524 exam 2.2

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cong10
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43548
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524 exam 2.2
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2010-10-24 19:53:55
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exam dr bryant
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skelital muscle mechanics
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  1. what are the functions of skeletal muscle? (6)
    • 1. produce skeletal movement: they pull on tendons to move bones
    • 2. maintain posture and body position
    • 3. support soft tissues: can support organ's weight or shield them from injury
    • 4. guard entrances & exits: provide voluntary control over swallowing, defecation, urination
    • 5. maintain body temperature: contraction of muscles uses energy which produces heat
    • 6. store nutrient reserves: skeletal muscle contains large amounts of proteins that if necessary, can be broken down and used for energy
  2. organization of the skeletal msucel: what are the 3 layers of connective tissue?
    • 1. epimysium: surrounds entire muscle
    • 2. perimysium: surrounds muscle fascicle
    • 3. endomysium: surrounds muscle fiber (muscle fiber = muscle cell)
    • -endomysium contains (a) capillary networks, (b) myosatellite cells, (c) nerve fibers

  3. at the end of each muscle, collagen fibers of the epimysium, perimysium and endomysium come together to form a ______; that then attaches to bone
    bundle (tendon) OR sheet (aponeurosis)
  4. how are skeletal muscle fibers formed???
    • MYOBLASTS are muscle germ cells that during development, fuses to form skeletal muscle fibers
    • each nucleus reflects the contribution of a single myoblast cell
  5. myoblast that don't fuse with developing muscle fibers; important if there's damage to muscle cells because they can become enlarged and fuse; how skeletal muscles regenerate itself; basically: embryonic stem cells that function in the repair of damaged muscle tissue
    • MYOSATELLITE CELLS
    • muscle cells can't divide but new muscle fibers are produced through the divisions of myosatellite cells
    • skeletal muscle tissue can repair itself after injury!!!
  6. characteristics of skeletal muscle
    • 1. mutinucleated
    • 2. large size: some can be up to a foot long!
  7. how does muscle repair itself?
    myosatellite cells can enlarge and fuse with damaged muscle fibers
  8. describe the different elements that make the structure of the skeletal muscle:
    1. sarcolemma
    2. sarcoplasm
    3. T tubules/transfer tubules
    4. myofibrils
    5. sarcoplasmic reticulum (SR)
    6. triad

    • 1. sarcolemma: muscle membrane fiber; plasma membrane of a muscle fiber
    • 2. sarcoplasm: cytoplasm of a muscle fiber
    • 3. T tubules: narrow tubes that are continuous with sarcolemma; extends into sarcoplasm at right angles to cell surface; action potentials travel down these tubules to initiate muscle contraction; so AP that goes through sarcolemma filters through muscle through T tubules
    • 4. myofibrils: bundles of protein filaments (myofilaments) that are attached at each end of sarcolemma; actively shorten during contraction; mitochondria surround these myofibrils since these myofibrils need lots of energy
    • 5. sarcoplasmic reticulum SR: similar to smooth ER of other cells; expands near T tubules to form chambers called terminal cisternae; see how it wraps around myofibril!
    • 6. triad: pair of terminal cisternae and T tubule
  9. made of thick and thin filaments and titin (elastic myofilaments associated with thick filaments); organized into repeating functional units called SARCOMERES
    myofibrils
  10. describe the different sections of a sarcomere:
    1. A band
    2. I band
    3. within the A band: M line, H band, and zone of overlap
    4. within the I band: Z lines
    • 1. A band: (dArk) length of thick filaments
    • 2. I band: (lIght) contains only thin filaments, no thick!
    • 3. M line: connection point of thick filaments
    • 4. H band: light region on either side of M line that only has thick, no thin!
    • 5. zone of overlap: region of overlap between thick and thin filaments
    • 6. Z line: boundaries between adjacent sarcomeres; where sarcomeres connect

