1. Identify and list characteristics of three types of muscle
Skeletal
Cardiac
Smooth
Location
Attached to bones
and a few tubes
Heart
Internal organs and
tubes
Function
Moves the skeleton
and a few sphincters
Generates heart
contraction
Moves internal
organs and tubes
NS Control
Somatic
- Part of
nervous
system that
we have
voluntary
control over
Autonomic
- Under
automatic
control
Autonomic
Initiation of
Contraction
Membrane
Depolarization
Membrane
depolarization
Membrane
depolarization
Cell Structure
Large Multinucleated
fibers/cells
- each fiber
independently
activated by NS
Smaller uninucleated
cells; branched fibers
Small uninucleated
cells
Coordination of
muscle contraction
One neuron
depolarizes many
fibers (motor unit) →
activates large
number of muscle
fibers through
synapses
Gap junctions
Gap junctions and
motor units
Contractile
Filaments
Actin and Myosin
Actin and myosin
Actin and myosin
Appearance
Striated
striated
Not striated
2. Name anatomical features of skeletal muscle
Antagonistic muscle groups: move bones in opposite directions
- Has one set of muscles that move it in one direction, and one set that moves it in the
opposite direction
- Fibers move bone by shortening and pulling bone
Muscle contraction can pull on a bone but cannot push a bone away
Tricep: agonist
Bicep: antagonist
Muscle fiber: is the same as one muscle cell
- Contains sarcoplasmic reticulum: surrounds all myofibrils and has calcium storage
- T tubules: connected openings in sarcolemma which gives opportunity for ECF to come
around internal structures
- Sarcolemma: membrane of cell
- Myofibril: fiber within muscle (different from muscle fiber)
- Z disk: light part
- H zone: thick dark fibers (myosin)
- Sarcomere: distance between z disks
- A band: where myosin and actin meet
- Actin: thin filament
- Myosin: thick filament
- Accessory proteins: troponin and tropomyosin
Thick filaments: contain myosin heads: atpase, binding sites for actin, atp hydrolysis
Thin filaments: Tropomyosin: wraps g actin and covers part that myosin can bind to (prevents
binding of myosin)
Troponin: interacts with tropomyosin and shifts it when troponin binds with calcium, allowing
actin-myosin binding
Troponin and Nebulin: regulatory proteins
T tubules bring action potentials into interior of muscle fiber and creates opportunity for
signaling with t tubule and sarcoplasmic reticulum
Myosin heads interact with thin filaments
Sarcoplasmic reticulum stores calcium 2+
Sarcomere shortens during contraction, as contraction takes place actin and myosin do not
change length but instead slide past one another
A band stays the same and represents the physical length of thick filaments
Overlap changes, not length of thick filaments
Muscle relaxed → sarcomere shortens with contraction → muscle contracted when h zone and I
band both shorten but a band remains constant
3. Explain steps of excitation-contraction coupling
Excitation
1. Action potential
reaches axon terminal
of motor neuron
2. Acetylcholine
(neurotransmitter) is
released from motor
neuron axon terminal
into synapse
3. ACh binds to nicotinic
ACh receptors
(AChR) on the motor
endplate on muscle
fiber. Ion channel
requires first
messenger to bind to
receptor protein and
open channel →
increases membrane
permeability to Na
and K
4. AChR are ligand
monovalent cation
channels
5. Na+ flows into and K+
flows out of the
muscle fiber,
generating a large
depolarizing graded
potential
Coupling
1. Somatic motor neuron
releases ACh at
neuromuscular
junction
2. Net entry of Na+
through ACh receptor
channel initiates
muscle action
potential
3. Action potential in t
tubule alters
conformation of DHP
receptor (voltage
sensitive protein that
is connected to RyR
in sarcoplasmic
reticulum)
4. DHP receptor opens
RyR calcium 2+
release channels in
sarcoplasmic
reticulum and Ca2+
enters cytoplasm
5. Ca2+ binds to
troponin, allowing
actin myosin binding
Contraction
1. Ca2+ binds to
troponin, allowing
actin myosin binding
2. Myosin heads execute
power stroke
3. Actin filament slides
toward center of
sarcomere
Sliding filament theory: actin
and myosin slide past each
other
Power stroke cycle: myosin
cross bridges move actin
filament
1. Calcium release from
sarcoplasmic
reticulum
2. Calcium binds
troponin
3. Troponin pulls
tropomyosin from
myosin binding sites
on actin
4. Myosin binds tightly to
and moves actin
(power stroke) and
releases ADP plus Pi
5. ATP binds to myosin,
myosin hydrolyses
(breaks down) ATP →
ADP + Pi
6. The energy releases
the actin myosin bind
and rotates the
myosin head that then
binds weakly to actin
down the molecule
7. Head of myosin is
cocked ready for the
next power stroke
Action potential in t tubule during excitation:
1. DHP receptors in t tubule are voltage sensitive and change shape
2. Ry Receptors in sarcoplasmic reticulum contain Ca2+ channels that are physically linked to
