Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
316 Cards in this Set
- Front
- Back
|
Sensory systems transform physical energy into
|
neural inforation
|
|
|
Motor systems transfrom neural inforation into
|
phsycial energy
|
|
|
What are the 3 overlapping classes of movements
|
1. voluntary movements
2. reflex 3. rhythmic motor patterns |
|
|
What does succesfull movements in each of these classes requires that the motor systems
|
convey accurately timed commands, compensate for changes in position, take ino account limb inertia and mechanical arrangement of muscles, bones and joints
|
|
|
What is volntary movement
|
purposeful, primarily learned movements, goal directed
|
|
|
What is the most complex type of movement
|
voluntary movement
|
|
|
What is reflex movement
|
involutnary response, tends to be sterotype (withdrawal of a hand from a hot objet, coughing)
|
|
|
What is the simplest most primitve type of motor movement
|
reflex
|
|
|
What is rhythimic motor patterns
|
inititation and termination is voluntary, seqeunce itself tends to be sertotype, repetivie, and relex-like (walking, running)
|
|
|
What are the 3 levels in the hierarchy of motor control
|
Spinal cord (lowest level_
Brain stem Cortical motor areas (highest) |
|
|
What is the spinal cord level of heracy motor control
|
directly controls the activation of skeletal mucles
|
|
|
Where does spinal cord receive sensry input
|
from skelteal muscle, tendons and skin
|
|
|
How does spinal cord control output of muscle activity
|
alpha and gamma motor neurons
|
|
|
What does teh brain stem contorl
|
many--respiration, cardio, and can serve as a command center--
|
|
|
How is brian stesm a command center
|
receves singals from higher cetners and from sensory input
|
|
|
Where does brain stem receive input from
|
higher centers and sensory inputs
|
|
|
What is the output control of brain stem
|
control muscle activity via activation of inhibitor of motor neurons
|
|
|
What does crotical motor areas control
|
all planned and intentional movemetn
|
|
|
Where does cotrical motor area receive input from
|
internal and external sensory inputs and other brain centers
|
|
|
What is output of cortical motor areas
|
sends signals to sensorimotor corext, which conncect brain stem and spinal cord
|
|
|
Skeletal muscles are made up of a group of elongated, mutinulceated cells called
|
muscle fibers
|
|
|
What does muscle fibers contract in response to
|
neural or electrical stimuli
|
|
|
A single contraction/relaxation cycle is called
|
a twitch
|
|
|
What are tough conncetive tissue taht connect a muscle to bones
|
tendons
|
|
|
The attached of the tendon to the bine the remain stationary during muscle contration is known as
|
the orgin
|
|
|
The tendon that is moved is
|
the insertion
|
|
|
What is motor unit compsed of
|
single alpha motor neuron and all the fivers taht are innervated by it
|
|
|
Motor neurons syynpase onto muscle fibers at
|
the neuromuscle juntion
|
|
|
Since muscles can only contrat, must agnoinst and antagoins muscle work in a coordinated fashion to achieve the desired movement
|
YES
|
|
|
A single alpha motor neurons innervates 10 to 2000
|
extrafusal msucel fibers
|
|
|
The smaller the inneravation ratio 1:20 verus 1:1000 means
|
greater degree of fine control of muscle movement
|
|
|
The cell body of teh alpha motor neuron reside in
|
ventromedial ro dorsolateral nuclues of gray matter
|
|
|
Alpha otor neurons are myelinated, and release what are the neuromuscle junction
|
AcH
|
|
|
What does AcH stimulate
|
the opening of the nicotinic-cholinergic cation channels
|
|
|
What does a flexor do
|
decrease the angle at a joint
|
|
|
What does an extensor do
|
increases the angle at a joint
|
|
|
What does an agonist do
|
flexors that attach to same bones or extensors that attach to same bones
|
|
|
What is an antagoinst
|
flexors and extensory that attach to SAME bone
|
|
|
What is isotonic
|
contraction that results in muscle shortening
|
|
|
What is isometric
|
contraction that results in muscles staying the same length
|
|
|
What is summation of muscle contraction
|
is teh additive effect of consecutive twitches
|
|
|
What happens is a muscle is stimulated before is has completely relaxed
|
the contraction force is increased
|
|
|
What is tetanus
|
