produced
when a muscle contracts
-based on movement from
anatomical position
-muscles work in groups for complex
motions
Agonist: (prime mover) muscles
that’s contracting to create a
particular movement
Antagonist: muscle whose action
opposes the motion of the
agonist
e.g. biceps brachii vs. triceps
brachii – functional opposites
Synergist: helps agonist work
more efficiently, provide more
pull, stabilize origin
-fixators: synergists that
stabilize origin by preventing
movement in other joints
Naming
1. Location – Temporalis
st
nd
2. Origin/Insertion – (1 /2 ) –
Sternocleidomastoid
3. Fascicle organization
-Rectus (straight)-Rectus
abdominis
-Oblique/Transversus
4. Relative position
-Superficialis/Externus
-Internus/Profundus
5. Structure
-Biceps (2 heads), Triceps (3
heads)
-Trapezius (triangle)
-Longus, Brevis, Maximus,
Minimus, Major, Minor
6. Action
-Flexor, Extensor, Pronator,
Abductor, etc.