A polygraph measures the Galvanic skin response, heart rate, skin temperature, respiration

rate, and blood pressure.

 Galvanic response: sweating, more you sweat the more conduction
 How does a polygraph work?
 Measuring sympathetic response
 Increased conductivity, rise in blood pressure, respiration, hr
 How to trick the test?
 Elevate baseline
Muscle Physiology
 3 classes
 Skeletal
 Innervated by the somatic nervous system
 Attached to bone
 Functions to move the skeletal system
 Origin: the more stationary end of the muscle
 Insertion: the more movable end of the muscle
 Belly: the center of the muscle
 Smooth
 Innervated by the autonomic nervous system*
 Parts of the GI that are also able to move on their own and they are
influenced by the autonomic nervous system
 Surrounds hollow organs and vessels
 GI, respiratory tract, cardiovascular tract, uterus
 Functions to move contents within organs/vessels and to provide vascular
resistance
 Cardiac
 Innervated by the autonomic nervous system *
 Increase heart rate and contractility of the heart
Skeletal Muscle
 There are differences in skeletal muscle forms because there are differences in
function
 Don't need to memorize all the specific types
 Skeletal muscle structure
 Muscle attached to tendon attached to bone
 Muscle body: wrapped in an epimysium (connective tissue), it migrates
around groups of muscle fibers- fascicles, at that level it's perimysium
 Endomysium: inside the fascicles
 Muscle fibers encased in a thin sheath of connective tissue: endomysium
 Perimysium: more connective tissue, extends into the body, diving into fascicles
(bundles of individual muscle cells)
 Sarcolemma: muscle fiber's plasma membrane
 Sarcoplasm: packed with mitochondria and myofibrils
 Myofibrils: contain thick and thin filaments made up of actin and myosin
 Sarcoplasmic reticulum: surrounds each of the myofibrils, and is associated with
T tubules
 Lateral sacs/ terminal cisternae: near the T tubule, the sarcoplasmic reticulum
has these enlargements which store calcium
  Each T-bubule is associated with 2 lateral sacs: forming a triad
 ***T tubules help transmit signals from the sarcolemma to the myofibrils
 Muscle fiber: muscle cell
 Multiple muscle fibers in the fascicle
 Multi nucleated
 Inside each muscle cell are myofibrils and inside those protein filaments
 Skeletal muscle fiber
 Sarcoplasmic reticulum
 T tubules: allows the extracellular fluid to go through the middle of cell
 Allows for maximum access to extracellular fluid
 Myofibrils in clusters that contain the
 Mitochondria scattered through
 Striated
 The sarcomere
 The structural and functional unit of muscle contraction
 What we contribute the striations to the orderly arrangement of protein fibers
in the myofibrils
 Thick filament: myosin
 Thin filament: actin
 The thick and thin filaments are in a 2:1 ratio
 Myosin is anchored by titin to the Z-line
 The thin filament is directly attached to the Z-line
 Z line: Z disk
 Anchors thin filaments
 Each sarcomere is bordered at the ends by Z-lines
 Consists of alpha actinin and CapZ
 M line
 Where thick filaments are going to be lined up
 Connects thick filaments in the sarcomere
 Links bipolar thick filaments
 Made of M-protein, myomesin, and creatine kinase
 I-band
 Mostly thin filaments
 Cuboidal arrangement, square lattice
 The Z line is in the center of the I-band
 A-band
 Thick and think filaments
 Overlap is a hexagonal lattice
 H-zone
 No thin filaments
 These zones change size during contraction, we can measure the zones to
understand the physiology of what's going on
 We can see them so well bc all the sarcomeres are lined up so we can see the
thick filaments and thin filaments and where they overlap
 The thin filament
 Made of actin: second most abundant protein on earth
 Monomeric actin (G-actin) has 1 polypeptide chain
 42 kDNA
  Contains one molecule of ATP and one myosin binding site
 G-actin polymerizes to form filaments (F-actin, the filaments)
 Double helical actin strands, found in thin filaments
 Filament is polarized
 Barbed ends: plus ends
 Anchored at Z-line
 Pointed ends: minus ends
 Important for orientation at the sarcomere
 Tropomyosin
 Overlaps myosin binding sites
 Binds troponin
 Troponin Complex
 Complex of 3 proteins: one attached to the actin strand, another that
binds to tropomyosin, and a third with a site to calcium
 Binds Ca2+ reversibly
 Tropomodulin
 Regulates actin polymerization and depolymerization at the pointed ends
 CapZ
 Regulates actin polymerization and depolymerization at the barbed ends
 Actin treadmiling
 Don't want that to happen in muscle tissue
 So tropomodulin and CapZ, capping proteins stabilize the actin filament,
reduce treadmilling
 The thick filament
 Made of myosin II
 Six polypeptide chains
 2 heavy chains
 4 light chains
 525 kDa
 Globular head region: very important
 Heads are called crossbridges bc they bridge the gap b/w the thick
and thin filaments
 Properties of myosin II
 Ability to split ATP and release energy
 Has actin binding site and ATPase site
 Dimers form thick filaments
 Important for physiology of contraction
 Binds strongly to actin
 Crossbridges, bare zone, all the tails point towards one another which is
important for physiology
 Other important proteins
 Titin
 Giant size (>3500 kDa)
 Forms elastic connections between Z-line and myosin filaments
 Titin strand extend along each thick filament fro the M line to each Z line
anchoring the thick filament in their proper positions relative to the thin
filament
 When contraction occurs, help stabilize the sarcomere
  Primarily responsible for the passive forces within muscle
 More important with cardiovascular physiology
 When you pull the muscle apart, recoil, or force against you in part
due to titin keeping the muscles from splitting apart
 Intermediate filaments
 Connect Z-disks to one another and to the sarcolemma
 Dystrophin
 Along with other associated proteins, stabilizes the sarcolemma with the
cytoskeleton and extracellular matrix

