Skeletal Muscle Mechanics

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monchi
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Skeletal Muscle Mechanics
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2010-10-13 23:22:33
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Skeletal Muscle Mechanics Lecture Dr Bryant IBHS Exam
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Skeletal Muscle Mechanics Lecture (Dr. Bryant) IBHS Exam 4
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  1. Functions of Skeletal Muscle
    • Produce Skeletal Movement
    • Maintain Posture & body position
    • Support soft tissues
    • Guard entrances & exits
    • Maintain body temperature
    • Store nutrient reserves
  2. Functions of skeletal muscle

    Produce skeletal movement
    Skeletal muscles pull on tendons to more bones
  3. Functions of skeletal muscle

    Maintain posture & body position
    Enables you to keep head up during lecture... or not =)
  4. Functions of skeletal muscle

    Support soft tissues
    Can support organs weight or shield from injury
  5. Functions of skeletal muscle

    Guard entrances & exits
    Provide voluntary control over swallowing, defecation, urination
  6. Functions of skeletal muscles

    Maintain body temperature
    contracction of muscles uses energy which produces heat
  7. Functions of skeletal muscle

    Store nutrient reserves
    Skeletal muscles contains large amounts of proteins that if necessary can be broken down and used for energy (its converted to amino acids)
  8. Organization of Skeletal Muscles

    Each Muscle Contains 3 layers of connective tissue
    • 1. Epimysium - surrounds the ENTIRE muscle
    • 2. Perimysium- surrounds muscle fascicles (bundles of muscle fibers)
    • 3. Endomysium - surrounds individual muscle fibers (muscle fiber= muscle cell); contains capillary network, myosatellite cells, nerve fibers
  9. Which of the following layers contain capillary network, myosatellite cells, and nerve fibers?
    A. Epimysium
    B. Endomysium
    C. Perimysium
    B. Endomysium (endo=inner)
    (this multiple choice question has been scrambled)
  10. Layer that surrounds the entire muscle
    Epimysium
  11. Layer that surrounds muscle fascicles (bundles of muscle fibers)
    Perimysium
  12. Layer that surrounds individual muscle fiber
    Endomysium
  13. What connects muscle to bone?
    Tendons
  14. Organization of skeletal muscle
    At the end of each muscle, collagen fibers of the epimysium, perimysium & endomysium come together to form a bundle (tendon) or sheet (aponeurosis) that attaches to bone
  15. Formation of skeletal muscle fibers
    • Myoblasts (muscle germ cells) fuse to form skeletal muscle fibers
    • Myoblasts that do NOT fuse with developing muscle fibers reamin & are called myosatellite cells
  16. Myosatellite cells
    • Myoblasts that do not fuse with developing muscle fibers remain
    • Help with muscle repair... Can enlarge & fuse with damaged muscle fibers
    • Found in endomysium
  17. Structure of a skeletal muscle fiber

    Muscle fiber membrane
    Sarcolemma
  18. Structure of a skeletal muscle fiber

    Cytoplasm of muscle fiber
    Sarcoplasm
  19. Structure of a skeletal muscle fiber

    T (transverse) tubules
    • Narrow tubes, continuous wiht sarcolemma, extend into sarcoplasm at right angles to cell surface
    • Action potentials travel down these tubules to initiate muscle contraction
  20. Structure of a skeletal muscle fiber

    Myofibrils
    • Bundles of protein filaments (myofilaments) attached at each end of sarcolemma
    • Actively shorten during contraction
    • Contain thick & thin filaments
    • Mitochondria surround these myofibrils (energy)
  21. Structure of a skeletal muscle fiber

    Sarcoplasmic reticulum (SR)
    • Similar to smooth ER of other cells
    • Expands near T tubules to form chambers called terminal cisternae
  22. Structure of a skeletal muscle fiber

    Triad
    Pair of terminal cisternae & a T tubule
  23. Myofibrils structure
    • Made up of thick and thin filaments, titin
    • Organized into repeating sarcomeres (functional units)
  24. Sarcomeres Structure
    • A bands (dArk) -length of thick filaments
    • I bands (LIght)- contains thin filaments but NOT thick
  25. Sarcomere structure