  11. sarcomere structure: length of thick filaments; dArk band
    A band
  12. sarcomere structure: contains thin filaments but not thick, lIght band
    I band
  13. connection point of thick filaments
    M line
  14. light region on either side of M line that contains only thick filaments
    H band
  15. boundaries between adjacent sarcomeres; responsible for the banded/striated appearance of muscle!!!
    Z lines
  16. elastic protein that attaches thick filaments to Z lines; allows for contraction; allow stabilization of thick filaments
    titin
  17. describe thin filament structure:
    1. actin
    2. nebulin
    3. tropomysin
    4. troponin
    • 1. actin: F (filamentous actin) composed of two rows of G (globular) actin molecules; each G actin molecule has an active site that can bind to myosin... thick filament attaches to this active site
    • 2. nebulin: runs through middle of F actin strand; basically holds it together
    • 3. tropomysin: double stranded protein that covers seven active sites on G actin molecules; each is bound to one troponin molecule; goes across G actin molecules like a rope; lays on top of active site to cover the active sites during muscle relaxation
    • 4. troponin: contains 3 subunits; when its bound to calcium changes conformation and moves tropomysin off active sites; exposes active site and muscle contraction can occur
    • - troponin C: binds calcium that triggers muscle contraction (calcium levels are low in resting phase and only increase to initiate contraction)
    • - troponin T: binds to tropomysin
    • - troponin I: binds to actin

  18. describe thick filament structure:
    1. myosin
    2. titin
    • 1. myosin: contains about 300 myosin molecules; contains a head and a tail region; the head interacts with actin to form cross bridges while the tails are pointed toward he M line
    • 2. titin: elastic protein that can recoil; organizes myosin, prevents overstretching and helps return sarcomere to resting length (look at pic)

  19. what happens to the thick and thin filaments during contraction? (what happens to the thick and thin filaments? H band? I band? zone of overlap? Z lines? A band?)
    • sliding filament theory: thin filaments slide toward center of sarcomere, alongside thick filaments
    • H band and I bands get smaller
    • zones of overlap get larger
    • Z lines move closer together
    • width of A band remains the same

  20. what controls skeletal muscle activity?
    nervous system; voluntary control
  21. control of skeletal muscle activity: neuromuscular junction (NMJ)
    where nerve and skeletal muscle meet and communicate
  22. control of skeletal muscle activity: nerve axon branches & ends here; contains vesicles filled with acetylcholine (ACh = neurotransmitter)
    synaptic terminal
  23. control of skeletal muscle activity: narrow space between synaptic terminal and sarcolemma; contains enzyme acetylcholinesterase (AChE) which breaks down ACh - a way to turn off signal after a certain amount of time, allows ACh to be recycled to make new ACh
    synaptic cleft
  24. control of skeletal muscle activity: sarcolemmal surface containing ACh receptors
    motor end plate
  25. describe: neuronal stimulation of a muscle fiber (5 steps)
    • 1. arrival of action potential at synaptic cleft: action potential causes calcium ions to enter synaptic terminal and causes vesicles to release ACh (step 2)
    • 2. release of acetylcholine: vesicles in the synaptic terminal fuses with the neuronal membrane and dump their contents (ACh) into the synaptic cleft
    • 3. ACh binding at the motor end plate: the binding of ACh to the receptors increase the membrane permeability to sodium ions... sodium ions rush into the cell!
    • 4. appearance of an action potential at the sarcolemma: an action potential spreads across the surface of the sarcolemma... while this occurs, AChE breaks down the ACh
    • 5. return to initial state: if another action potential arrives at the NMJ, the cycle begins again at step 1

    • action potential in muscle leads to muscle contraction!!!
    • sodium going in creates action potential --> stimulates muscle
  26. link between generation of action potential in sarcolemma and start of muscle contraction; occurs at triads; action potential travels down T tubules, triggers calcium release from terminal cisternae of SR
    • excitation-contraction coupling
    • stimulation of a nerve coupled to muscle contraction
    • calcium seen as the trigger for muscle contraction
    • remember: troponin C binds to calcium, so once nerve stimulates muscle, SR releases calcium... calcium interacts with troponin C...
  27. how are active sites on the thin filaments exposed???
    • action potential triggers release of calcium ions from SR
    • calcium binds to troponin C
    • troponin moves tropomysin, exposing active sites (at rest... active sites are blocked by tropomysin!)
    • exposure of active sites leads to cross bridge formation
  28. describe the 5 steps of the contraction cycle:
    • 1. exposure of active sites: the calcium ions entering the SR bind troponin; troponin changes position and removes tropomysin away from active sites and allows interaction with myosin head
    • 2. formation of cross bridges: once active site exposed, myosin head binds to them and forms cross bridges
    • 3. pivoting of myosin heads: (stored energy is released (ADP+Pi), myosin head pivots toward the M line to create a power stroke) at rest, the myosin head points away from the M line = cocked... requires energy... at cocked position = ADP and phosphate group are still bound to myosin head! soooo... using stored energy, myosin head pivots, when it moves, it pulls the actin and essentially slides across from each other
    • 4. cross bridge detachment: when a new ATP molecule binds to the myosin head, the link between the active site on actin and the myosin head is broken
    • 5. myosin reactivation: back to initial resting phase by reactivating the myosin head... occurs when ATP is broken down to ADP+P, myosin head recocks... if calcium ions are still present and there's sufficient ATP, this cycle will continue to be repeated several times per second