The Mechanism of Force and Generation in Muscle

 The sliding filament model: describes how contractions are a result of thick and thin
filaments sliding past one another
 The cross bridge cycle describes how muscles generate force
 Responsible for the sliding filament model
 Excitation-contraction coupling: describes how muscle contractions are turned on and
off
 How we're transferring energy from action potential to mechanical force
 Muscle cell metabolism: describes how muscle cells provide ATP to drive the
crossbridge cycle
The sliding-filament model
 Muscle contraction
 Shortening of muscle
 Originally it was thought that the proteins themselves shortened
 Filaments slide past each other
 Note how each region changes with contraction
 During contraction the actin filaments are sliding inwards toward the
center, shortening some of the zones. A band remains the same bc it's a
measure of the length of the thick filament but the other ones are
shortening , sarcomere as a whole is shortening
 Shortening of the I bands bc the thin filaments slide pat thick
filaments, moving deeper into the H zone and decreasing it width. A
band move closer together, which decrease the width of the I
bands so the Z lines move closer together and the sarcomere
shortens
 Myosin filaments are dimerized tail to tail with the heads and as
contraction is occuring the heads are moving inwards and that is pulling
the actin filaments toward the center that is shortening the sarcomere
 Sliding is due to cyclical formation and breaking of cross bridges=cross bridge cycle
 When we have myosin binding to actin, it's called a crossbridge
Myosin Binding to Actin
 In the absence of ATP
 Myosin bind to actin at an angle
 In the presence of ATP
 Myosin/actin bond is weak
 Actin stimulates myosin ATPase activity
 Myosins move toward the barbed end
The Crossbridge Cycle
  Binding of myosin to actin
 energized state: ADP and Pi are bound to the ATPae ite of the myoin head
 Myosin ha a high affinity for actin and bind (only in the presence of calcium)
 Inorganic phosphate is released
 ADP molecule will be released shortly as well
 Power stroke
 The ADP is coming off
 The head pivots toward the middle of the sarcomere, pulling the filament along
 Rigor
 ADP is released and myosin is still tightly bound to actin- rigor, lowest energy
form
 Rigor mortis: stiffening of the body that occurs after death bc the cross bridge
cycle is stuck at this step due to excess calcium and a lack of ATP.. Continues
until enzymes leaked by disintegrating components begin to break down the
myofibrils
 New ATP binding to myosin head
 Unbinding of myosin and actin due to conformational change
 ATP is hydroylzed
 Cocking of the myosin head, myosin in high-energy form, ready to bind with the actin
filaments
 Role of calcium
 Calcium binds to troponin and that will expose the binding site for the myosin
head
 Without calcium, no contraction
 Once we remove the calcium, muscle relaxation
 A crossbridge generates force only during the power stroke but a muscle cell
generates force constantly during a contraction. Many crossbridges occur out of
phase with each other so at any point there is some crossbridge. There are always
several crossbridges attached to actin at any time to make the cycle efficient.
 During contraction, each myosin head completes 5 crossbridge cycles/sec. But each
filament has several 100 heads so thousands of power strokes occur and sarcomeres
and muscle fibers can shorten rapidly.
Excitation-contraction Coupling
 Describes how an action potential in the sarcolemma causes contraction
 When a muscle cell receives input from a motor neuron, the cell depolarizes and fires
an action potential that stimulates contraction