    A Band
    • M line: connection point of thick filaments
    • H band: light region on either side of M line
    • * contains ONLY thick filaments

    Zone of overlap: region of overlap between thick & thin filaments
  26. Sarcomere Structure

    I Band
    Z lines: boundaries between adjacent sarcomeres

    • responsible for the banded (striated) appearance of muscle
    • Titin: elastic protein that attaches thick filaments to Z lines
  27. Connection point of thick filaments
    M line (in A band)
  28. Light region on either side of M line
    H Band (in A band)
  29. Elastic protein that attaches thick filaments to Z lines
    Titin
  30. Responsible for the banded (striated) appearance of muscle
    Z lines ( in I BAND)
  31. Region of overlap between thick & thin filaments
    Zone of overlap
  32. Light region on either side of M line
    H band ( contains only thick filaments)
  33. Connection point of thick filaments
    M line (in A band)
  34. Sarcomere structure

    Thin & Thick filaments are organized 3-dimensionally too
    (ex. in the zone of overlap, 3 thick filaments surround each thin filament & 6 thin filaments sound each thick filament)
  35. What makes up the thin filaments?
    Actin, Nebulin, Tropomyosin, Troponin
  36. Thin Filaments

    Actin
    • F (filamentous) actin: composed to 2 rows of G (globular) actin molecules
    • Each G actin molecule contains an active site that can bind to myosin
  37. Thin Filaments

    Nebulin
    Runs through middle of F actin strand, holds it together
  38. Thin Filaments

    Tropomyosin
    • Double stranded protein that covers 7 active sites on G actin molecules
    • Each is bound to one troponin molecule
  39. Double stranded protein that covers 7 active sites on G actin molecules
    Tropomyosin
  40. Thin Filaments

    Troponin
    • Contains 3 subunits, when bound to calcium changes conformation & moves tropomysosin off of active sites
    • 1. Troponin C: binds Calcium (calcium levels are very low in resting state & only increase to initiate contraction)
    • 2. Troponin T: binds to Tropomyosin
    • 3. Troponin I: binds to actin
  41. Which of the following binds to actin?
    A. Troponin I
    B. Troponin A
    C. Tropomyosin I
    D. Tropomyosin A
    E. Troponin T
    A. Troponin I
    (this multiple choice question has been scrambled)
  42. Double stranded protein that covers 7 active sites on G actin molecules
    Tropomyosin
  43. Composed of 2 rows of G actin molecules
    F actin
  44. Runs through middle of F actin strand, holds it together
    Nebulin
  45. Thick Filaments

    Myosin
    • Contain about 300 myosin molecules
    • Contains head & tail region ( head interacts with actin... formation of cross bridges) (tails are all pointed toward M lines)
  46. Thick Filaments

    Titin
    • Elastic protein that can recoil
    • Organizes myosin, prevents overstretching & helps return sarcomere to resting length
  47. What happens to these filaments during contraction ?
    • 1. Thin filaments slide toward center of each sarcomere, alongside thick filaments (sliding filament theory)
    • 2. H band & I bands get smaller
    • 3. Zones of overlap get larger
    • 4. Z lines move closer together
    • 5. Width of A band remains constant.
  48. Big Picture of Contraction
    If sarcomeres shorten during contraction then:

    • Myofibrils will shorten
    • Entire muscle will shorten
  49. What controls Skeletal Muscle Activity?
    Nervous systerm (but remember it is VOLUNTARY)
  50. Control of Skeletal Muscle Activity:

    Where nerve & skeletal muscle meet & communicate
    Neuromuscular junction (NMJ)
  51. Control of skeletal muscle activity:

    Synaptic terminal
    • Nerve axon braches & ends here
    • Contains vesicles filled with acetylcholine (ACh)
  52. Control of skeletal muscle activity:

    Synaptic Cleft
    • Narrow space between synaptic terminal & sarcolemma
    • Contains enzyme acetylcholinesterase (AChE) which breaks down ACh
  53. Control of skeletal muscle activity