contact is smooth and sustained, b/c of a constant stimulus, where there is no evidence of muscle relaxation
|
|
|
What is recruitment
|
lower levels of stimulation active smaller cell bodes, as more strength is needed, larger and larger motor units are activated
|
|
|
The size of msucel is proportionate to
|
the number of muscle of fibers,
|
|
|
The more muscle fivers
|
the greater the amount of force that can be genrated
|
|
|
Spinal relfexes can act independly of higher brain centers, howevver the brain is continously informed of teh current state of muscles by
|
Golgo tendon organs and muscle spindels
|
|
|
Spinal reflex play a critical role in what
|
posture and locoamtion
|
|
|
Stimulation of muscle spindles sends information to the CNS about
|
muscle length or rate of change of length
|
|
|
What is anatomy of a muscle spinle
|
made of 3-12 intrafusal muscle fibers, surrounded by extrafusal muscle fibers
|
|
|
Streching of the muscle spindle stimulates what 2 types of sensory neurons
|
Type Ia or Type II
|
|
|
Type Ia or Type II synapse directly on
|
alpha and gamma motor neurons in teh spinal cored to cause contaction of the muscle
|
|
|
What is the strech reflex
|
streching stimulates Type Ia or II, that synapse of alpha and gamma, and cause contraction
|
|
|
What type of information does Type Ia convey
|
RATE of strech
|
|
|
What type of information does Type II convey
|
CHANGE in muscle length
|
|
|
Does stimulation of Type Ia and II cause contraction to OPPOSE the sudeen change in length
|
YES
|
|
|
What is reciprocal innervation with stimulation of Type Ia fibers
|
causes inhibiton or relaxtion of antagoinst muscle
|
|
|
What do Gamma motor neurons stimulate, which is important for
|
contraction of intrafusal muscle fibers, proper functioning
|
|
|
What do Gamma motor neurons contribute to maintaince of
|
muscle tone via activation of a reflex arc
|
|
|
Are Golgi tenond organs located in tendons
|
YES
|
|
|
What is the fuction of the Golgi tendon organ
|
provide teh CNS with instantanoues information on the degree of tension in each muslce
|
|
|
Singals from teh Golgi tendon organ are sent via
|
Type Ib nerve fibers to SPINAL CORD and higher brain centers
|
|
|
What does Golgi tendon organs respond to (opposite of Muscle spindle)
|
contraction via type IB nerve fiber which causes inhibition of inhibiotin of the alpha motor neurons, leading to muscle relataction and lengthing
|
|
|
What is the 1st step that happens after tapping the tendon of the knee
|
1. Passive streching of muscle spindle (intrafusal fibers)
|
|
|
Streching of the spinde stimulates what
|
sensory neurons and the AP are conducted into the spinal cord via dorsal root, synspase on aplha motor neruons
|
|
|
What happed after axons of sensory nerves synapse on alpha motor neurons
|
effeert nerve impulese go to extrafusal muscle fibers causing the release of Ach
|
|
|
The release of Ach form teh ending of the alpha motor neruons stimulated what
|
contraction of the extrafusal fibers,
|
|
|
Does contraction fhte msucle relives teh stretch of the spindle
|
YES, and decreasing its electrical activity in the spindle afferent fibers
|
|
|
What is the crossed extensor refelx AKA
|
withdrawl reflex
|
|
|
What is general mechanism of crossed extensory reflex/ withdrawl refelx
|
withdrawls of ipsilateral limb, and extension of contralteral limb
|
|
|
What is the flexor reflex
|
step on glass exitation of flexor, and that inhibits that extensors of same limb
|
|
|
Reciprocal innervation is
|
interneurons that connect to motor neurons to inhibit antagonist muscles
|
|
|
What is double reciprocal innervation
|
interneurons that connect to motor neurons of muscles on limbs on opposite side of the affected limb
|
|
|
What is an example of double reciprocal innervation
|
step on glasses inhibit flexor and excite the extensor on OPPOSITE limb
|
|
|
The Type Ia of the Muscle spindles and Type Ib of Golgi tendon sned infromation to higher brain centers via interneurons in
|
the drosal columns to the thalamus
|
|
|
What is posture
|
the overall position of the body and limbs relative to one another
|
|
|
Is posture very dependent on refelx loops, especaily
|
YES--vestibular reflexes,
|
|
|
What is locomation (walking) dependent on
|
rhythmic motor pattersn ath are generated by spinal reflex circuits
|