 Requires Ca2+
 Dependent on input from the motor neuron
 Each motor neuron innervates several muscle cells
 Each muscle fiber receives input from a single motor neuron
 The neuromuscular junction: connection b/w a motor neuron and muscle cell
 The motor end plate: the motor neuron's terminal boutons fan out of the
sarcolemma, and opposite of these is the region of the sarcolemma, the motor
end plate
 Increase surface area
 High density of acetylcholine receptors, helps to increase the signal
 Highly folded
  Neurotransmitter: acetylcholine
 Motor neuron action potentials always create muscle cell action potentials
 End-late potential is much later than an ordinary PSP; it's always above
threshold and triggers an action potential
 Ca2+ determines the ability of myosin to bind to actin
 Without calcium, tropomyosin is going to cover the binding site
 Relaxed muscle: low Ca2+ concentration, little binding b/w Ca2+ and
troponin
 Low calcium levels due to : calcium pumps in the membrane of the SR
that actively transport calcium ions from the cytosol into the SR & the
voltage-gated calcium channels are closed, preventing calcium leak out
 In the presence of calcium, it binds to troponin, that alters the structure of the
tropomyosin which exposes the binding site
Calcium-induced Calcium release
 T-tubule system
 Invaginations of the sarcolemma
 Allows for extracellular fluid to permeate through muscle fiber
 Sarcosplasmic reticulum
 Storage site for Ca2+
 Together these form the triad
 Action potential triggers opening of DHP receptor, which in turn, opens the ryanodine
receptor
 The electrical signal that triggers gating occurs in the membrane of the T tubule
not the membrane of the SR itself
 Action potential in the T-tubule (electrical signal that trigger gating occur in the
membrane of the T tubule and not the membrane of the R membrane) trigger
the release of Ca2+ from the SR bc of DHP and ryanodine receptors.
 Receptors for CICR
 Sarcoplasmic reticulum is connected to the T-tubules by receptors
 DHP: dihydropyridine receptor responds to change in Vm
 Voltage gated channel on the T-tubule membrane
 Ryanodine receptor: Ca2+ release
 On the sarcoplasmic reticulum, calcium channels that are gated by the
DHP receptors
 In skeletal muscle, the DHP receptor is directly linked to the ryanodine receptor
 Called the Ca2+ release unit
Excitation-contraction coupling steps
 Action potential traveling down the motor neuron, triggering the release of ACH
 ACH is released from the axon terminal of a motor neuron and binds to receptors in
the motor end plate. This binding elicits an end-plate potential, which triggers an
action potential in the muscle cell
 Action potential propagates along the sarcolemma and down T tubules
 The action potential triggers Ca2+ release from SR
 Ca2+ binds to troponin, exposing myosin binding sites
 Crossbridge cycle begins (muscle fiber contracts)
 Ca2+ is actively transported back into lumen of SR following the action potential
 Tropomyosin blocks myosin-binding sites (muscle fiber relaxes)
Muscle Relaxation
  Influx of Ca2+ into the sarcomplasm ceases
 Ryanodine receptors close when membrane potential returns to normal
 As cytosolic Ca2+ rise, SR Ca2+ channels close
 Ca2+ is removed from the sarcoplasm
 Ca2+ is actively transported back into the sarcoplasmic reticulum via the
sarco/endoplasmic reticulum Ca2+-ATPase pump SERCA
 Ca2+ is also pumped out of the cell via active transport channels located on the
sarcolemma
 As Ca2+ levels fall, bound Ca2+ dissociates from troponin
 The release of Ca2+ causes a conformational change in the tropomyosin complex that
once again blocks the tight interaction of myosin with actin
 Muscles cease to contract