    Motor end plate
    Sarcolemmal surface containing ACh receptors
  54. Which of the following is the sarcolemmal surface containing ACh receptors?
    A. Neuromuscular junction
    B. Synaptic Terminal
    C. Motor end plate
    D. Synaptic Cleft
    C. Motor end plate
    (this multiple choice question has been scrambled)
  55. Narrow space between synaptic terminal & sarcolemma
    Synaptic Cleft
  56. Neural Stimulation of a muscle fiber:
    • Step 1: Arrival of an action potential at the synaptic terminal
    • Step 2: Release of acetylcholine: Vesicles in the synaptic terminal fuse with the neuronal membran and dump their contents into the synaptic cleft
    • Step 3: ACh binding at the motor end plate: the bind of ACh to the receptors increase the membrane permeability to sodium ions. Sodium ions then rush into the cell
    • Step 4: Appearance of an action potential in the sarcolemma: An action potential spreads across the surface of the sarcolemma. While this occurs, AChE breaks down the ACh
    • Step 5. Return to initial state: If another action potential arrives at the NMJ, the cycle begins again at step 1
  57. Excitation- Contraction coupling

    E-C Coupling
    • Link between generation of action potential in sarcolemma & start of muscle contraction
    • Occurs at triads
    • Action potential travels down T tubules, triggers Ca2+ release from terminal cisternae of the SR
  58. Exposure of active sites
    • Action potential triggers realse of Ca2+ from SR
    • Ca2+ binds to troponin C
    • Troponin moves tropomyosin, exposing active sites
    • Exposure of active sites leads to cross-bridge formation
  59. Contraction Cycle
    • 1. Release of Ca2+ that binds to troponin, which pulls tropomysin off , ACTIVE SITE EXPOSURE
    • 2. Myosin head attaches to acting: CROSS-BRIDGE FORMATION
    • 3. Stored energy is release (ADP+P), myosin head pivots toward the M line= power stroke: PIVOTING OF MYOSIN HEAD
    • 4. When a new ATP molecule binds to the myosin head, the link between the active site on actin & the myosin head is broken: CROSS BRIDGE DETACHMENT
    • 5. Myosin reactivation occurs when ATP is broken down into ADP+P, myosin head recocks: MYOSIN REACTIVATION
  60. Contaction Cycle
    1. ACTIVE SITE EXPOSURE
    2. CROSS-BRIDGE FORMATION
    3. PIVOTING OF MYOSIN HEAD
    4. CROSS BRIDGE DETACHMENT
    5. MYOSIN REACTIVATION
    ***if calcium ions are still present & there is sufficient ATP, this cycle will continue to be repeated (several times per second) until calcium gets taken up***
  61. Shortening during a contraction
    • A) During contraction, if neither end of myofibril is held in place, both ends move towards middle
    • B) In intact skeletal muscle, one end of muscle is usually fixed (the origin) while the other end moves (the insertion)- THE FIXED END MOVES THE FREE END
  62. Muscle Contraction Summary (simplified version)
    • 1. ACh released, binding to receptors
    • 2. Action Potential reaches T tubule
    • 3. Sarcoplasmic Reticulum releases Ca2+
    • 4. Active site exposure, cross-bridge formation
    • 5. Contraction begins
  63. Muscle Relaxation Summary (simplified version) aka steps that END a contraction
    • 6. ACh removed by ACHe
    • 7. Sarcoplasmic reticulum recaptures Ca2+
    • 8. Active sites covered, no cross-bridge interaction
    • 9. Contraction ends
    • 10. Relaxation occurs, passive return to resting length
  64. Muscle Contraction Summary (extended version)
    • 1. At the neuromuscular junction (NMJ), ACh released by the synaptic terminal binds to receptors on the sarcolemma
    • 2. The resulting ∆ in the transmembrane potential of the muscle fiber leads to the production of an action potential that spreads across the entire surface of the muscle fiber and along the T tubules
    • 3. The SR releases stored Ca2+, increasing calcium concentration of the sarcoplasm in & around the sarcomeres
    • 4. Ca2+ bind to troponin, producing a ∆ in the orientation of the troponin-tropomyosin complex that exposes active sites on the thin (actin) filaments. Cross bridges form when myosin 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.
  65. Muscle Relaxation Summary (extended version)
    • 6. Action potential generation ceases as ACh is broken down by acetylcholinesterase (AChE)
    • 7. The SR reabsorbs Ca2+ & the concentration of Ca2+ in the sarcoplasm declines
    • 8. When Ca2+concentrations approach normal resting levels, the troponin -tropomyosin complex returns to its normal position. This ∆ re-covers the active sites & prevents further cross-bridge interaction.
    • 9. Without cross-bridge interactions, further sliding cannot take place, & the contraction ends
    • 10. Muscle relaxation occurs & the muscle returns passively to its resting length
  66. Death: no oxygen & nutrients, so muscle runs out of ATP, calcium leaks into sarcoplasm; without ATP cross-bridges can't be broken= RIGOR MORTIS: sustained contraction, starts 15-25 hours after death & ending 72 hours or more later
  67. Muscle Tension

