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194 Cards in this Set
- Front
- Back
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A skeletal muscle cell is called a _____.
It is formed by the fusion of _______. |
muscle fiber
myoblasts (these cells are extremely loud) |
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A muscle is a _______ of ___________ bound together by _________.
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bundle
muscle fibers connective tissue |
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Muscle Cells (myofibers) are composted of _________.
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Myofibrils
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Myofibrils are composed of ______ and _____ ___________.
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thick and thin filaments
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Thick filaments are composed of _______.
Thin are made of ______, ______, and _________. |
myosin
actin, troponin, and tropomyosin |
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Band of the sarcomere composed of ONLY thick filmaents
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A Band
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Part of sarcomere that contains ONLY THIN filaments
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I Band
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In the middle of the A Band, the part of the sarcomere between the opposing ends of 2 sets of thin filaments
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H Zone
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Dark band in the center of the H zone liks together the middle of adjacent thick filaments
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M line
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Protein between Z line and M line, linked to both M line proteins and thick filaments?
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titin
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cross-bridges
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portions of myosin molecules from surface of thick filaments toward the thin filaments: the parts that make contact w/ thin filaments during muscle contraction
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Sliding-filament Mechanism: What moves past one another?
What shortens? (sarcomeres or filaments?) |
-thick and thin fils move past
-sarcomeres shorten: FILAMENTS DO NOT |
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During the X-Bridge cycle, where do the thin filaments move? Which filament moves more?
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Thin filaments move toward the center of the sarcomere, shortening it.
Thick filaments move a lot more than thin. ***Often one end of muscle is FIXED, and xbridge-inducd shortening pulls the entire sarcomere toward the fixed end, shortening the entire muscle |
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Cross-Bridge Cycle in 4 steps
1. Attachment of ______ to ______ 2. Movement, producing _______ in thin fil. 3. __________ of x bridge and thin fil. 4. ________ the x bridge |
1. Attachment of Xbridge to thin fil
2. Movement of X bridge 3. Detachment of Xbridge from thin fil 4. Energizing X bridge so it can again attach |
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Resting muscle fiber: Ca concentration?
This means WHAT for myosin and actin? Cross-bridges energized or no? What is bound to myosin? |
LOW
Myosin CANNOT bind Crossbridges energized by SPLITTING ATP ADP and P are bound to myosin (storing Energy!!) |
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What initiates X-Bridge Cycling?
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Ca entering cytoplasm
Then, one myosin X bridge binds to a thin filament actin molecule |
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After myosin binds to actin (cross bridge cycle) what happens?
What is released? |
Cross bridge moves (power stroke)
ADP and P ARE RELEASED |
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When the cross-bridge moves, myosin and actin are bound. What breaks this link?
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Binding of NEW ATP molecule to Myosin
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When ATP binds (step 3) in cross bridge cycle on myosin--what happens to myosin's affinity for actin?
Is ATP providing energy at this step? A |
decreases
NO!!!! no E from ATP! just regulation. |
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After actin and myosin dissociate (step 3), what happens to the ATP bound to myosin (and consequently, the xbridge?)
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Hydrolyzed!! back into ADP + P
re-forms the energized state of myosin; returns X bridge to pre-power stroke position |
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Do hydrolosis of ATP and movement of cross-bridge simultaneous events?
What does this mean for the cycle? |
NO.
If Ca is still present, the X-bridge can reattach to a new actin monomer in the thin filament and the cycle repeats. |
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ATP's 3 roles in the X-bridge cycle
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1. Energy released from hydrolysis provides E for the movement
2. ATP binding to myosin BREAKS link b/t actin and myosin so the cycle can repeat 3. Hydrolysis of ATP by Ca2-ATPase in SR provides E for active transport of Ca into the reticulum. Lowers cytosolic Ca to prerelease levels, ending contraction, allowing fiber to relax. |
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rigor mortis.
what happens? hint: after death, there is no _ _ _. |
ATP concentration declines after death.
W/o ATP--breakage b/t actin and myosin does not occur, thick and thin filaments remain bound by stationary X-bridges: rigid condition |
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What prevents myosin cross bridges from making contact with actin in skeletal muscle (at rest)?
What moves it out of the way? |
Tropomyosin
When Ca binds with troponin. This changes troponin's shape, allows tropomyosin to move. |
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how long does an action potential in skeletal muscle last?
How long does the resulting mechanical activity last? Does the AP directly cause contraction? |
AP=1 to 2 msec, it's over before signs of mech activity
Mech Activity: 100 msec or more No, it produces a state of increased Ca, which continues to activate the contractile machinery long after the AP stops. |
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What does troponin do in skeletal muscle?
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holds tropomyosin in the way of the actin binding sites, preventing cross bridges from making contact
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3 Functions of ATP in Skeletal Muscle
1. Hydrolosis of ATP by myosin does what? 2.Binding of ATP to myposin? 3. Hydrolysis of ATP by Ca2+-ATPase |
1. Hydrolysis of ATP by myosin energizes cross-bridges and gives ENERGY for power stroke.
2. Binding of ATP to myosin dissociates x-bridges bound to actin so they can repeat their cycle 3. Hydrolysis of ATP by Ca2+-ATPase in the SR provides ENERGY for active transport of Ca2+ ions into reticulum, LOWERING cytosolic Ca, ENDING contraction, letting muscle fiber RELAX |
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force exerted on an object by a contracting muscle
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muscle tension
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force exerted on the muscle by an object
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load
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Whether a muscle fiber shortens depends on the magnitudes of the ______ and the ______.
For muscle fibers to shorten, ______ must be greater than ______. |
tension
load tension load |
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When a muscle develops tension but does not shorten or lengthen, what type of contraction?
When does this occur? (concrete example) what is happening in the cross-bridge cycle? what happens when isometric contraction is prolonged? |
isometric contraction
when muscle supports a load in a constant position attempts to move an otherwise supported load that is greater than the tension developed by the muscle cross bridges exert force on the thin filaments but ARE UNABLE TO MOVE IT. Rather than filaments sliding, rotation absorbed within the structure of the x-bridge. If prolonged, x-bridges repeatedly rebind to the SAME actin molecule |
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Contraction in which the muscle changes length while load remains constant
how does the X-bridge cycle work for this type (i.e. step 2--the power stroke) |
isotonic contraction (either shortening or lengthening)
cross bridges rotate thru power stroke, shortening sarcomeres |
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type of contraction when tension exceeds load and shortening occurs?
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concentric (type of isotonic)
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type of contraction when load is greater than tension and muscle lengthens?
does muscle lengthen as result of contractile protein activity? what happens during the cross-bridge cycling? |
eccentric contraction
load pulls muscle to longer length in spite of opposing force produced by x-bridge **lengthening of muscle fibers is not active process produced by contractile proteins, but CONSEQUENCE of external forces being applied to muscle.** the load pulls the cross-bridges in step 2 BACK toward the Z lines while they are still bound to actin and exerting force |
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What determines the end result of single-fiber contraction?
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THE MAGNITUDE OF THE LOAD
-chemical changes in each type of contraction are the same |
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mechanical response of a muscle fiber to a single action potential?
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TWITCH
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latent period
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following AP, interval of a few ms before the tension in the muscle fiber begins to increase.