|
|
The brain stem is made up of, and does it control autonomic and motor
|
Medulla, Pons, and Midbrain, YES
|
|
|
What are 2 important patways for motivation aspexts of movement
|
mesolimbic and nigrostriatal DOPAMINERGIC pathways
|
|
|
Where are the cell bodies of the mesolimbic
|
ventral tegmentum
|
|
|
Where are the cell bodies of teh nogrostrital
|
substantia nigra
|
|
|
What is the orgin of the Red nucleus
|
midbrain
|
|
|
The red nuclues controls, and sends out via
|
coordinates control of arms and hands---rubospinal tract
|
|
|
What does reticular nucles control
|
activation of large msucles involved with upright posture (axial and legs) by interacting with alpha and gamma motor neurons
|
|
|
Where does vestibular nucleus responsible for and location
|
MEDULLA--activation of limb and axial muscles involved with upright postures by interacting with alpha and gamma motor neurons
|
|
|
Sudeen movements esecially of the head activate what
|
the vestibular nucleus
|
|
|
All voluntary movement involves conscious activity in
|
the cerebral cortex
|
|
|
The corex exerts some control over lower brain areas, in which they send specifc signals to msucles
|
YES
|
|
|
However what movements does the cortex make DIRECT CONNECTIONS to the muscles
|
fingers and hands
|
|
|
What are the 3 phases of simple voluntary movement
|
1. Target identification
2. Plan of action 3. Execution |
|
|
What areas of the cortex control
1. Target identification 2. Plan of action 3. Execution |
1. posterior parietal cortex
2. premotor areas of frontal 3. primary motor cortex |
|
|
What does somatic sensory cortex and somatic assciation area provide sensory info to
|
primary motor cortex
|
|
|
The primary motor corex is important in
|
initiation, control, and termination ofo skilled voluntary movements
|
|
|
How is the primary motor cortex arranged
|
somatoopically, a specfic region of the cortex corresponds to a specific body part
|
|
|
Half the motor corext is concerned with controlling
|
hands and muscles of speech
|
|
|
What is the most important descending motor output pathway from the primary motor cortex
|
corticospinal tract
|
|
|
Why do size of the body parts in the motor homunclus do not correspond to their actual size
|
corrrespond to skill level
|
|
|
Where do most coticopsinal tracts terminate
|
on interneurons of the spinal cord or on alpha motor neurons
|
|
|
What does dorsolateral corticospinal tracts control
|
control DISTAL limbs
|
|
|
Does Dorsolateral decussate
|
YES
|
|
|
What does ventromedial corticospinal tract control
|
trunk and axial muscles
|
|
|
What does the premotor cortex do
|
prepares for more complex movements for exampling position the shoulders and arms in prepartion
|
|
|
Typically signals from the premotor cortex are sent to what
|
basal ganglia, then thalamus then primary motor cortex *sometime directly to primary motor cortex
|
|
|
What do the supplementary motor areas do
|
aid in the programming and coordination of complex movements (thinking not doing_
|
|
|
What does teh Somatic sensory cortex do
|
assigns sensations of pressure and textures to discrete parts of the body, also judges weight and shapes or forms of objects
|
|
|
What are two main ascending tracts the bring sensory information those types of sensory sensation
|
Dorsal Colum-touch sensation
ALS----pain and temp sensation (desscuasate @ spinal cord) |
|
|
What does the Somatic ASSOCIATION are do
|
combines and interpret, allow person to "feel"
|
|
|
Does electrical stimulation of cerebellum cause any sensation or motor movement
|
NO
|
|
|
What does Cerebellum do
|
sequences motor activites, and monitors and makes adustments
|
|
|
What does it mean that the cerebellum has a comparator function and what specifc region
|
its compares actual movements with inteneded movements and makes corrections
(Spinocerebellum) |
|
|
The cerebellum also help plan or calculates the next sequential movement, which helps with, and specifc region of cerebellum
|
smooth the procession of movements
(Cerebrocerebellum) |
|
|
Does the cerebellum learn from its mistakes
|
if a movement does not occur exactly as intended, is it modified next time
|
|
|
What are 3 division of cerebellum
|
1. Spinocerebellum
2. Cerebrocerebellum 3. Vestibulocerebellum |
|
|
Which region of the cerebellum is arragned somatotopically