DHP receptors and Ry receptors open
3. Ca2+ goes in cytoplasm
4. Ca2+ binds to troponin → thin filament
5. Tropomyosin shifts relative to G actin → thin filament
6. Myosin binding sites on G actin are exposed → thin filament
7. Dynamic cross bridge formation between myosin and G actin (strong bonds)
Causes onset of muscle tension (contraction)
Initiation of contraction:
1. Ca2+ levels increase in cytosol
2. Ca2+ binds to troponin (TN)
3. Troponin Ca2+ complex pulls tropomyosin away from actin’s myosin binding site
4. Myosin binds strongly to actin and completes power stroke
5. Actin filament moves
Relaxation:
1. Sarcoplasmic Ca2+ Atpase pumps Ca2+ back into SR
2. Decrease in free cytosolic Ca2+ causes Ca2+ to unbind from troponin
3. Tropomyosin re-covers binding site. When myosin heads release, elastic elements pull
filaments back to their relaxed position
Motor endplate: region on muscle fiber that receives acetylcholine (where nicotinic AChR are)
Neuromuscular Junction: motor neurons always depolarize skeletal muscle fibers
- There are no voltage gated channels in the motor endplate, only nAChR
- Because of the nAChR, the motor endplate only generates large depolarizing
graded potentials that spread to sarcolemma (outside of synapse) where the
voltage gated Na+ channels are
- Action potentials cannot be generated on the motor endplate
- Voltage gated Na+ channels are adjacent to the motor endplate - action potentials can
be generated at these regions
- One action potential in a motor neuron always generates an action potential ina skeletal
muscle fiber which shows high safety factor
Action potentials in skeletal muscles: always reach threshold and graded potentials are always
depolarizing (more positive)
Hyperpolarization: more positive after reaches negative
Repolarization: 0 to negative
Roles of ATP in skeletal muscle contraction:
1. Ca2+ atpase in the sarcoplasmic reticulum membrane
2. ATP binds to myosin and provides energy for power stroke
3. ATP binds to myosin and causes release of myosin from actin
4. Na+ K+ ATPase is critical for membrane potential
Identify factors that influence skeletal muscle contraction strength and duration
Factors that affect tension:
1. Sarcomere length within muscle fiber
- Sarcomeres contract with optimum force if at optimum length (neither too long nor too
short) before the contraction begins
- - tension generated proportional to number of crossbridges
- Too much overlap of thick and thin filaments leaves no room for them to move so no
tension, too little overlap leaves no opportunity for actin and myosin to interact, thus no
shortening
2. Summation of twitches within a muscle fiber
- Neuromuscular junction has a high safety factor → synapses are strong and
depolarization at motor end plate is so big that there is always an action potential
created (every time there is an action potential in motor neuron there will be an action
potential in muscle fiber, and each action potential in muscle fiber will cause muscle
contraction)
- Each action potential in the motor neuron produces a twitch contraction in all of the
muscle fibers innervated (synapses many muscle fibers, and each one of those fibers
will contract and contribute to twitch) by that motor neuron
- Latent period: short delay between muscle action potential and start of contraction
because theres a delay in the time required for Ca2+ in to increase
- Delay between action potential coming into t tubule and release of calcium from
sarcoplasmic reticulum
- End of muscle twitch is caused by low sarcoplasmic calcium 2+ (when calcium is high,
contraction happens, when calcium is low contraction stops)
- As a result of latent period, a muscle fiber is not refractory during a contraction and is
able to generate multiple action potentials
- Temporal summation: multiple action potentials occurring by muscle fiber during
contraction together due to latent period that causes summation of contractions
- Each twitch is caused by an action potential generated that causes release of
calcium into SR that leads to tension, calcium is then removed and tension
returns to where it was before
- Short duration action potential in muscle fiber coupled with latent period before
contraction develops causes ability for multiple muscle fibers to create action potentials
due to excitability
Twitch contraction: contraction response to single action potential
Tetanus: high tension simulation caused by multiple action potentials creating twitches that
occur in summation
Fatigue: when muscle fibers are stressed operating at high frequency tension, there will be
fatigue and tension decreases even though action potentials are still occuring
3. Recruitment of additional motor units
- More motor units can be recruited to increase muscle tension
- Motor unit: 1 motor neuron and all of the muscle fibers it innervates (synapses)