During this time=processes associated w/ excitation-contraction coupling are occurring |
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contraction time
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interval from beginning of tension develoment (END OF LATENT PERIOD) to the peak tension
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Do all muscle fibers have the same twitch contraction time? What does the duration of a contraction depend on?
Is Ca2+ ATP-ase greater or less with fast twitch fibers (v. slow)? |
NO (some 10 msc, some 100 ms)
duration depends on TIME CYTOSOLIC CA REMAINS ELEVATED -how long for x-bridges to cycle and detach -how long for Ca to be removed Ca2+ATP-ase activity in the SR is GREATER in fast twitch fibers and less in slow twitch. |
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which has longer latent period? (isotonic or isometric?)
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Isotonic: includes both time for excitation-contraction coupling AND time to accumulate enough attached X-bridges to lift the load.
***Before shortening, there is a period of ISOMETRIC CONTRACTION during which tension increases.** the heavier the load, the longer it takes for tension to increase to the value of the load WHEN SHORTENING WILL BEGIN. Isometric latent period only has to wait for excitation-contraction coupling since it DOES NOT LIFT LOAD |
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Which is longer duration: mechanical event (shortening/lengthening) in isotonic OR force generation in an isometric twitch?
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Isometric Twitch is LONGER: takes longer for all cross-bridges to detach
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What do characteristics (amt. of tension, length of shortening/shortening velocity, latent period, etc) of an ISOTONIC twitch depend upon??
At heavier loads, the latent period is ______, velocity of shortening is ________ the duration of twitch is __________, and the distance shortened is ________. |
the MAGNITUDE of the load being lifted!
-latent pd longer velocity of shortening slower duration of twitch shorter distance shortened less |
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When there is no load, the shortening velocity of an isotonic twitch is ______.
When the load is equal to the maximal isometric tension, the shortening velocity is ___. At loads greater than max isometric tension, the fiber will _________ (lengthen/shorten) at a velocity that ______ (increases/decreases) with load. |
maximal
zero lengthen increases |
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How many ATPs split during a skeletal muscle X-bridge cycle?
What determines the rate of a fiber's shortening velocity? What slows it down? |
one
The rate of ATP splitting determines velocity. If you increase the load, the ATP hydrolysis slows and so does velocity of shortening. |
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When a stimulus is applied before a fiber has completely relaxed from a twitch, the resonse in a peak tension _______ than that produced by a single twitch. What happens as the interval b/t stimuli is reduced even further?
What is this called? What is a maintained contraction in response to repetitive stimuli? What is going on in the X-bridges? |
GREATER--the shorter the interval, the greater the peak tension
Summation Tetanus; xbridges=more and more xbridges attaching. Fused Tetanus: no oscillations (at high stim frequencies): increase until MAX FUSED TETANIC TENSION Unfused: oscillates (at lower stim frequencies) |
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Maximal tetanic tension
how much greater than single twitch? same/diff for each muscle? |
-3 to 5x greater than single twitch
different fibers have diff contraction times--so stim frequency that produces tetanus AND max tetanic tension vary per muscle fiber |
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Why is tetanic tension so much greater than twitch tension?
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When Ca is released, all thin fil. binding sites initially available, BUT not all X-bridges can bind in time! Calcium is pumped back into SR *before* ALL x-bridges attach. (in single twitch)
In tetanic: -successive APs EACH release Ca from SR at a rate greater than pumpking Ca back out=prevents decline in binding sites, many more X-bridges bind. |
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Isometric tension at any instant depends on total number of _______ bound to _______ and completing ______ ________s.
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-x-bridges, actin, power strokes
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What is responsible for passive elastic properties of relaxed muscle fiber?
What happens w/ increased stretch? What is elongated to cause this? |
TITIN
"springlike"-increased stretch, passive tension INCREASES b/c titin filaments elongate. |
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Amt. of ACTIVE TENSION a muscle fiber produces varies with what?
when does fiber develop greatest isometric active tension? What keeps muscle fibers at this place? |
*LENGTH*
greatest isometric active tnesion at Lo (optimal length) At 60% and 175% of L0=NO ACTIVE TENSION WHEN STIMULATED (in b/t this is Lo, bell shape) Passive elastic properties and being attached to bones keeps fibers at L0. Filament overlap is ideal at Lo!!! |
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3 Ways a muscle fiber can form ATP
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1. Phosphorylation of *creatine phosphate*
2. oxidative phosphorylation of ADP in mitochondria 3. phosphorylation of ADP by glycolytic pathway in cytosol |
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Phosphorylation of ADP by Creatine Phosphate (CP)
1. fast/slow? 2. What happens? 3. Does Energy drive x-bridge cycling? |
1. FAST
2. Creatine and Phosphate break bond, CP + ADP=>C + ATP 3. Does not drive cycling; builds up storage DURING REST. When muscle first starts contracting, ADP levels rise, so CP *WANTS* to create ATP--happens so fast there is almost no fluctuation. Limited by amt. of CP in cell--provides few seconds for oxidative phosph and glycolysis to make ATP |
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at moderate levels of muscular activity, what is the main way of making ATP for muscle?
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OXIDATIVE phosphorylation
breakdown of muscle glycogen to glucose, then blood glucose and fatty acids contribute |
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when exercise is intense, what creates atp?
where does this method obtain glucose? as intensity increases, more ATP made w/o O2, leading to buildup of ____? |
GLYCOLYSIS: glycolytic pathway can produce ATP pretty quick and w/o O2.
glucose obtained from blood or muscle fibers lactic acid |
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at the end of muscle activity, must replace CP and glycogen in muscle, and lactic acid must be metabolized. What does muscle use for this?
what process? |
MUSCLE CONSUMES O2!
increased ATP by OXIDATIVE PHOSPHORYLATION after exercise repays the O2 debt |
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decline in muscle tension as a result of previous contractile activity
what are characteristics of this state? |
muscle fatigue
1. decreased shortening velocity 2. shorter rate of relaxation DEPENDS ON: -type of muscle fiber -intensity/length of contraction -degree of fitness! |
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What accounts for muscle fatigue?
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NOT ATP: ATP concentration in tired muscle=only slightly lower than at rest--not enough to impair xbridge cycling.
*BUT* if cycling were to continue, ATP would get so low that X-bridges would become linked=RIGOR. |
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High-intensity exercise: what causes fatigue? (3 things)
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1. Conduction Failure: too much K+ in T-tubule during AP repolarization leads to persistent DEPOLARIZATION, and eventually--failure to produce APs in the T-tubes (bc Na+ channels inactive).
This halts release of Ca2+ from SR. Rapid Recovery w/ Rest. 2. Lactic Acid Build Up: changes Ca 2+ handling "machinery" 3. Inhibition of X-bridge Cycling: -buildup of ADP and P--slows rate of X-bridge cycling |
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Low-intensity, long-duration exercise: what causes fatigue?
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1. Changes in contractile proteins bc of leaky Ca channels=weakness and soreness till damaged proteins are repaired
2. depletion of fuel substrates 3. NOT ATP DEPLETION, but decrease in muscle glycogen CORRELATES. |
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Central Command Fatigue
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-regions of cerebral cortex failt o send excitatory signals to motor neurons (person needs will to win!)