|
spinocerebellum
|
|
|
What does spinocerebellum controls
|
the execution of movement and regulates muscle tone
|
|
|
What region is where comparison and correction between intetnion and execution are made
|
Spinocerebellar
|
|
|
What does the cerebrocerebellum do
|
planning/calculating of sequential movments and correct timing--allowing smooth and coordinated
|
|
|
Where are input rececived and outputs of the cerebrocerebllum sent
|
Input from premotor corex and somatic and association sensory
motor and premotor cortexes |
|
|
What does Vestibulocerebellum do
|
balance and coordination between the head and eyes
|
|
|
Where are outputs sent of the vestibulocerbellum
|
vestibular nuclues
|
|
|
What composes the basal ganglia
|
globus pallidus, caudate nuclues, and putamen
|
|
|
Is the basal ganglia like the cerebellum, it DOES NOT act by themselves, but acts to modify singals from the cortex
|
YES
|
|
|
Where does Basal ganglia receive inputs and send to
|
from the cortex, and send back to cortex
|
|
|
The role of the basal ganglia in motor control is in the regulation of motor function via
|
INHIBITION of singals from the cortex
|
|
|
What does the Putamen Ciruct do
|
important in subconscious execution of learned patterns of movment
|
|
|
What is an example of Putamen Circuit
|
writing letters of the alphabet, throwing a ball
|
|
|
What is the importance of the Caudate circuit
|
programming and INIATION of complex voluntary movements
|
|
|
What is beginning to run an example of
|
Caudate circuit
|
|
|
What is the importance of the Caudate circuit
|
programming and INIATION of complex voluntary movements
|
|
|
What happens if there is a lesion in the motor cortex
|
paralyisi of muscles on opposite side of body
|
|
|
What is beginning to run an example of
|
Caudate circuit
|
|
|
Lesions in Cerebellum DO NOT cause paralysis rather
|
awakwardsness of intentionial movments
|
|
|
What happens if there is a lesion in the motor cortex
|
paralyisi of muscles on opposite side of body
|
|
|
Lesions of basal ganglia DO not cause paralysis rather
|
meaningless uninitetnioal movemetns occuring unexpectdely
|
|
|
Lesions in Cerebellum DO NOT cause paralysis rather
|
awakwardsness of intentionial movments
|
|
|
What is an disease example of Basal ganglia
|
Parkinson's
|
|
|
Lesions of basal ganglia DO not cause paralysis rather
|
meaningless uninitetnioal movemetns occuring unexpectdely
|
|
|
What is an disease example of Basal ganglia
|
Parkinson's
|
|
|
Do all pathologies of the in some matter affect motor systems
|
YES--directly or indirectly
|
|
|
What is the primary cause of Parkinson's
|
degeneration of the DA cells in the substantia nigra
|
|
|
Is parkinson's genetic or environmental
|
BOTH
|
|
|
What are 4 symptoms of Parkinson's disease
|
STUD
1. Slow movement (bradykinesia) 2.Tremor at Rest 3. Unique increase in muscle tone or rigidity 4.Difficultly in iniation of movement |
|
|
What disease has ratchet-like characteristic
|
Parkinson's
|
|
|
What is the cause of Tetanus or Lockjaw
|
bacteria that is taken up by alpha and motor neurons, and goes to spinal cord or brainstem
|
|
|
What happens aften the toxin goes to spinal cord or brainstem
|
it blocks release of GABA and Glycine
|
|
|
Signs and symptoms of Lockjaw
|
Ridigty adn violent spams, and death from interferance with respiration
|
|
|
What is saprin used as
|
an isectices, and weapon of mass destruction
|
|
|
What does Sarin do
|
blocker of Acetylcholinesterase
|
|
|
What are signs and symptoms Sarin toxicity
|
Miosis, wheezing, weakness, N/V respiaratory failure
|
|
|
What is cause of Cerbebral stroke
|
blood clot, or break, interupting blood flow to brain
|
|
|
What happens after the brain cell "infarct"
|
they release chemicals that set off a chain reaction called an ischemic cascade
|
|
|
Given teh rapid pace of the ischemic cascade the window of opporunity for inervation is...and what would happen
|
6 hrs, and if no intervation, then the PENUBRA dies
|
|
|
Signs and symptoms of stroke
|
Numbness on one side of body, confusion, difficuly speaking
|
|
|
What is main roles of Muscle
|
convert chemcial energy to mechanial enery,
|
|
|
What do muscles generate heat
|
energy conversion not 100% effecient
|
|
|
What are 3 types of muscle
|
skeletal, cardiac, and smooth