    Amount of tension produced by a muscle fiber depends on the number of cross-bridges, but can vary depending on:
    • 1. Fiber's resting length at time of stimulation (relates to degree of overlap between thin & thick filaments)
    • Optimal length= most efficient = most tension produced
    • Overstretch= cross-bridge interaction is reduced or absent
    • Decreased resting lengths= thin filaments extend across center of sarcomere= decrease of tension
    • 2. Frequency of stimulation
  68. Muscle tension

    Frequency of stimulation
    • A single stimulation produces a single contraction , or twitch
    • Repeated stimulation produces a sustained contraction
  69. Muscle tension

    Treppe ("stairs")
    • When a second stimulus arrives immediately after relaxation phase has ended, the next contraction will develop slightly higher tension
    • --due to increased Ca2+ in sarcoplasm (because Ca2+ doesnt have enough time to all be pumped back into SR)
  70. Muscle Tension

    Wave Summation
    When a second stimulus arrives before relaxation phase has ended, the second contraction will have increased tension
  71. Muscle Tension

    Incomplete Tetanus
    Increased stimulation frequency, muscle almost never allowed to relax completely, 4 times the tension produced compared to wave summation
  72. Muscle tension

    Complete Tetanus
    Higher frequency stimulation completely eleminates relaxation phase, causes continuous contraction.
  73. Tension production by skeletal muscles

    Tension produced by whole skeletal muscles depends on:
    • The tension produced by the stimulated muscle fibers
    • The total number of muscle fibers stimulated
  74. Motor unit:
    all the muscle fibers (usually around 100) controlled by a single motor neuron
  75. Tension production by skeletal muscle

    The total number os muscle fibers stimulated
    • Recruitment: increasing the number 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 a rotating basis- asynchronous motor unit summation (TO PREVENT FATIGUE)
  76. Muscle Tone

    Resting Tension: some motor units are active, but not enough to produce movement
    • Stabilizes postitions of bones and joints
    • Prevents uncontrolled, sudden ∆s in position
    • Related to basal metabolic rate... the more muscle tone the higher the basal metabolic rate
  77. Some motor units are active, but not enough to produce movement
    Resting tension
  78. 2 Types of contractions:
    Isotonic and Isometric
  79. Isotonic Contraction

    Tension rises, skeletal muscle length changes (ex. running, picking up laptop)
    • 2 Types:
    • 1. Concentric:muscle tension exceeds the resistance, muscle shortens
    • 2. Eccentric: muscle tension does not exceed the resistance, muscle elongates
  80. Isometric Contraction (iso=same, metric= length)
    Tension rises, no change in skeletal muscle length (ex. flexed arm hang, holding a yoga pose)
  81. Muscle tension does not exceed the resistance, muscle elongates
    Eccentric (e for elongate)
  82. Muscle tension exceeds the resistance, muscle shortens
    Concentric
  83. Tension rises, skeletal muscle length changes
    Isotonic contraction
  84. Effects of aging on Muscular System
    • Skeletal muscle fibers become smaller in diameter (due to decrease in # of myofibrils, and decrease in skeletal muscle size, strength & endurance)
    • Skeletal muscle become less elastic (increase amouts of fibrous connective tissue (fibrosis))
    • Tolerance for exercise decreases (result of rapid fatigue & reduction in ability to thermoregulate)
    • Ability to recover from muscular injuries decreases (# of myosatellite cells decrease & scar tissue formation occurs instead of muscle repair/regeneration)
  85. TETANUS (the DISEASE)