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Slow-oxidative Fibers
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(Type I)
Combine low myosin-ATPase activity with high oxidative capacity Rate of X-bridge cycling is slow, but same force produced as in fast fibers. Oxidative=most of ATP dependent upon blood flow to deliver O2 and fuel molecules. Surrounded by many blood fessels AND myoglobin (all to increase O2) red muscle ibers (bc of myoglobin) |
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Fast-oxidative-glycolytic fibers
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Fast twitch (Type IIa)-contain myosin w/ high ATP activity
-high oxidative capacity -intermediate glycolytic capacity: few mitochondria but HIGH concentration of glycolytic enzymes and large store of glycogen |
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fast-glycolytic fibers
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type IIb
combine high myosin-ATPase activity with high glycolytic capacity (white muscle fibers--not a lot of myosin) surrounded by few blood vessels fatigue rapidly!! slow-twitch fatigue slow, middle=middle |
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which develops more tension (has more strength) when it contracts--glycolytic or oxidative fiber?
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glycolytic: LARGER DIAMETER
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All muscle fibers in a motor unit are of the ______ fiber type.
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same (i.e. slow-oxidative motor unit)
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Total tension a whole muscle can develop depends on:
1. Number of Fibers in each Motor Unit 2. Tension developed by each Fiber 3. Number of active Fibers *expand on #s 2 and 3 |
2. Each Fiber's Tension:
a. action potential frequency b. fiber length c. fiber diameter d. fatigue 3. # of Active Fibers a. number of fibers per motor unit b. number of active motor units |
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Recruitment
How is this achieved? How does motor neuron SIZE play a role? Smaller motor neuron=__________ (earlier/later) recruitment? What units are recruited first? Recruitment provides the primary means of varying ________ in a whole muscle. |
when muscle is composed of small motor units, tension can be increased by activating ("recruiting") additional motor units
Achieved by *activating excitatory synaptic inputs to more motor neurons* size of Motor NEURON: axon diameter -small motor neuron=undergo greater DEPOLARIZATION, THEREFORE--smaller neurons recruited first, will be able to generate APs first. These innervate SLOW-OXIDATIVE MOTOR UNITS, so these are recruited first, then fast-oxi-glyco, then fast-glyc. varying TENSION |
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recruitment of motor units leads to increases in both _____ nad __________.
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force, velocity (more workers helping)
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denervation atrophy
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neurons to skeletal muscle are destroyed, muscle fibers become smaller in diameter, amt. of contractile proteins decrease
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disuse atrophy
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nerve supply stays intact but muscle fibers decrease in size/contractile proteins
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hypertrophy of muscle fibers
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usually w/ exercise--increase in fiber SIZE AND ATP production
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"aerobic exercise"
-duration/intensity? -increases # of what in muscle fibers? (2 things) |
low intensity and long duration exercise
increases number of mitochondria and Number of capillaries (NOT FIBER DIAMETER) |
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strength training exercise (short-duration, high-intensity) affects what fibers?
what happens w/ exercise? (what increases size, what is created, what activity increased?) |
affects fast-twitch fibers
-these undergo increase in fiber diameter -form more myofibrils (more synthesis of actin and myosin) glycolytic activity increases (more synthesis of glycolytic enzymes) -big strong muscles, small endurance, fatigue quickly **neural pathways modified ALSO cause gain in strength while not involving hypertrophy at all |
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Exercise produces _______ change in proportions of fast/slow fibers in a muscle.
However, exercise DOES change the ______ at which metabolic enzymes are _________. This leads to changes in the proportion of _________ and _______ fibers within a uscle. |
LITTLE CHANGE
does change RATE at which enzymes are SYNTEHSIZED changes proportion of OXIDATIVE and GLYCOLYTIC fibers (w/ endurance, decrease in fast-glyco, increase in fast-oxi-glyco) |
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Max force a muscle generates decreases by __ to __ percent between ages of 30 and 80.
This is b/c of decrease in _____ _________. |
30 to 40%
decrease in fiber diameter (ability of muscle to adapt to exercise decreases w/ age) |
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muscle soreness?
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structural damage to muscle cells and their membranes, activates inflammation response
most often occurs from lengthening contractions |
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Flexion
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bending of a limb toward a joint
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extension
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straightening of a limb
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Purpose of Muscle?
1. Receive _____ 2. Initiate _______ that produces _________ _______. Requires _________! |
Receive signals.
Initiate (in muscle cell) biochemical cascade that produces MECHANICAL FORCE Requiers ENERGY (in form of ATP made in muscle cells' mitochondria) to generate force and often MOVEMENT |
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Roles of Muscles in Homeostasis
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1. acquire nutrients/fuel (body move around in environ)
2. Process food (chew, swallow, digest) 3. breathing 4. escape from harm 5. generate heat (convert fuel into Energy. Same chemical process of respiration. Carbs, proteins, oxygen BURN chemically. Energy stored in ATP molecules |
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skeletal muscle:
how many nuclei? |
mULTIPLE (myoblasts fusing)
organized parallel sarcomeres |
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Cardiac muscle; striated? organized?
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Striated, not necessarily multinucleus cells
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Smooth Muscle: striated? organized?
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Not organized as tightly as skeletal
-often wrapped around organs/lining of gut, etc. (doesn't necessarily contract longitudinally like skeletal) ONE NUCLEUS/CELL NO STRIATIONS |
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How do APs turn into force in skeletal muscle?
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-AP in presynaptic cell--neurotrans onto muscle-->postsyn cell receptor binds neurotrans-->postsyn cell-->biochem cascades-->proteins interact--> mechanical force!
excitable tissue propagates APs along membranes Membranes have VOLTAGE GATED Na and K channels--can fire APs -when excited by presynaptic nerve there is a DEPOLARIZATION and AP--AP propagates along muscle like axon of nerve (**but in both directions) |
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Skeletal Muscle:
what % of body mass? consumes lots/little nutrients? waste? |
30-40% of body mass!
#1 consumer of nutrients, O2 high metab-ABUNDANT WASTES that disrupt ECF homeostasis if they weren't cleared away by excretory sys |
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"muscle belly"
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whole muscle--composed of multiple muscle cell bundles
muscle--muscle cell bundle--muscle cell (myofiber)--myofibrils **in ea myofibril=force generating material |
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Sarcoplasmic Reticulum:
-surrounds WHAT? -extension of what? -role? |
wraps all thru and SURROUNDS ALL MYOFIBRILS.
-extension of ENDOPLASMIC RETIC -membrane tubes are full of Ca, when APs arrive, SR dumps Ca2+ out=CONTRACTION |
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T-tubules
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makes contact w/ all myofibrils
bunch of tubes in membrane (like SR) -part of OUTSIDE membrane of cell--starts as pockets of plasma membranes and goes down into cell |
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lateral sacs
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thick parts where t-tubules and SR are alligned
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ICF of myofiber has lots of ____
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ATP!