Mechanics of Skeletal Muscle Contraction

 Innervation of skeletal muscle
 A single somatic neuron innervates multiple fibers
 Each muscle cell is innervated by only one neuron
 Motor unit: a motor nerve and all of the muscle fibers it innervates
 Functional contractile unit
 All muscle cells within a motor unit contract synchronously when the nerve fires
 Size of the unit varies depending on function
 Muscle twitch
 Mechanical response due to a single action potential
 Can refer to an individual muscle cell, a motor unit, or a whole muscle
 Berief
 Tension= force

 Phases of twitch
 Latent period: period before the contraction starts (time lag bc excitation-
contraction coupling must occur before cross-bridge cycling)
 Contraction phase: where we have cross bridging
 Ends when muscular tension peaks
 Cytosolic calcium levels are increasing as release of the ions exceeds
uptake
 Relaxation phase: calcium is leaving the sarcoplasm
 cytosolic Ca2+ decreases
 Number of active crossbridges are decreasing
 A twitch is reproducible: talking about one muscle cell
 Repetitive stimulation produces several twitches in a row, each with the same
magnitude and shape
  All or nothing principle
 An action potential always triggers the same degree of calcium release from the
SR, which causes the same rise in cytosolic calcium levels, exposes the same #
of binding sites for the myosin crossbridges, produces the same force
 Force can vary from one muscle or cell to another
 Subsequent action potentials can also cause a change in force
 Also some muscle fibers are stronger than others, larger diamter fibers can
exert more force than smaller diameter fibers
 The speed of the twitch differs between fast and slow twitch muscle fibers
 Types of twitch (depends on whether the muscle is allowed to shorten as it contracts)
 Isometric: the muscle develops force at a constant length
 The load is greater than the force generated by the muscle
 Increase in tension than decrease in tension
 Ex: trying to lift the desk glued to the floor
 Ex: standing still and postural muscles hold your body upright, held in
place by bones
 Isometric contraction: sarcomeres shorten even though the whole muscle
does not. Because the sarcomeres (contractile component, CC) of muscles
do not extend the entire length. SEC, series elastic component, transmit
the force to the ends of the muscle. When CC shortens, SEC lengthens so
the overall length doesn't change.
 Isotonic: the muscle shortens under a constant load (textbook says it can
also increase??)
 Increase in tension than plateau
 Muscle is getting shorter, the load is lifting
 Only when the force is equal to the load does the muscle begin to
shorten
 The muscle generates a constant tension just greater than any forces
opposing it
 Concentric contraction: shortening of muscle (lifting objects with curling
motion)
 Eccentric contraction: the muscle length increases (biceps contracting
when lowering an object)
 Not an all or nothing event: size and shape depend on the size of the
load. Latent period increases as load increases bc it takes the muscle
longer to develop the force needed to move the load
 When the load exceeds the amount of the force the muscle can generate,
muscle can't move and contracts isometrically
 Isotonic contraction is rare in the body
 Factors affecting the force generated by individual muscle fibers
 Depends on force generated in indivudal muscle fiber & the # of muscle fibers
contracting
 Force: depends on the # of myosin-binding sites on actin that are
exposed, so on the # of active crossbridges
 At higher frequencies
 The rate of Ca2+ release from the SR exceeds the rate of return to the SR
 An increase in peak tension results
  As stimulation frequency increases, twitch contractions move to treppe,
to summation, to tetanus
 Treppe: independent twitches follow one another closely such that the
peak tension rises in a stepwise fashion until reaching a constant level
 Summation: additive effect of increased stimulation rate
 Additional action potentials arrive before twitches are completed
 The calcium is not removed as rapidly as it is released so the muscle
fiber can't relax completely between twitches
 Tetanus
 Unfused: small oscillations, brief periods of relaxation between
peaks, peaks are reached when calcium levels are high enough to
saturate troponin
 Fused: binding sites are continually exposed, resulting in plateau
 Maximum tetanic tension: muscle is generating all the force it can
 Muscle fiber diameter
 More crossbridges in larger diameter fibers leads to more force-
generating capacity
 More sarcomere, more thick and thin filaments in parallel
 Hypertrophy results from training
 Hyperplasia is not common in mature muscle
 Skeletal muscle growth and hypertrophy
 The total # of skeletal muscle fibers is probably fixed early in life
 This is regulated by myostatin, a protein synthesized in muscle cells
 Myostatin suppresses skeletal muscle development
 Cattle, dogs, and mice with inactivating mutations in their myostatin gene
develop much larger muscles
 Changes in muscle fiber length
 The length is associated with the possible number of crossbridges (length-
tension relationship)
 Length of sarcomeres is important not the # of sarcomeres in series
 An optimum length can generate the most force due to max myosin
crossbridges
 Length tension curve pg 338
Regulation of force generated by whole muscles
 Recruitment: an increase in the # of active motor units
 Fibers within a motor unit are activated simultaneously
 A muscle recruits more fibers by recruiting more motor units
 Fiber type affects timing of recruitment
 Slow twitch: small (100-500 fibers); innervated by an easily excitable
neuron
 Fast twitch: large (1000-2000 fibers); neuron is more difficult to excite
 The size principle
 Motor units vary in both size and the size of innervating neurons
 Correspondence b/w size of motor units and order of recruitment
 When larger forces are needed --> larger motor units are recruited
 When smaller forces are needed --> smaller motor units are recruited
 The basis of this principle: motor units vary in size but ALSO motor neurons that
control them vary in size
  Velocity shortening : the rate of change of the distance shortened
 In a muscle contracting isotonically
 Latent period of shortening increases with increasing load, duration of
shortening decreases, velocity of shortening decreases