- When a motor neuron generates an action potential, all of the muscle fibers it
innervates will generate action potentials and contract
- each muscle fiber is innervated by only one motor neuron, but one motor neuron can innervate
may muscle fibers
- all of the muscle fibers within a motor unit have the same properties
- different motor units within the same muscle may have different properties
- motor neuron only determines timing of contraction, how it contracts and strength is due to
muscle fibers
4. The properties of recruited motor units (muscle fibers in motor units)
Slow twitch fibers (ST or type I myosin): muscle fibers used for posture
- Rely primarily on oxidative phosphorylation
- slow , relatively weak contractions
- Fatigue resistant
- Large amounts of red myoglobin
- Numerous mitochondria
- Extensive capillary blood supply
Fast twitch fibers (Type II myosin)
- Develop tension faster
- Split ATP more rapidly
- Pump Ca2+ into sarcoplasmic reticulum more rapidly (Ca2+ atpase in SR)
- Fast twitch oxidative glycolytic fiber (FOG or type IIA): used for routine
movements
- Use oxidative and glycolytic metabolism
- Fast, strong contractions
- Fatigue resistant
- Has mitochondria
- High myoglobin content
- Fast twitch glycolytic fibers (FG or type IIB/X): muscle fibers used to generate rapid
and/or maximum force
- rely primarily on anaerobic glycolysis
- fast, very strong contractions
- rapidly fatiguing
- large diameter
- pale color
Muscle fatigue: inability to maintain tension during periods of sustained, repetitive activation
- Occurs in fibers that use glycolytic metabolism to produce ATP and is correlated with
lactic acid production
Define proprioception and identify sensors involved with proprioception
Proprioception: sense of body’s position, movement, and effort
- Muscle spindles are small bundles of muscle fibers (intrafusal fibers: inside spindle fusal
form structure), sensory receptors, sensory neurons, and motor neurons that lie in
parallel with the rest of the muscle (extrafusal fibers)
- Muscle spindles are fusiform, meaning they are tapered at both ends
Diagram and explain three types of reflexes
Proprioceptor types
Muscle spindles: in skeletal muscles
- Sense position
- Monitor length
- Sensory organ
- Structures within muscle spindle are intrafusal
- Contains sensory receptors, sensory neurons, intrafusal muscle fibers, and gamma
motor neurons
- Intrafusal muscle fibers maintain the sensitivity of the muscle spindle to stretch
- Some components of the muscle spindle respond to the actual length of the muscle
- Some components of the muscle spindle respond to change in length of the muscle
- Increase in frequencies of action potentials when muscle gets longer
- Spindles accelerate during change in length
- Tonic response: responds to information about length
- Phasic fiber/response: provides information about rate of change of length
Golgi tendon organs: in tendons
- Sense load (tension)
- Monitor tension
- These pinch more than they stretch
- Normally tendon organs are quiet until there is tension on them, then the GTO become
active
Joint receptors: in joint ligaments and capsules
- Sense joint position
Muscle spindles, golgi tendon organs, and skin receptors can elicit reflexes if these receptors
detect a sudden, unexpected change
Muscle Spindle Reflex
1. Stimulus: tap to tendon stretches muscle
2. Receptor: muscle spindle stretches and fires
3. Afferent path: action potential travels through sensory neuron
4. Integrating Center: sensory neuron synapses in spinal cord onto either somatic motor
neuron or interneuron inhibiting somatic motor neuron
5. Efferent path 1: somatic motor neuron
- 6. Effector 1: Quadriceps muscle
- 7. Response: quadriceps contracts, swinging lower leg forward
Or
5. Efferent path 2: interneuron inhibiting somatic motor neuron
- 6. Effector 2: hamstring muscle
- 7. Response: hamstring stays relaxed, allowing extension of leg
Golgi Tendon Reflex
1. Neuron from golgi tendon organ fires
2. Motor neuron is inhibited
3. Muscle relaxes
4. Load is dropped
Flexion Reflex and the Crossed Extensor Reflex
1. Painful stimulus activates nociceptors
2. Primary sensory neuron enters spinal cord and diverges
3. a) One collateral activates ascending pathways for sensation (pain) and postural
adjustment (shift in center of gravity)
b) withdrawal reflex pulls foot away from painful stimulus
c) crossed extensor reflex supports body as weight shifts away from painful stimulus
Action Potential in Skeletal Muscles
- Membrane potential is stable at -70-80mV
- Events leading to threshold potential: net Na+ entry through ACh operated channels
- Rising phase: Na+ entry
- Repolarization phase: rapid; caused by K+ efflux
- Hyperpolarization: due to excessive K+ efflux at high K+ permeability. When K+
channels close, leak of K+ and Na+ restores potential to resting state
- Duration: 1-2ms
- Refractory period: generally brief