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AP propagation in muscle cell:
-where does it go? |
down plasma membrane, INTO T-TUBULES!!
sends AP straight down into muscle cell--comes right up next to parts of SR. depolarizaing INSIDE |
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Synaptic Cleft of motor neurons (from spinal cord and brainstem) that synapse onto the sarcolemma
what type of receptors? channels? neuromuscular junction-big/small terminal? how much neurotrans? |
has junctional folds=specialization, increase Surface Area, increase Receptors for ACh (nicotinic receptors)
nicotinic receptors=let Na and K in and produce EPP! termina=HUGE. TONS of docking sites (active zones), thousands of vesicles filled w/ ACh 2. AP triggers Ca influx, dumps TONS (millions) of ACh molecules |
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each muscle cell gets input from _____ motorneuron(s).
One Motorneuron can signal onto _____ cells. One motorneuron signals ___ motorunit(s). |
ONE! (unlike neurons)
MANY. when it synapses, WILL trigger APs reliably. One motorneuron=MANY motorunits. arranged specifically to coordinate muscle cells' movements. |
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Motorunit:
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-divide up labor for CONTROL and COORDINATION
one motor neuron branches to activate many cells all part of same unit. separate motor units in one muscle can be activated at different times |
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Events @ Neuromuscular Junction (ACTION POTENTIAL PROCESS)
1. Presynaptic AP _______ 2. Lets in ___ thru ____-gated channels. 3. Interacts w/ ______, causes _________ of vesicles. 3. ____released, binds to _________ 5. ________ receptors let __ in, ___ out. 6. ____________ EP membrane. 7. Sends _____ ________. 9. Termination: _____ chews up ACh |
1. Presynaptic AP depolarizes terminal
2. Lets in Ca2+ thru Voltage Gated channels 3. Interacts w/ SNARE in Presynaptic neuron-causes FUSION of vesicles. 4. ACh released into junctional cleft, binds to ACh receptors that are themselves ion channels (ionotropic!) 5. Ionotropic receptors let in Na, let out K 6. Depolarizes EP membrane 7. Depolarization sets up + at End Plate, but - membrane regions nearby==sends LOCAL CURRENT! 8. AP propagates away from synapse 9. TERMINATION: ACh diffuses away (inefficient) OR *Acetylcholinesterase chews up ACh (super fast!) *Most of ACh chewed up before even gets to end plate but enuf released to activate channels. |
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Interaction b/t T-Tubules (carrying AP) and SR (not carrying AP)
role of Ca? how does contraction occur? |
SR membranes full of Ca
when APs arrive, SR dumps out Ca when Ca is dumped=contraction Triggers contractile proteins!! Ca is there immediately after AP then gets taken away. |
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Excitation-Contraction Coupling in Skeletal Muscle
1. AP where? 2. what receptors sense this? what do they do? 3. influx of what ion? 4. What cycle happens? 5. How is Ca removed? What are the 2 reasons for this? |
1. AP in plasma membrane and T-tubules (propagates)
2. DHP receptor SENSES voltage change-moves when AP arrives 3. Mechanically TUGS on ryanodine receptors (ion channels) 3. When this happens, RRs open and LARGE Ca2+ influx from SR! spills into cytosol where contractile proteins are 4.Cross-bridge Cycling: creates force! 5. Ca2+-ATPase pumps Ca2+ back into SR=muscle relaxation. -primary active transport -hydrolyze ATP to ADP, pumps Ca2+ back into SR 1. clears Ca from cytosol, letting muscle relax AND 2. restores Ca to SR so muscle can contract again |
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Contraction: I bands and H bands _________ in size.
Relaxtion: I and H bands _____________. |
1. decrease
2. increase |
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thick filament: what protein?
-what regulates this protein's force generation? |
-myosin!
-Ca2+ regulates binding to actin and force generation |
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thin filament: what proteins?
how is binding site exposed so x-bridge cycling can occur? *sliding-filament mechanism* |
-actin
-tropomyosin (BLOCKS binding of myosin to actin at rest)-troponin holds it in place -Ca2+ binds to TROPONIN, changes its shape, this changes the shape of TROPOMYOSIN, moves it. Leaves actin available for myosin to bind. "ratcheting" of crossbridge cycle=CONTRACTION |
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Contraction
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activation of cross-bridges to exert force on thin filaments (length may or may not change)
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*Cross Bridge Cycling*
Myosin Head Group: what binding sites? 1. At rest: what 2 molecules bound to myosin? 2. When Ca present, can ____. 3. Interacting w/ what protein? 4. Let's go of ____ and ___. 5. changes shape 6. what type of movement? called the ______ stroke. 7. When power stroke complete, open ____ binding site. What binds? 8. Myosin lets go of ______. 9. __________ ATP, take sEnergy and does what? 10. Ready for next cycle: what 2 molecules bound? |
*Mysoin head grp has ATP binding site and ACTIN binding site.
1. At rest: ADP and P. Makes it want to bind actin but can't b/c tropomyosin in the way. 2. When Ca present, troponin binds it, tropomy moves, Ca activates actin 3. Myosin binds actin 4. RELEASES ADP and P 5. changes shape of the "neck" 6. ratcheting movement-POWER STROKE** cross bridge moves! 7. When power stroke complete, open binding site on myosin-ATP binds 8. Causes X-bridge to DETACH, myosin LETS go of actin but still in "ratcheted form," ATP is favored and binds to myosin 9. Hydrolyzes ATP into ADP and P, takes energy and puts it into mechanical motion=reprimes headgroup 10. Now primed, ADP and P bound, ready for another cycle |
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Botulinum toxin ("botox")
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gets into presynaptic terminal and interferes w/ FUSION:
vesicles cannot fuse OR release ACh makes muscles go lax because no contraction was triggered |
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Curare
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example of LOCAL ANESTHETIC/MUSCLE RELAXANT
affects post-synaptic ACh receptors Bind to these receptors and stop it from binding ACh |
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Organophosphates (pesticides/nerve gases)
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Bind to AChase and prevent it from chewing up ACh.
Will have LOTS of ACh around-gives better muscle contraction for short pd of time. Activating receptors-->depolarizing muscle membrane, KEEPs depolarizing, can't regenerate APs (Na inactivated states and can't recover) will get a few spikes then no more, muscle incontrollably contracting=frozen in contracted state |
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Succinylcholine
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muscle relaxant
Mimics ACh and binds to receptors, depolarizes muscle and doesn't allow it to recover doesn't have permanent effects, can be used safely by doctors |
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smooth muscle characteristics
arrangement? nuclei? special proteins? big/small cells? t-tubes? Ca2+? |
-arranged in sheets
-NO sarcomeres -dense bodies instead of z-lines anchor thin filaments -SINGLE nuclei -nO troponin --SMALL CELLS -no T-tubes (no mech for AP to propagate in cell body--different Ca mechanism) -minor Ca2+ stores--no store in SR |
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Smooth Muscle Contraction: ca2+ activation of X-bridges in smooth muscle
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Ca 2+=special 2nd messenger
Proteins in the cell are binding sites for Ca, Ca binds and changes shape. 1. Ca 2+ in cytosol increases, binds to CaM and activates it. 2. CaM + Ca activates myson light-chain kinase 3. Active Kinase phosphorylyzes ATP into ADP +PO4 (O from myosin) 4. Phosphorylyzation forces x-bridge toward thin filament. 5. Binds to actin, same x-bridge cycle as skeletal muscle (P + ADP fall off myosin head, releasing energy and power stroke occurs) 7. ATP binds to myosin, lets go of actin 8. Myosin light-chain phosphatase decreases Ca2+. Phosphorylation="recocked" **^^cleaving off of phosphate by light-chain phosphatase ENDS x-bridge cycle and contraction, NOT CA2+ LEVELS LIKE SKELETAL MUSCLE. As long as myosin light chain kinase is attached, crossbridge cycling will continue. |
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Smooth Muscle Contractile Properties
1. x-bridge cycle: fast/slow? 2. economical or not? (fast/slow ATP?) |
1. SLOW: twitch=3 seconds!
-myosin slower -thick and tin filaments disorganized--geometric readjustment must occur before force -depends on extra enzymes (kinase and phosphatase) 2. ECONOMICAL (SLOW ATP splitting)--can operate long periods of time, generally light load 3. |
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Smooth Muscle length/tension curve? (vs. skeletal?)