    Occurs if you have a deep puncture wound because of decreasing oxygen levels allows CLOSTRIDIUM TETANI to thrive
    • Bacteria release neurotoxins which block release of neurotransmitters that normally inhibit motor neurons
    • -Results is sustained , powerful skeletal muscle contractions
    • -Often shorter neurons are affected first, so difficulty opening jaw- lockjaw
    • Severe tetanus has 40-60% mortality rate
    • Immunization : DTap vaccine for infants, then "boostered" every 10 yrs (body makes antibodies to neurotoxin)
    • If unimmunized can receive "anti-toxin"= antibodies (VACCINES CAN'T REVERSE DAMAGE THAT HAS ALREADY BEEN DONE)
  86. Inherited diseases caused by a mutation in one of the many genes that affect muscle function
    Muscular Dystrophy
  87. Muscular Dystrophy

    Inherited Diseases caused by a mutation in one of the many genes that affect muscle function

    ** NO CURES**
    • Symptoms: Progressive muscle weakness & deterioration occurs
    • Variable severity depending on the type of mutation
    • Ex: Duchenne's muscular dystrophy (DMD)- mutation in gene that codes for dystrophin (protein that attaches thin filaments to anchoring proteins on sarcolemma) - X-linked inheritance pattern, so more males affected
    • Myotonic dystrophy- alteration in gene that codes for a myosin kinase
  88. Malignant Hyperthermia

    Symptoms cause by inherited defect in receptor that allows calcium to be released from SR & initiate muscle contraction
    • Hereditary impairment to sequester calcium, leads to prolonged released of calcium (body can't keep up)
    • Symptoms include: rapid rise in body temperature greater than 105 degrees F
    • Muscle rigidity & stiffness
    • Dark brown urine (due to rhabdomyolysis)
    • Increased heart rate
    • Acidosis (low blood pH)
    • Usually triggered by general anesthetic
    • Patients given DANTROLENE (muscle relaxant that dissociates excitation-contraction coupling)
  89. Symptoms cause by inherited defect in receptor that allows calcium to be released from SR & initiate muscle contraction
    Malignant Hyperthermia
  90. Patients that have _________________are given DANTROLENE
    Malignant Hyperthermia
  91. Drugs that Relax Skeletal Muscle

    Spasmolytics
    Acts to decrease muscle spasms & increase muscle tone

    (ex. Diazepam, Baclofen)
  92. Which of the following is a spasmolytic drug?
    A. Succinylcholine
    B. Diazepam
    C. Cisatracurium
    D. Tubocurarine
    B. Diazepam
    (this multiple choice question has been scrambled)
  93. Drugs that relax skeletal muscle

    Neuromuscular blocking drugs
    • Nondepolarizing: Antangonist at ACh receptor, prevents ACh from binding, prevent depolarization
    • Used as adjuncts during general anesthesia to facilitate tracheal intubation & optimize surgical conditions
    • Can be reversed by cholinesterase inhibitors (ex. Tubocurarine, Cistatracurium)
    • Depolarizing: acts as a depolaring agonist at ACh receptor: phase 1 it binds to receptor & causes depolarization, not metabolized effectively at synapse, so membranes remain depolarized & unresponsive to subsequent impulses (depolarizing block); in phase 2 acts as if channel is prolonged closed state (desensitized)
    • Can be reversed by cholinesterase inhibitors, but only during phase 2 (ex. Succinylcholine-only one approved in US)

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