|
|
|
What are functions of skeletal muscle
|
1. used for posture/movement/respiration
2. contraction 3. voluntary control |
|
|
What are functions of cardiac muscle
|
1. propel blood
2. spontaneous contractile and regulated by autonomic/hormones |
|
|
What are functions of smooth muscle
|
1surrounds hollow organs and tubes, and blood veseels
2. contraction regulated and spontaneous |
|
|
Does smooth muscle play a role in iris and hairs in skin
|
YES
|
|
|
What is organization level of skeletal muscle
|
1. muscle
2. fascicle 3. muscle fiber 4. Myofibril 5. Sacromere 6. Myofilament |
|
|
What is whole muscle and what covers teh muscle
|
groups of fasciculi---connective tisue called the
epimysium |
|
|
What is Fascicle and covers teh fascile
|
groups of muscle cells (fibers) covered by perimysium
|
|
|
What is a muscle cell (fiber) and sourroned by
|
group of myofibrils surronded by a cell membrane (sarcolemma)
|
|
|
What is the myofibril
|
numerous sacomers
|
|
|
Is the myofibril a long protein structure is AKA
|
contractile ELEMENT
|
|
|
What is sarcomere
|
composed of myofilaments
|
|
|
What is teh sarcomere AKA
|
BASIC unit of contractile machinery in skeletal muscle
|
|
|
What is the the myofilament
|
made of thick and thin filaments
|
|
|
What is the central portion of the myofibril
|
A-band --thick mylofilaments (myosin)
|
|
|
What is the lateral portion of the myofibril
|
thin filaments
|
|
|
What is the Z line or disc
|
ends of the thin filament and attaches to other sarcomeres
|
|
|
What are the elastic elements composed of
|
protein titin
|
|
|
What do elastic elements do
|
attack thru the thick filaments to the M-line, and hold in place and return to orginal spahe after strech
|
|
|
What is the M-line composed of
|
M-protein, paramyosin, and C-protein
|
|
|
What does the M-line do
|
binds the ends of the thick filament together
|
|
|
What is overlap of thick and thin during relaxed
|
small overlap and Z far apart
|
|
|
During contraction, overlap increase, what happens
|
A bands remain constant (thick stay same), and H and I bands decrease in size, and Z closer together
|
|
|
What is intrepation of what happens during contraction
|
thin filaments move closer, the sarcomere shortens, and muscle shorterns
|
|
|
What is strcute of myosin
|
thick, heavy protein with a tail and a double globular head
|
|
|
What is strcutre of thick filament
|
comprised of 300-400 molecules of myosin where globular heads project out
|
|
|
Myosin are are packed together in oppostie driection which results
|
in a middle region devoid of globular heads
|
|
|
What 3 proteins compose the thin filaments
|
actin, tropomyosin, and troponin
|
|
|
What is strcutre of actin
|
Globular proteins that form long bead chain (F-actin)
|
|
|
Two stands of F-actin combine to form
|
the healical backbone of the thin filament
|
|
|
What is Tropomyosin
|
long fibrous protein that lies near goove formed by the 2 F-actin
|
|
|
What is Tropoin
|
protein complex made of 3 gobular proteins
TNI, TnT, TnC |
|
|
What is TnI
|
inhibitory subunit that binds to actin
|
|
|
What is TnT
|
binds to tropomoysin
|
|
|
What does TnC do
|
binds calcium
|
|
|
What is the plasma mebrane of the muscle cell
|
sarcolemma
|
|
|
What are inward extension of the sarcolemma that enter deep into the muscle cell
|
T-tubules (transvere)
|
|
|
What is the sarcoplasmic reticulum
|
forms an extensive sleeve-like structure aroudn eacch and every myofibril
|
|
|
What are the enlarged ends of the SR called
|
terminal cisternac
|
|
|
Are the terminal cisternae connected to the T-tubles
|
NO
|
|
|
What is the triad
|
terminal cistera, t-tuble and terminal cistera
|
|
|
What does the sarcoplasmic reticulum store
|
large amounts of Ca+
|
|
|
Are there many mitcohondria around SR
|
YES
|
|
|
Do either the thick of thin filaments change in length
|
NO--only the thin move, and only over lap
|
|
|
What is force (tension) generation of the slidiing filament theory
|
refers to activation of muscle NO VISIBLE OR EXTERNAL SHORTENING
|
|
|
What does contraction means in sliding filament theory
|
means EXTERNAL shortening, and overlaping of filaments
|
|
|
Explain actin-link regulation under resting SKELETAL muscle conditions
|
Tropomyosin blocking actin site preventing myosin from binding
|
|
|
What happens when there is increase intracellular Ca+