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BROAD
-wrapped around stomach/bladder so must frequently undergo changes in volume doesn't have specific optimal length(Lo)-will act at many lengths to do it's job |
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How is cytosolic Ca2+ elevated in smooth muscle?
Is it the same for all muscles? |
MECHANISM VARIES IN DIFF MUSCLES
1. voltage-gated Ca2+ channels 2. 2nd messenger release of SR Ca2+ 3. Receptor-gated Ca2+ channels 3. Stretch-activated channels 5. Chemosensor-gated Channels |
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1 way of elevating Ca2+ in smooth muscle: voltage-gated Ca2+ channels
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Plasma membrane has resting potential
--things can change the ion channels that are open and therefore the V. When Ca2+ channels open, triggers contraction Ca2+ comes from ECF? |
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2. elevating Ca2+ in smooth muscle=2nd messenger release of SR Ca2+
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G-Pro receptors activate IP3 receptor (like ryanodine in skeletal); cascade opens Ca2+ *Intracellular Store*
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3. elevating Ca2+ in smooth muscle:
Receptor-gated Ca2+ channels |
i.e. NMDA receptor
Neurotransmitter receptor IS ITSELF an ion channel permeable to Ca2+. Huge Ca2+ concentration gradient, if opened, LOTS of Ca2+ influx *or* metabotropic g-pro coupled to Ca2+ channel in membrane (not intracellular Ca2+) |
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Ways of elevating Ca2+ in smooth muscle:
4. Stretch-activated Channels 5. Chemosensor-gated channels |
4. "trip channels" =sense pressure
5. chemosensor senses simpler molecules than neurotransmitters like O2, NO, etc. |
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Removing Ca2_ relaxes smooth muscle: 2 ways
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1. Transporters return Ca2+ to ECF by primary active transport (and/or secondary active transport-Countertransport w/ Na)
2. Ca2+ ATPase pumps refill SR: Pumps in SR, can't interact wo CaM or myo light chain kinase, decreases Ca2+ in cytosol and replenishes SR |
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Smooth Muscle: differences from skeletal muscle Ca2+ handling(4 ways)
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1. Basal ICF [Ca2+] causes "smoothm uscle tone" (resting intracellular Ca2+-always some contractile force being generated "muscle tone," steady level of activity
---in skeletal muscle, resting state=very little X-bridge cycling. 2. Depending on stimuli intensity, smooth muscle [Ca2+] and thus contraction strength ARE GRADED-can do this in a continuous manner by opening more Ca2+ channels. 3. Many inputs can simultaneously influence Ca2+ levels and contraction strength (can have excitatory Ca stimuli or inhibitory) 4. APs are not necessarily associated w/ contraction (lots of muscle cells don't fire AP. Don't need APs in smooth muscle cells to get contractions |
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Activation/Inhibition of Smooth Muscle Membrane
1. Electrical 2. Nerves/Hormones 3. Local Factrs |
1. Some cells=pacemakers: hYPERPOLARIZATION (not depolar!!) TURNS ON cation channel "H channels," and brings cell back up (depolarization). This depolarization will reach threshold and cause AP.
Other cells: rhythmic subtreshold oscillations. Until an Excitatory stimulus eventually causes cell to reach AP. (they have a head start from the subthres waves) 2. Nerves and hormones 3. Local factors (i.e. pressure, pH, O2, etc) |
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Single Unit smooth Muscle
1. Gap Junctions (syncytium) what connects them? where do they occur in body? what excites them? |
-many muscle cells modulated by neurotransmitter, all connected by GAP JUNCTIONS.
Vericosities: neurotransmitter released at all vericosities Gap junctions=ion channels (all cells electrically connected); if ONE gets AP, all get ap. WHOLE Unit contracts together=syncytium Most useful in pulse/rhytmic contracts (bladder, peristalsis) tend to be self-excitatory: autonomic nerve modulating their activity, not activating other things) |
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2 types of smooth muscle single-unit OTHER THAN gap junctions?
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2. self-excitatory (pacemaker)
3. autonomic nerve modulation found in--gi tract, reproductive organs, urinary bladder, small blood vessels |
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Multi Unit Smooth Muscle characteristics
-gap junctions? -how activated? -where found? |
few/no gap junctions
autonomic nerve activated (and/or inhibited) found in large blood vessels, airways, eye, hair follicles |
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paracrine signal
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diffuses right into tissue until it finds cell w/ a receptor (not into bloodstream!)
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autocrine signal
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receptor ON SAME CELL=cell produces sbstance and regulates amount by sensing how much it producd
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neurohormone
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released by enrve terminal DIRECTLY onto blood vessel serface (just like endocrine hormone but source is *nerve* not gland)
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3 Chemical Types of Hormones
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1. Amines
2. Peptides/Proteins 3. Steroids |
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Amine hormones
1. examples? 2. hydrophil/hydrophob? 3. receptors on target cell? |
1. norep/ep
2. dopamine (1&2=catecholamines; neurotransmitters but also have hormonal functions) 3. T3, T4 Catecholamines=hydrophilic; receptors extracellular Thyroid hormones=hydrophobic; intracellular receptors |
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Steroid Hormones: Name the 5, what glands/organs they come from.
what do they come from?? polar/non? diffuse easy/diff? how stored/transferred? where are receptors on target cell? |
5 steroids:
*from adrenal gland*: cortisol aldosterone *from gonads*: testosterone estradiol progesterone come from CHOLESTEROL! (important of all cell membranes in body. has FEW CHARGES, so all steroid hormones are NONPOLAR, HYDROPHOBIC!) -membrane permeant! -can't package b/c they'll just diffuse out of vesicle -stored in 'oil droplets" -enzymes convert oil drops into hormone when signaled, hormone simply diffuses outside of cell. -now in blood (h2o filled), dislike so it must find PROTEIN CARRIER in plasma. Steroid will go to nearest hydrophobic "pocket" on a plasma protein. **imperfect-allow hormone to attach/detach until it finds correct receptor intracellular receptors |
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peptides/protein hormones:
come from what? hydrophil/phob? stored how? where are receptors on target cell? |
come from AMINO ACIDS (long chain of amino acids)
"R" group is what makes them able to interact w/ only some SPECIFIC cells HYDROPHILIC, love water, have polar groups Stored in VESICLES like neurotrans. -wait for Ca to cause fusion so they can be secreted. Once in blood (filled w/ h2o), they're happy and can diffuse as free molecules receptors extracellular |
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Hydrophilic Hormones; Extracellular Receptors for hormones: what occurs in cell?
fast/slow? excretion fast/slow? fast/slow? |
Often g-protein mediated cascade--modify existing proteins--->desired effect
FAST effect, TEMPORARY changes. When hormone is gone, cell goes back FAST metabolism/excretion (thru enzymatic breakdown or taken up by liver/kidneys) |
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Hydrophobic Hormones, Intracellular receptors (thyroid hormones and steroids): fast/slow? how does signal work?