    remember: don't mix what happens between reactivation and crossbridging!!!
  29. describe the shortening of a muscle during a contraction
    • during contraction, if neither end of myofibril is held in place, both ends move towards middle
    • if intact skeletal muscle, one end of muscle is usually fixed (the origin) while the other end moves (the insertion)... fixed end moves to free end
  30. muscle contraction summary: steps that initiate a contraction (5)
    • 1. at the NMJ, ACh released by the synaptic terminal binds to receptors on the sarcolemma
    • 2. the resulting change in the transmembrane potential of the muscle fiber leads to the production of an AP that spreads across the entire surface of the muscle fiber and along the T tubules
    • 3. the SR releases stored calcium ions, increasing the [calcium] of the sarcoplasm in and around the sarcomeres
    • 4. calcium ions bind to troponin, producing a change in the orientation of the troponin-tropomysin complex that exposes active sites of the thin (actin) filaments. cross bridges form when mysin heads bind to active sites on F actin
    • 5. the contraction begins as repeated cycles of cross bridge binding, pivoting, and detachment occur, powered by the hydrolysis of ATP. these events produce filament sliding, and the muscle fiber shortens
  31. muscle relaxation summary: steps that end a contraction
    • 6. action potential generation ceases as ACh is broken down by AChE (acetlycholinesterase)
    • 7. the SR reabsorbs calcium ions, and the [calcium] in the SR declines
    • 8. when calcium ion [ ] approach normal resting levels, the troponin-tropomysin complex returns to its normal position. this change re-covers the active sites and prevents further cross bridge interaction
    • 9. without cross bridge interactions, further sliding cannot take place and the contraction ends
    • 10. muscle relaxation occurs and the muscle returns passively to its resting length
  32. the amount of tension produced by a muscle fiber depends on: (3)
    • 1. number of cross bridges
    • 2. fiber's resting length at the time of stimulation - see an "optimum"
    • - relates to degree of overlap between thick and thin filaments
    • - optimal length = most efficient = most tension produced
    • - overstretch = cross bridge interaction is reduced or absent... can't form cross bridges because muscles are pulled to farm apart... no sliding if they can't attach
    • - decreased resting lengths = thin filaments extend across center of sarcomere = decrease tension... if it's too close together, there's no room to compress further, not efficient
    • 3. frequency of stimulation - twitch vs treppe vs wave summation vs incomplete tetanus vs complete tetanus
  33. produced by a single stimulation
    • twitch
    • a single contraction
    • repeated stimulation produces a sustained contraction
  34. muscle tension: when a second stimulus arrives immediately after relaxation phase has ended, the next contraction will develop slighty higher tension; due to increased calcium in sarcoplasm (calcium doesn't have enough time to all be pumped back into the SR)