|
Ca+ enters cytoplasm and bind to troponin C moving troponin away from myosin binding site
|
|
|
The actin-myosin interaction is AKA
|
powerstoke or cross bridge cycling
|
|
|
What is 1st step powerstoke or cross-brigding
|
attachment of the myosin cross bridge to actin at a 90 degree angle
|
|
|
Is myosin in its HIGH energy state in step one, and why
|
YES, ATP has already been hydrolzed and ADP and Pi remain bound
|
|
|
What is step 2
|
power stoke and release of ADP and Pi
|
|
|
The energy from ADP and Pi does what
|
casues globular head to go from a 90 degree angle to a 25 degree angle and move it actin inward
|
|
|
What is step 3
|
detachment of myosin from actin by the binding of ATP
|
|
|
What is step 4
|
ATP is split and cocking of myosin head occurs
|
|
|
This cycle repeat as long as Ca+ and ATP are present, the more cycles means
|
the greater force generation and greater potential of contraction
|
|
|
What happens when there is lack of ATP
|
myosin remains bound to actin and remains in contractile state AKA Rigor mortis
|
|
|
What are 2 functions of ATP
|
1. Energy source
2. allosteric regulator |
|
|
What are the 2 fuctions of myosin
|
structual protein and
an enzyme that hydrolzyes ATP |
|
|
Does myosin convert chemical energy into mechanial energy
|
YES
|
|
|
THe normal resting state of skeletal muscle is
|
relaxation
|
|
|
Motor neurons divides into many braches that innervated many fibers
|
YES
|
|
|
But each muscle fibers is controleed by how many motor neurons
|
ONE
|
|
|
After the alpha motor nerve temminal synapase on the muscle fibers what happens 1st
|
relase of AcH which binds to and actvivates nicotinic acetylcholine receptons
|
|
|
What happens after the activation of of nocotinic ACh receptors
|
the LIGNAD channels are opened allowing Na+ ions and and some K+
|
|
|
What is the result of the opening and allowing Na+ ions and some K+
|
End-plate potention
|
|
|
Action of ACh is terminated by
|
enzymatic acetylcholinesterase
|
|
|
What do end plate potentials cause
|
an ACTION POTENTIAL, opening of VOLTAGE-GATED Na+ channels
|
|
|
What does an action potential do at an end plate potential
|
propagated alson the sarcolema membrane, and down the T-tuble, which transmits AP into interior of muscle cell
|
|
|
What happens after AP travels down the T-tuble
|
activates the SR, causing ot it release Ca+ down its concentration gradient into the muscle cell
|
|
|
What does Ca+ do onces its released into the muscle cell
|
binds to TROPONIN TNC, causes a conformational change and tropomyosin uncovers the myosin binding site on actin, and muscle contraction
|
|
|
How is Calcium removed from the muscle cell cytoplams
|
by the action of Ca+ ATPase pumps
|
|
|
Where are the Ca+ ATPase pump
|
on the SR
|
|
|
What happens when Ca+ falls low enough
|
tropomyosin blocks the myosin binding site, and the muscle returns to RELAXATION
|
|
|
How long is the AP in SKELETAL MUSCLE
|
Very short duration (5msec)
|
|
|
What is the time realtionships of the muscle action potential, after release of AP
|
next calcium released peaks at 7-8 sec, and up to >30msec
|
|
|
When does Skeletal Muscle contratation occur after generation of an AP time-wise
|
peaks at 20-30 secs and last up to >50sec (depends on muscle)
|
|
|
When is beneift of have slower skeletal muscle contraction
|
Mutiple AP can be generated before muscle tension reaches a peak, allows SUMMATION
|
|
|
What does a single AP genere in a muscle
|
single twich
|
|
|
What type of contractile force does a single twitch produce
|
little, and CANNOT effectively move a load
|
|
|
Is Tatanus the maximal capability of the muscle
|
YES
|
|
|
What is Isometric tension
|
contraction WITHOUT shortening
|
|
|
What is Isotonic tension
|
contraction with SHORTENING
|
|
|
What is the Length-tension relationship
|
refers the length of a msucle prior to activation
|
|
|
The Length-tension relationship is important b/c the amount of contractile force generated depends on
|
the degree of overlap between myosin and actin
|
|
|
What happens when a muscle starts out at very short length
|
little contractile force development, b/c actin overlap interferes with muscle force production
|
|
|
What happens in intermediate or optimal length
|
produces maxiumum force generation and contraction, maxium amount of cross bridge formation