Changes drastic/minimal/termporary/longterm? |
SLOW!
Does not go away quickly; hours or days, effect will stay even in hormone's absence. SLOW metab/excretion easy to get into cell, majority directly interact w/ protein inside cell so must get DEEP into cell (like to the nucleus) often want to change DNA transcription!! determine ratios of proteins that cell makes=what makes cell specific!! (differentiation) **DRASTIC CHANGES* |
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Destinies of a hormone? (4 options)
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1. excreted in urine/feces
2. inactivated by metabolism (enzymatic breakdown; turned into another molecule that does not have receptors) 3. Activated by metabolism (THEN target cells)--broken down into molecule w/ diff structure (i.e. progesterone) OR metabolites 4. Target cells: bind to receptor and produce response |
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Characteristics of Endocrine receptors
1. affinity 2. biochem cascades mean... 3. down/up regulation? 4. permission 5. secretion |
1. HIGH SENSITIVITY!! (10^-12 M!)=high affinity. Hormone concentration DILUTED in body tissues so receptors must be verrryyy sensitive/have high affinity for hormone.
2. amplification! 3. hormone levels influence expression of their OWN receptors: receptors are expressed in certain tissues but expression NOT FIXED. Tissues can alter the amt of receptors they make and insert at surface; this process of making, trafficking, and inserting receptors is ITSELF under hormonal control. Affict gene transcription-->genes transcribed are receptors for same hormone or others. Hormone levels influence SENSITIVITY of tissues for that same hormone. If hormone levels ^, - feedback downregulates and vice vers; hOMEOSTASIS--keep levels of sensitivity constant 4. have permissive effect on other hormone's receptor's expression: i.e. tissue w/ receptor--its expression is influenced by other hormones (w/o enuf ster/thyroid hromone heart won't make enuf receptors for epineph, e.g.) 5. Hormones regulate hormone secretion (not just reception)--paracrine, autocrine. TROPIC effect!! example=any hypothal-pit-gland-target cascade w/ neg. fdbk loop |
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tropic effect of hormone
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affect secretion
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trophic effect of hormone
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stimulate/reduce GROWTH
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hyposecretion: primary, secondary
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primary: gland itself not secreting enuf
secondary: gland not stimulated enough |
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hypersecretion: primary, secondary
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gland secreting too much=primary
gland overstimulated=secondary |
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hyporesponsiveness/hyperresponsiveness
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enough horm secreted but not enough/too much receptors being made/coupling too much/too little
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pituitary: which is slower--ant/posterior hormones
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anterior
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posterior pituitary hormones (2)
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1. oxytocin: reproductive functions--triggers lactation reflex, mediates contractions
2. vasopression--salt balances, blood pressure |
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hypothalamus input (4)
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1. peripheral receptors (pain, touch, temperature, suckling)
2. higher centers (emotions) 3. special senses (light/dark-->circadian rhythm!) 4. blood conditions-glucose conc, osmolarity, temp, hormones |
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T4
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90% of secretion, circulating "storage pool," most common IN BLOOD
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Thyroid Gland: follicles trap ____ for synthesis of ____
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iodide
T3, T4 |
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T3
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most ACTIVE form
tissues make T3 from T4 (target cell mainly responds to T3; hence T4 converted to T3) **BOTH T3 AND T4=hydrophobic molecules! (along w/ steroids) |
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Thyroid Gland functions?
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metabolism
GROWTH |
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TSH: tropic or trophic/both?
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TROPHIC: stimulates thyroid to MAKE hormones, enlarges thyroid
tROPIC: stimulates thyroid to SECRETE them! |
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Goiter caused by *what* being stimulated?
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TSH receptor!!
Many ways it can occur: 1. hypothal stimulating pituitary too much 2. thyroid too response 3. not making enough T3/T4 so lose -- fdbk |
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actions of thyroid hormone: specific target cells?
What effects does it have? 4) |
not really, BODY-WIDE
1. Metabolic Rate (heat production) increased use of ATP via increased Na/K ATP ase. --Increased USE of ATP, means less ATP, makes glycolytic pathway more active, this produces heat (calorigenesis) 2. Permissive of adrenergic receptor expression (permits receptors for hormones produced by adrenal glands, SENSITIZES body for sympathetic/parasympathetic signals) 3.Permissive of GROWTH and DEVELOPMENT (if lack T3/4 early in development-->Cretinism/congenital hypothyroidism (inability of other tissues to develop!) -poor nervous sys/intellectual/phys development. Can be corrected w/ Thyroxine and/or dietary IODIDE 4. Adult nervous sys function: ^thyroid=^nS excitability (increases responsiveness/development of NS) |
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Graves' disease
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Autoimmune disease: body treats tissues as though foreign.
-stimulate TSH receptor as if it were stimulated by TSH (by binding), act AGAINST it. Promotes signals to excessive degree-->hyperthyroidism hot, sweaty, thin, weak muscles, swelling around eye sockets, GOITER |
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hypothyroidism
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caused by iodine deficiency/radiation
low metab, cold intol, weight gain, fatigue, weak pulse, decreased alterness, cardio probs, lose smooth muscle tone |
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linear growth: at epiphyseal growth plates
how? |
growth hormone triggers release of IGF-1.
IGF1 stimulates mitosis, leads to cell division in growth plate. New cells are produced and spread out on either side, other processes convert connective tissue to calcified bone. |
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normal growth requires: 4 things
what 5 hormones? |
1. adequate nutrition (esp protein)
2. freedom from chronic illness (free of physio and psycho stress bc during sress response, body prepares for disaster (slow processes like growth not priority) 3. freedom from chronic psychosocial stress 4. normal suite of hormones: -growth hormone -IGFs -Thyroid Hormone -Insulin (regulates how food is stored for later use) -Androgens (like testosterone) -Estrogens -Other peptide growth factors |
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You can stimulate growth.
Explain Hormone Cascade. |
1. Stimulate Nuclei in Hypothalamus (w/ sleep, exercise, fasting, stress, etc). Releases: GHRH (growth horm releasing horm), decreases Release of SomatoStatin.