Questions
 Isometric and isotonic contractions. How about instances the muscle lengthens during
contraction?
 Slowly putting the barbell back down
 Isometric: the muscle develops force at a constant length
 Isotonic: the muscle shortens under a constant load
 Types of twitch
 Concentric contractions: shortening of muscle (isotonic)
 Eccentric contractions: lengthening of muscle
 Cross bridging is still happening
 Don't the exact mechanisms involved with the lengthening in muscle
 A lot of passive forces generated from the connective tissue that's in the muscle
 Thinking about the physiology of contraction and how a sarcomere shrinks
(generating force), if the muscle does not shrink during an isometric contraction, then
where does the force come from?
 Contractile component: comprised of the sarcomeres
 Series elastic component: connectie tissues at the ends of cells
 Mostly tendon
 Parallel elastic component: connective tissue that lies parallel to muscle fibers
 Paramyeium, epimieieum etc
 The net shrinkage of the muscle is going to be zero
 There is a significant role in the connective tissues as well
 What is rigor mortis? How does it happen?
 The muscles are frozen
 Happens when you die
 ATP is not allowing the detachment of myosin from the binding site because
there is no more ATP produced after you're dead, you're not breathing.
 You need ATP to detach the myosin head from the actin filament

12.4 Skeletal Muscle Metabolism

 ATP is crucial for contraction
 The pool of ATP in skeletal muscle cells is only enough to support a few
contractions
 ATP must be continuously replenished
 Oxidative phosphorylation, substrate level phosphorylation, anerobic
glycolysis, creatine phosphate
 Creatine phosphate is used to convert ADP to ATP for a quick supply of ATP
 Creatine phosphate + ADP <---Creatine kinase--->creatine + ATP
 Once the muscle rests the reaction slides the other way
 This is sufficient to give ATP-producing reactions time to gear up
 Metabolism changes with demand for energy
  Important factors determining ATP sources: intensity of exercise & oxygen
availability
 What do you think the primary sources for ATP are during
 Low oxygen levels: anerobic processes
 Light exercise: oxidative phosphorylation
 Creatine phosphate occurs very fast so we need other ways
 Some anerobic glycolysis but mainly oxidative phosphorylation
 Heavy exercise:
 More anerobic glycolysis involved than oxphos
 The muscles also utilize glycogen stores. After creatine phosphate is used,
glycogen sources and glucose and fatty acids delivered by the bloodstream can
also be used
 Glucose- glut 4 expression increased in sarcolemmas
Types of Skeletal Fibers
 3 skeletal muscle fiber types
 Slow oxidative
 Fast oxidative
 Fast glycolytic (rare)
 *Muscles contain all 3 types, but in different proportions
 Differences in the speed of contraction: fast-twitch and slow twitch fibers
 Dependent on rate of myosin ATPase activity
 Different isoforms of myosin and they hydrolyze ATP at different rates
 ATP hydrolysis is the rate limiting step of the crossbridge cycle