|
|
|
What happens in the over-streched length
|
little number of crossbridges taht can be formed, reduces the potential for developing force
|
|
|
What happens if a muscle is streched so far that actin and myosin do not overlap at all
|
crossbridges cannt be formed, and no tension development
|
|
|
The length at which a muscle is actvited determines
|
the amount of force it can gerneation, and the load it can overcome
|
|
|
What causes Epilepsises
|
overstimulation of alpha motor neurons
|
|
|
What causes MS
|
loss of myelin sheaths and neuronal injury causes loss of AP conductance
|
|
|
Muscle cramps are often releated to altered extraceullar ions or osmoslarity, that causes
|
rapid firing of motor neurons cauing intense contractions
|
|
|
What causes Myasthenia gravis
|
autoimmune diesases with a decrease number of AcH receptors in NMJ,
|
|
|
What happens in Myasthenia gravis when you have a dreased number of AcH receptors
|
leads to a reduced contractile response
|
|
|
Does myasthenia gravis reduce endurance an lead to repiratory failure
|
YES
|
|
|
Muscular dystrophy is a genetic disease caused by mutated protein dystrophin, that leads to
|
degeneration of skeletal and cardiac muscle
|
|
|
What is Rhadomyolysis AKA
|
drug-induced muscle degradtion, associated with statins
|
|
|
What is muscle strophy
|
loss of neural stimulated causing muscles to arophy as much as 5% a day
|
|
|
Many insectidicies and nerve agents are hibitiors of what
|
Acholineesterase, leading to overstiluation of muscle-seziures, death by respiratory failure
|
|
|
What 4 simialatires of Cardiac to Skeletal muscle
|
1. Striated muscle with sarcomers
2. Sarcoplasmic reticulum 3. Sarcolemma with T-tubules 4. Mitochondria |
|
|
What are 2 main differance of cardiac from skeletal muscle
|
1. Short cells
2. Intercalated disks |
|
|
What are 2 types of intercalated disks that CARDIAC muscle have
|
1. Desmosomes
2. Gap junctions |
|
|
What are Desmosomes
|
strong mechanical connections required to keep cells from spea
|
|
|
What are Gap juctions
|
provide electrical couplinh
|
|
|
Do gap junctions allow heart to act as a "syncytium"
|
YES
|
|
|
What is the sliding filament theroy for Cardiac muscle
|
same as skeltal
|
|
|
What are differance in Exciation -Contraction coupling with Cardiac
|
1. Inititation of contraction
2. Sources of calcium for contraction |
|
|
What do skeletal muscles require for iniation of contraction
|
NEURAL activation to iniate AP and EC coupling
|
|
|
What do Cardic muscles require for iniation of contraction
|
DO NOT require neural, but instead has spontaneous activity
|
|
|
The only input to skeletal muscle is excitory, inputs to cardiac muscle
|
can be excitory or inhibitory
|
|
|
Only Ca+ from the SR is needed for skeletal muscle, what types of calcium is needed for Cardiac
|
extraceullar caclium and SR Ca+
|
|
|
How is extraceullar calcium essential for iniation contraction in cardiac muscle
|
Ca+ enters from extracellualr space though volatage senstve calcium channels in T-tubles and plasma memebrane
|
|
|
What does the extracellualr cause
|
further release of caclium from SR
|
|
|
Which mechanism provides the bulk of calcium for contraction
|
SR
|
|
|
How is calcium removed in cardiac muscle
|
Ca ATPase pump in SR and the sarcolemma Na-Ca antiport exchange mechanism
|
|
|
What is differrent about cardiac muscles AP and contraction
|
LONGER ACTION potential (200ms) and AP and contratile force OVERLAP (occur same time)
|
|
|
What are 3 ion voltaged-gated channels important in Cardiac muscles
|
1. Fast-gate Na
2. Slow gated Ca+ 3. K+ channels |
|
|
Once the heart membrane reaches theshold, what happens
|
opening of voltage gates Na+ channels causes in inital AP spike
|
|
|
What prolongs the AP in cardic
|
slow voltage gated Ca+2 ion channels
|
|
|
Because there is overlap of the action potential and contraction of cardiac what does this mean
|
SUMMATION cannot occur in heart or teatunus
|
|
|
What is the length-tension relationship main differance between skelatal and cardiac
|
The princial differance Frank-Starling Law of the Heart
|
|
|
Where does cardiac muscle normally operate on teh length-active tension curve
|
low to middle region
|
|
|
Is there a substntial amount of reserve in cardiac muscle, which allows it