2. Increase Plasma GHRH, decrease plasma SS in portals 3. Anterior Pit: ^ secretion Growth Hormone 4. ^ plasma GH (goes all over body in blood, mobilizes glucose and fat from storage, signals protein synthesis) 5. Liver and Other Cells ^ IGF-I secretion (also goes thruout blood, stimulates MITOSIS, hypertrophy of muscle/other tissues, hyperplasia: mobilization of tissues to change from 1 type to another, and differentiation: maturation of tissue) 6. Increase Plasma IGF-I |
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lots of iGF-I in the blood: what type of feedback on
1. GHRH? 2. SS? 3. GH? (short loop fdbk) |
1. lots of IGF-1 in the blood exerts NEG. feedback on GHRH (downregulating it)
2. lots of IGF-1 in the blood exerts POS. feedback on SS (upregulating) 3. lots of IGF-1 in the blood exerts NEG. feedback on GH (short loop) |
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Growth Hormone Abnormalitiles:
1. Dwarfism: --what deficiency? --what not working? 2. Gigantism: what hormone elevated? when? 3. Acromegaly: what hormone elevated? when? |
1. Dwarfism: GH deficiency, RECEPTOR insensitivity
2. Gigantism: elevated GH *before puberty* (before growth plates ossify) --early death, probs w/ all organs 3. Acro: GH elevated AFTER puberty (only extremities huge) |
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adrenal glands, cortex secretes (3) what hormones?
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1. Aldosterone
2. Cortisol 3. Androgens |
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adrenal gland: medulla secretes what 2 hormone?
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1. epineph
2. norepineph |
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Epinephrine/Norepinephrine function:
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fight or flight
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Cortisol: "main stress hormone"
basal levels: functions (4) |
"hypothalamic-pituitary axis hormone"
neg feedback keeps basal levels in check 1. permissive of adrenergic receptors in cardio system: regulate/enhances responsiveness of this system 2. Liver glucose production b/t meals (glucocorticoid): stimulates liver b/t meals to release glucose to be used 3. Anti-inflammatory/anti-immune (cortisone shots) 4. Fetal/neonatal development of brain, intestines, lungs |
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INCREASED cortisol levels functions (6)
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1. Metabolic effects (glucose SPARING): mobilize glucose, fatty acids, aminos (prepare body to heal itself after injuries)
2. Bone RESORPTION (Ca2+ mobilization): reabsorb parts of extracelular matrix that are making scaffolding, take Ca2+ up and release it in rest of body (long term decrease in bone mass is side effect of steroid treatment like cortisone shot) 3. Support sympathetic responses (fight/flight): high blood pressure w/ prolonged excess of glucocorticoids. Co-released w/ epineph/norep 4. Stimulates Erythropoietin to replace RBCs (again, prolonged elevation=too many RBCs) 5. Anti-inflammatory/immunosuppression: body can ignore pain to deal w/ emergency at hand (this helps treatment to prevent rejection of transplanted organs) 6. Psychological/Analgesic: cortisol elevates mood, arousal, awareness --endorphins co-released w/ACTH; inhibit pain (body's endogenous opiods) 7. Inhibition of non-essential functions like growth/reproduction |
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ratio of cortisol to sympathetic activity (epin/norep) is influenced by what?
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perception of stressor
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how long w/o blood glucose kills neurons?
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15 mins.
blood/ECF nutrient levels must remain relatively constant |
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Give the mobile form and storage form for each (and where they are stored):
1. Carbs 2. Proteins 3. Fats |
Mobile:
1. glucose 2. amino acids 3. fatty acids, monoglycerides Storage: 1. glycogen (liver, muscles) 2. proteins (muscles) 3. triglycerides (adipose) |
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Absorptive State:
1. What is it? 2. To what tissues does each go? |
1. When food/fuel is in GI tract, being broken down and released into blood: glucose, aminos, and fats are available In blood (also starts storage for long term)
Glucose: goes to almost all tissues to be used as energy. -goes to adipose, converted to triglycerides, stored as fat -goes to muscle: stored as muscle glycogen goes to liver: transfered to triglycerides and glycogen, those triglycerides ALSO go to adipose (stored as fat) Triglycerides: straight to adipose and stored (turned into fatty acids, monoglyc, and back to triglyc) Amino Acids: go to all tissues, go to liver as well, some turned to triglyc. |
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Postabsorptive State:
1. What happens/ |
body starts to USE stored fuel: rereleased into blood, moving FROM liver, etc.
1. Muscle releases: amino acids, lactate and pyruvate (from glycogen) 2. Adipose releases triglycerides as: glycerol and fatty acids ***Both of the Above go to Liver*** EXCEPT some fatty acids--dir. to blood to tissues (except nervous tissues) 3. Liver: intake of glycerol, glycogen, lactate and pyruvate, aminos, fatty acids, all made into glucose or ketones. Glucose goes to blood and nerve tissue. Ketones go to other tissues. |
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Some fatty tissues in postabsorptive state go directly into blood and to almost all tissues but nervous system. What is this called? How does it help during postabsorptive state?
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GLUCOSE SPARING
Can use Energy from fat and leave glucose alone |
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Pancrease secretes main hormones that regulate absorptive/postabsorptive processes (what are these?)
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1. Insulin (by Beta cells)
2. Glucagon (by alpha cells) Both are secreted by Islets of Langerhans Their balance determines whether in absorptive/post state |
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Insulin
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Stimulates absorptive processes and INHIBITS postabsorptive (net storage)
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Glucagon
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stimulates postabsorptive processes and inhibits absorptive (net mobilization)
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Control of Insulin Secretion (negative feedback loop)
start w: increased plasma glucose |
1. Increased plasma glucose
2. Islet BETA cells sense this, increase insulin secretion 3. Increased plasma insulin 4. Adipocytes and muscle all over body increase glucose uptake AND, LIVER: cessation of glucose output, net glucose uptake 5. Restoration of plasma glucose to normal (arrow back to beginning (-) fdbk |
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mechanism of insulin action in muscle/fat cells:
1. hydrophil/phob? 2. where is receptor? 3. how transported? (diffusion, endocyt, etc) 4. what happens in exercising muscles? 5. Brain? |
1. HydroPHILLIC
2. Must bind to ExtraCellReceptor-->signal transduction pathway stimulates: 3. FUSION of vesicles that have glucose transporter 3. More transorters=cell can suck up more glucose. Cycling of vesicular insertion and vesicular endocytosis stimulated by insulin 4. In exercising muscles, glucose transporters go to membrane W/O insulin stimulation 5. Brain does NOT need insulin for glucose transport |
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Control of glucagon (-) feedback
Start w/ decrease plasma glucose What other hormones are stimulated by low plasma glucose?? |
1. Decrease Plasma Glucose
2. Sensed by ALPHA cells, secrete glucagon 3. Increased plasma glucagon 4. Liver: -glycogenolysis (break glyco down into precursor molecules) -gluconeogenesis (making new glyc from precursors) -ketone synthesis (produced from aminos) 5. Increase plasma glucose and plasma ketones arrow to beginning: - fdbk Epinephrine and norep Cortisol Growth Hormone ^^these all help glucagon mobilize glucose! |
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diabetes mellitus:
Type 1: insulin dependent/juvenile onset |
Not enough insulin to signal absorptive state
Pancreas' inability to secrete insulin-->hyperglycemia, fatty acid mobilization, ketoacidosis treatment by insulin injections |
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Diabetes Mellitus: Type 2
noninsulin dependent/adult-onset |
1. Desensitization of insulin receptors on target tissues often assoc. w/ obesity: becomes less responsive even tho stim is normal (sometimes stimulus ITSELF desensitizes receptor)
More glucose is around than necessary, constantly stimulatig insulin, insulin constantly stimulating receptor-->desens. Hyperglycemia and other symptoms like type 1 but milder treatable w/ DIET and EXERCISE |
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Gonad roles: (2)
feedback (+ or -?) |
steroid production (tropic)
gametogenesis: production of cell and ova (trophic) --development of glands and differentiation into these cells at development feedback: negative in males, females - or + depending on stage of development and stage of menstrual cycle |
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Ovary
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where egg cells are made (oogenesis)
and estrogens/progestins are made (steroidogenesis) |
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endometrium
myometrium fallopian tubes |
1. lines cavity, produces nutrients for developing fetus
2. smooth muscle on outside: contractions 2. ciliated epithelial cells=wave of movement carries egg to uterus, if fertilized, will implant |
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Follicle Development (reproductive):
1. takes place where (in female)? 2. order of events (roughly 2-3 steps) 3. How is corpus luteum ultimately formed? |
1. takes place INSIDE ovary
-millions of precursor oocyte cells go through this process 2. Process: 1. Oocyte and granulosa cells during fetal development of female. 2. Both oocytes and granulosa cells grow and divide. Theca cells also surround on outside. (both gran and theca=support/protective functions AND endocrine functions--important for development, menstruation, AND preg) PRODUCE ESTROGENS!! 3. fluid-filled space (antrum) forms around oocyte inside gran/theca. Oocyte is connected to one side of gran/theca cell covering 4. Mature oocyte to be released into fallopian tubes 3. Granulosa and Theca cells left behind once oocyte is released on surface of ovary. Continue to have ndocrine functions; left behind structure=CORPUS LUTEUM-secretes estro and progestoerone |
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Theca and Granulosa Cells (follicle development)
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Cooperate to manufacture estrogen
Dominant follicle develops LH receptors on its granulosa cells LH hormone from mom: theca cells synthesize ANDROGENS (testosterone). Testosterone diffuses to Granulosa Cells. FSH hormone from mom signals Granulosa cells toconvert androgens to ESTROGEN and later PROGESTERONE **developing egg sends signals to mom's body abt how it's doing so mom's body can respond |
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LH/FSH in fetus: effect on development (general)?