 Higher rate: faster crossbridge cycling, sarcomeres shorten faster
 Fast fibers: Myosin with fast ATPase activity
 Slow fibers: Myosin with slow ATPase activity
 Muscles usually have fast and slow fibers but one predominates
 Differences in the primary mode of ATP production: glycolytic and oxidative fibers
 Glycolytic fibers: glycolysis
 Lower numbers of mitochondria bc not doing oxphos
 Larger diameter and surrounded by fewer capillaries
 Lack myoglobin, white muscle
 Pyruvate is generated faster than consumed --> lactic acid, fatigue easily
 Oxidative fibers
 Smaller in diameter than glycolytic: oxygen can diffuse much more quickly
 Closer to capillaries: increased access to blood because blood is a source
of oxygen and need access to oxygen
 Have myoglobin: binds oxygen in the muscles to act as a small oxygen
store, similar to hemoglobin in the blood, gives the muscles a dark color
 Converts pyruvate to acetyl CoA as fast as it is produced
 Both fibers are found in all muscles of the body but their proportions vary
among muscles
 Response to exercise: correlation b/w size of motor unit and fiber type
 A motor unit has the same type of muscle fiber in the motor unit
 Slow oxidative
 Smaller motor units
 Recruited first
 Fast oxidative
  Intermediate motor units
 Recruited second
 Fast glycolytic
 Larger motor units
 Only recruited during high-intensity exercise (sprinting/weight lifting)
 Resistance to fatigue
 Fatigue: decline in muscle's ability to maintain a constant force of contraction in
the face of long term repetitive stimulation
 Low intensity exercise: likely result of energy reserve depletion (mainly
glycogen)
 Recovery in 24 hrs
 High intensity exercise:
 Buildup of pyruvate, convert to lactate, buildup of lactic acid
 strong contractions can also compress blood vessels
 Very high intensity exercise: can induce neuromuscular fatigue
 Depletion of acetylcholine at the end plate, reduced ability to have action
potentials triggered
 Fast twitch & slow twitch
 Fast twitch
 Type IIB: fast glycolytic, white
 Type IIA: fast oxidative, red
 Slow twitch
 Type I: slow oxidative, red
 Red color due to myoglobin
 Differences between breeds between a species as well as individuals
 Pay attention to Table 12.1

Long-term muscular response to exercise

 With training, you can change between oxidative and glycolytic fibers
 With aerobic exercise: increased oxidative capacity, some fast glycolytic fibers can be
converted to fast oxidative fibers, increase in size and number of mitochondria,
decrease in fiber diameter which facilitates oxygen movement but decreases force
generating capacity, increase in number of capillaries surrounding muscle fibers
 With high intensity exercise: decreased oxidative capacity, some fast oxidative fibers
can be converted to fast glycolytic fibers, decrease in size and number of
mitochondria, increase in fiber diameter, reduced resistance to fatigue
 Muscle growth is not due to the addition of new fibers bc muscle fibers are
postmitotic
 Can not change fast and slow twitches bc it has to do with the mysoin isoform and
that can't be changed