|
respond to changes in blood flow to the heart
|
|
|
What happens when there is increased blod flow to teh heart
|
the heart fills with more blood and in turn streches teh msucle more
|
|
|
How do you achieve maximal force and contraction in the heart
|
the greater volume and strech of the heart (bad)
|
|
|
What are differances between smooth muscles and skeletal
|
surround hollow organs, smaller cells, contain a single nucleus and dividie,
|
|
|
Skeletal muscles are multi-nucleiated, can they divided
|
NO
|
|
|
Is smooth muscle striated
|
NO--no MYOFIBRILS and no sarcomeres
|
|
|
What is only similarity between skeletal and smooth muscle
|
muscle contains actin and myosin (but arragned different
|
|
|
What are thin filaments anchored to in smooth muscle, similar to what
|
attached to dense bodies is a criss-cross pattern, analgous to Z line in skeletal and cardiac muscle
|
|
|
What do intermediate filaments of smooth attach to
|
Dense bodies
|
|
|
What does contraction look like in a smooth muscle cell
|
causes the muscle to assume a rounded and irregular apperance
|
|
|
Do smooth muscles have gap junctions
|
YES
|
|
|
Is the sliding filament theory of smooth muscle similar to cardiac and skeletal
|
YES, but 2 major differance
1. Smooth muscle does not contain troponin 2. biochemical activation of this process are different |
|
|
What is result of smooth muscle not contain troponin
|
actin always readily bind to myosin
|
|
|
Do smooth myscles require neural actiavtion to initaite AP and EC coupling like skeletal muscle
|
NO--spontaneous electrical activity
|
|
|
Smooth muscles DO NOT have a motor end plate rather have
|
autonomic nerves that innervate smooth muscles with varicosities
|
|
|
What are sources of Ca+ for smooth muscle
|
extracellular and SR
|
|
|
What is the major source of calcium for contraction in smooth muscle
|
extracellular calcium
|
|
|
AP stimulates release of Ca+ from SR, and how does extrceelular calium enter the smooth muscle cell cytoplam
|
through voltage-gate channels
|
|
|
Skeletal and cardiac msucle are muscle contraction is regulated by
|
actin-linked regulation, of troponin and tropomysoin inhibition
|
|
|
In contrast smooth muscle contraction is regulated by and why
|
myosin---smooth muscle does not contain troponin
|
|
|
What happens after Ca+ enters the cytoplams
|
binds to calmodulin, activating it
|
|
|
What does activated calmodulin do
|
activate MLCK (myosin light chain kinase)
|
|
|
What happens after the activation of MLCK,
|
they add a phosphate from ATP to myosin cross bridges
|
|
|
What happens once myosin is phosphorylated in smooth muscle
|
power-stroke or cross briding occuring
|
|
|
In skeletal and cardiac msucle decreased calcium means
|
tropin-tropomyosin change conforamtion black myosin from binding
|
|
|
What happens when calcium levels decrease in smooth muscle
|
MLCK is no longer activated, and phosphatases are inactivation myosin
|
|
|
Is a phosphatase enzyme always present in smooth muscle deactivating myosin, what happens when calcium apperear
|
phosphorlation is MUCH faster and myosin will bind to actin before phosphatase can deactivate
|
|
|
How is calcium removed from smooth muscle
|
SR-Ca+ ATPase pumps, and the plasma membranes Ca-ATpase pumps
|
|
|
Is calcium removed and relaxation of smooth muscle much SLOWER tha skeletal and cardiac
|
YES
|
|
|
Smooth muscle can sustain prolonged contraction with very low energy expenditure through a mechanism known as
|
latching
|
|
|
What is AP like in smooth muscle
|
short like skeltal, but much longer contraction
|
|
|
Can smooth muscle summate
|
YES
|
|
|
Does smooth perform isotonic or isometic contractions more
|
ISOTONIC---shortens, b/c is surrounds hollow organs
|
|
|
Is the length-tension relationship of skeletal, cardaic, and smooth similar
|
YES, the greater length of muscle, the greater amount of contractile force up to an optimal length
|
|
|
Does the optimal length for contraction vary for smooth mucles they are not alinged parallel
|
YES
|
|
|
Streching of cardiac and skeletal produces more vigourous contractions, can smooth smooth adapt to streching by RELAXING
|
YES--example is bladder
|
|
|
Skeletal and cardiac HYPERTROPY, but does only smooth do
|
hyperplasia, increase in number of cell, such as uterus during pregancy
|