Actions of estrogens/progestins at puberty (6)? |
LH and FSH direct development of reproductive tract in FETUS. LH and FSH levels stable till puberty.
At prepuberty--hypothal hormones stimulate: -growth spurt STOP -development of breasts/genitalia -pelvic widening -female fat distribution -osteoblast activation (build bone) -permissive of vasoconstriction (estrogen)--sensitizes cardio sys to respond to epin/norep |
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Actions on endometrium:
1. estrogen 2. prog |
1. Estrogen: proliferation of endometrium cells
2. Prog: secretory of nutrients for hospitable environment for fetus |
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Actions on Myometrium: estrogen,
2. progest |
1. estro: increases growth, contractility
2. prog: decrease contractility "antiestrogen effect"--fluctuating balance of est/pro--diffa ctions |
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Estrogen/Prog effect on Cilia/fimbria
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1. Estro: increases activity--promotes egg to be fertilized
2. prog: decrease activity |
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Cervical Mucus: effect of estro/progestins
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1. Estro: thin,watery, lots of mucus=hospitable for sperm cells
2. progestin: viscous, little: usually after fertilization occurs to prevent other foregin things/bacteria from implanting |
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effect of estrogen/progest on breast (pregnant)
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1. estro: duct development
2. progest: lobules/alveoli (both have support function) |
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Effect of estro/progest on follicle:
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1. estro: increases development
2. prog: decreases follicle devel (dying off of follicles that aren't necessary) |
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primary hypogonadism (male)
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testicular failure!!
i.e. Klinefelter's Syndrome (extra X chromosome by meiotic nondisjunction.) -small, firm testes, decreased sperm production, testosterone levels low from abnormal Leydig cell function, increased breast size, high LH and FSH bc of loss of androgen/inhibin negative fdbk |
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secondary hypogonadism (male)
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failure to supply the testes w/ appropriate gonadotropic stimulus (not enuf LH, FSH, GhRH, etc.)
ie. hyperprolactinemia (increased prolactin in the blood)-->tumor on pituitary gland inhibits LH/FSH production ex. 2: hypopituitarism: total loss of pituitary gland (anterior) function: must be treated w/ cortisol, thyroid hormone, and tesosterone (men), kids (growth hormone) |
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effects of testosterone in the male
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1. initiation/maintenance of spermatogenesis (via Sertoli cells)
2. decreases GnRH secretion (negative fdbk to hypothal) 3. Inhibits LH secretion via anterior pit gland (negative fdbk) 4. Differentiation of male accessory repro organs, maintains their function 5. Induces 2ndary sex characteristics 6. Stimulates protein anabolism, bone growth, cessation of bone growth 7. Sex drive/aggression 8. erythropoietin secretion by kidneys |
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5 Inputs Influencing Smooth Muscle Contractile Activity
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1. spontaneous electrical activity in plasma membrane of muscle cell
2. neurotrans released by autonomic neurons 3. Hormones 4. Locally induced changes in chemical composition of ECF (oxygen, acid, osmolarity, etc) 5. Stretch |
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Effects of Increased Plasma Cortisol Concentration During Stress (5)
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1. Effects on organic metabolism:
a. stimulation of protein catabolism in bone, lymph, muscle (breaks down these tissues) b. Stim of liver uptake of aminos and converts to glucose c. maintains plasma glucose levels d. stimulates triglyceride catabolism in adipose--release glycerol/fatty acid into blood 2. enhanced vascular reactivity (can maintain constricted vessels in response to norep) 3. nidentified protection against damaging influences of stress 4. Inhibits inflammation 5. Inhibits nonessential functions (growth/repro) |
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Actions of Sympathetic Nervous System (epinephrine etc) during stress
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1. Increased hepatic and muscle glycogenolysis
2. Breakdown of adipose tissue triglyceride (provides supply of glycerol) 3. Increased cardiac function (heart rate) 4. Diversion of blood from viscera to skeletal muscles by vasoconstriction in viscera and vasodilation in muscle 5. increased lung ventilation (stimulates brain breathin centers/dilating airways) |
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Nutrient metabolsim during absorptive pd (4 components)
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1. Energy provided by absorbed carbs in typical meal (primarily)
2. Net uptake of glucose by liver 3. Some carb stored as glycogen in liver/muscle, Most carbs and fats in excess are STORED as fat in adipose 4. Some synthesis of body proteins, some amino acids in diet protein used for E or converted to fat |
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Cortisol's effects on Metabolism
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--PERMISSIVE role ina djustments to fasting
-level doesn't need to increase much but presence of cortisol maintains concentrations of key liver/adipose tissue enzymes for gloconeogenesis and lipolysis. 2. Increased plasma concentrations cause: a. increase protein catabolism b. increase gluconeogenesis c. decrease glucose uptake by muscle/adipose cells d. increase triglyc breakdown NET RESULT: increased plasma [ ] of amino acids, glucose, and free fatty acids |
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Stages in Control of Reproductive Function (in both sexes) 4 Steps
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1. During fetal life-1st yr of life: GnRH, gonadotropins, gonadal sex hormones secreted at high levels
2. year 1-puberty: secretion hormones is low and constant 3 Puberty: hormonal secretion increase 4. Diminishes later in life bc gonads less responsive to gonadotropins |