12.5 Control of skeletal muscle activity

 Origin: point of attachment to stationary bone
 Insertion: point attachment to movable bone
 Muscle activity across joints occurs in an antagonistic fashion to accomplish
movement
 Muscle flexion: bicep contracts, tricep relaxes
  Muscle extension: bicep relaxes, tricep contracts
Muscle Receptors for Coordinated Activity
 Two types of receptors
 Muscle spindle: detect length or stretch receptors
 Golgi tendon organ:
 Muscle spindles
 Gamma motor neuron innervating it in efferent pathway
 Type Ia affarent and type II afferent
 Extrafusal fibers: bulk of the muscle body, innervated by the alpha motor
neuron
 Stretched muscle
 The sensory fibers release an increase in action potentials
 Contracted
 Decrease in action potentials
 Relaxed
 Have action potentials firing
 The muscle has a compensatory mechanism to maintain the sensitivity to receptor
 No gamma innervation
 Gamma motor neuron innervates the interfusual fiber
 Without that, we have a lose spindle fiber
 Coactiation of alpha and gamma motor neurons
 A bit of tension restored, hence some sensitivity restored
 Golgi tendon organs
 Located at the ends of muscles
 Innervated by type Ib afferent
 Connective tissue
 Protect against the over activity of the muscle, alert the body of overstretching
 If the muscle is being overstretched, the golgi tendon organ responds to that
increase in tension by signaling that the muscle needs to contract and come
back together.

Smooth Muscle
 Largely found in the walls of hollow organs and tubes
 Specialized for slow but powerful contractions
 Controlled by involuntary mechanisms
 Elongated, spindle-shaped cells; single nucleus (skeletal is multi nucleated)
 Gap junctions
 Varicosities along neuron
 Not every cell has a direct relationship with the neuron that innervates it
 Smooth muscle cells are arranged in sheets
 Like a tube??
 Irregular organization of the contractile machinery: lack sarcomeres, T-tubules, and
troponin
 There are thick and thin filaments but not arranged in sarcomeres
 Without the sarcomeres we don't have the striations
 We have thick and thin filaments anchored at dense bodies
 During contraction the whole cell squeezes in
  The filaments still slide one over another but not the same step as the skeletal
muscle
 Have a larger range for contraction bc it doesn't have sarcomeres (a limiting
factor)
 EC coupling
 Excitation and contraction coupling, how you turn an action potential to a
mechanical movement
 Still see EC coupling occurring
 Calcium plays an important role (as with skeletal and cardiac) but a slightly
different role
 The action potential travels down the sarcolema and triggers the opening of the
channels in the sarcoplasmic reticulum to release
 Dhp and rhyadenine receptor coupled together
 Rhyadenine receptor causes the sarcoplasmic reticulum to dump calcium
into the sarcoplasmic reticulum
 The calcium is coming from the sarcoplasmic reticulum??
 calmodulin: activates myosin light chain kinase
 Once that is activated, binds to myosin, phosphorylated myosin light chain,
myosin ATPase, cross bridge cycling, contraction
 In the absence of calcium, no binding to calmodulin, unphosphorylated myosin
light chain, no myosin atpase activity, no cross bridge activity (at rest)
 In skeletal muscle, calcium is binding to troponin which then shifts the
tropomyosin exposing the binding sites, acting on the thin filaments
 Here, we're acting on the thick filaments, the myosin heads
 Relaxation
 Phosphatases remove phosphate from myosin
 Ca2+ is removed from cytoplasm
 Smooth muscle contraction and relaxation is slower than skeletal and cardiac
muscle
Neural regulation of contraction
 Multi unit smooth muscle
 Consists of multiple distinct units that function independently of each other
 Must be stimulated by nerves to contract
 Single unit smooth muscle
 Contracts as a single cohesive unit due to gap junctions
 Forms dense sheets to facilitate simultaneous contraction
 Self-excitable "myogenic contraction" does not require nervous stimulation to
fire an AP and contract
 Examples: walls of hollow organs and viscera (GI, reproductive, urinary)
 Spontaneous depolarizations
 Have pacemaker potentials and slow-wave potentials that are spontaneously
generated form the cell
 Pacemaker: slow depolarization and when you cross threshold, potential
occurring
 Potassium, calcium, sodium channels
 Slow-wave: fluctuation
 Primarily sodium channels are involved
 The major differences are in the types of channels
  Smooth muscle has capacity for tone, very low level of contraction?

Cardiac Muscle
 Striated
 Troponin-tropomyosin regulation
 Gap junctions
 Pacemaker cells/myogenic
 Innervated by autonomic nervous system
 Ca2+ comes from extracellular fluid and sarcoplasmic reticulum
 Unique action potential plateau phase
 Prolonged plateau phase
 Don't want the concept of summation to happen here
 In skeletal muscle
 Very long refractory period, preventing another action potential to trigger
contraction

Study table 12.2