    treppe ("stairs")
  35. muscle tension: when a 2nd stimulus arrives before relaxation phase has ended, the 2nd contraction will have increased tension
    wave summation
  36. muscle tension: increased stimulation frequency, muscle almost NEVER allowed to relax completely, 4 times the tension produced compared to wave summation
    incomplete tentaus
  37. muscle tension: higher frequency stimulation completely eliminates relaxation phase, causes continuous contraction
    complete tetanus
  38. what determines the tension production by skeletal muscles? (2)
    • 1. the tension produced by the stimulated muscle fibers: motor unit = all the muscle fibers (usually around 100) controlled by a SINGLE motor neuron
    • 2. the total number of muscle fibers stimulated
    • - RECRUITMENT: increasing the # of active motor units to increase muscular tension produced
    • - max tension produced when all motor units in muscle are in state of complete tetanus
    • - typically during sustained contraction, motor units are activated on rotating basis - ASYNCHRONOUS motor unit summation
    • - typically we don't function at max motor unit capacity so that we don't get fatigued
    • - more like a RELAY... rotate through muscle motor units, change which muscles are used at a time to prevent fatigue
  39. what gives a person muscle tone?
    • the RESTING TENSION of a muscle... some motor units are still active but not enough to produce movement
    • this stabilizes positions of bones and joints
    • prevents controlled, sudden changes in position
    • so if we increase muscle tone, increase what you actually see as "muscle"
    • related to metabolism... increase muscle tone, increase basal metabolic rate
  40. what are the 2 types of muscle contraction?
    • 1. isotonic contraction
    • 2. isometric contraction
  41. decribe: isotonic contraction and the two types of isotonic contraction
    • isotonic contraction = tension rises, skeletal muscle length changes
    • 1. CONCENTRIC: muscle tension exceeds the resistance, muscle shortens (ex. lift water bottle, lift weight)
    • 2. ECCENTRIC = muscle tension doesn't exceed the resistance, muscle elongates (ex. unable to lift water bottle, unable to lift weight... muscle just elongates)
  42. describe: isometric contraction
    • tension rises, no change in skeletal muscle length
    • ex: flexed arm hang, don't actually do a pull up but your muscles are contracting, not changing in length... or if you're holding a pose...
  43. what are the effects of aging on muscular system? (4)
    • 1. skeletal muscle fibers become smaller in diameter
    • - decrease in myofibrils
    • - decrease in skeletal muscle size, strength & endurance
    • 2. skeletal muscles become less elastic
    • - increased amounts of fibrous connective tissue (fibrosis) vs elastic tissue; becomes stiffer
    • 3. tolerance for exercise decreases
    • - result of rapid fatigue & reduction in ability to thermoregulate
    • 4. ability to recover from muscular injuries decreases
    • - number of myosatellite cells decreases (ability to repair muscle damage decreases)
    • - scar tissue formation occurs instead of muscle repair/regeneration
  44. tetanus
    • deep puncture would has decrease oxygen levels and allows bacteria to thrive
    • caused by Clostridium tetani
    • bacteria releases neurotoxin blocks release of neurotransmitters that normally inhibit motor neurons
    • results in sustained, powerful skeletal muscle contractions
    • often shorter neurons are affected first so difficulty opening jaw - lockjaw
    • severe tetanus has 40-60% mortality rate
  45. treatment for tetanus
    • can be IMMUNIZED
    • DTaP vaccine for infants and then boostered every 10 yrs
    • body makes antibodies to neurotoxin
    • unimmunized can receive "anti-toxin" = antibodies
  46. muscular dystrophy
    • inherited group of disease caused by a mutation in one of the many genes that affect muscle function
    • progressive muscle weakness & deterioration occurs
    • variable severity depending on type of mutation
  47. treatment for muscular dystrophy?
    none =(
  48. muscular dystrophy example 1: duchenne's muscular dystrophy (DMD)
    • mutation in gene that codes for dystrophin... a protein that attaches thin filaments to anchoring proteins on sarcolemma
    • x linked inheritance pattern, so more males are affected
  49. muscular dystrophy example 2: myotonic dsytrophy
    alteration in gene that codes for myosin kinase
  50. malignant hyperthermia
    • symptoms caused by inherited defect in receptor that allows calcium to be released from SR and initiate muscle contraction
    • hereditary impairment to sequester calcium, leads to prolonged releases of calcium
    • may have been triggered by something
    • symptoms include: rapid rise in body temp, muscle rigidity & stiffness, dark brown urine due to rhabdomyolosis (breakdown of muscle tissue, proteins broken down clog up kidneys), increased heart rate, acidosis (low blood pH)
    • usually triggered by general anesthetics
  51. treatment for malignant hyperthermia
    • patients are given DANTROLENE
    • a muscle relaxant that dissociates excitation-contraction coupling
  52. type of drug that relaxes skeletal muscle:
    - antagonist at ACh receptor, prevents ACh from binding, prevent depolarization
    used as adjuncts during general anesthesia to facilitate tracheal intubation and optimize surgical conditions
    - can be reversed by acetylcholinesterase inhibitors (which inhibit AChE and increase the amt of ACh in synaptic cleft -reverse effect!)
    • NON DEPOLARIZING neuromuscular blocking drugs
    • 1. tubocurarine
    • 2. cisatracurium
  53. type of drug that relaxes skeletal muscle:
    - acts as a depolarizing agonist at ACh receptor
    - phase I, it binds to receptor and causes depolarization, not metabolized effectively at synapse, so membranes remain depolarized and unresponsive to subsequent impulses (depolarizing block)
    - in phase II, acts as if channel is in prolonged closed state (desensitized)
    - can be reversed by acetylcholinesterase inhibitors but only during phase II!!!
    • DEPOLARIZING neuromuscular blocking drugs
    • succinylcholine
  54. type of drug that relaxes skeletal muscle: acts to release muscle spasms and increase muscle tone
    • SPASMOLYTICS
    • 1. diazepam
    • 2. baclofen
    • both in the top 200

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