Anatomy - Exam 2.txt

  1. Cell membrane is a barrier
    • Separates inside of cell from outside fluid
    • -Inside = cytosol = intracellular
    • -Outside = extracellular = interstitial
    • -Allows inside concentration of electrolytes
    • and other solutes to be different from
    • extracellular concentration of solutes
    • -Higher inside:K+, proteins (negatively charged;A-)
    • -Higher outside:Na+, Cl, Ca+2
  2. Permeability
    • The ease with which substances can cross the cell membrane
    • -Nothing passes through an impermeable barrier(if 100%)
    • -Anything can pass through a freely permeable barrier
    • -Diff cells are permeable to diff substances (b/c of diff transport mechanisms)
  3. What level of permeability are cell membranes?
    Selectively permeable (because of different transport mechanisms)
  4. Passive Transport
    Cell doesn't expend energy (No ATP consumed)
  5. Active Transport
    Cell expends energy (ATP consumed from going against concentration gradient)
  6. Diffusion (in a solution or across a membrane)
    • Passive; Random motion of ions and molecules down their concentration gradient
    • -High to low concentration
  7. Carrier Mediated Transport (across membrane)
    Passive or active; requires transport protein in membrane
  8. Why can't anything hydrophilic or large pass thru a membrane alone?
    They MUST have a transport protein
  9. Diffusion (definition)
    Movement of a substance from an area of high concentration to low concentration
  10. How do molecules with no electrical charge diffuse?
    Diffuse down or along the chemical concentration gradient of the molecule
  11. How do charged ions and molecules diffuse?
    • -Diffuse based on electro-chemical gradient
    • -Chemical concentration gradient is one driving force
    • �Electrical concentration gradient is another driving force
    • -----positives go from positives to negatives on gradient
  12. Diffusion in body fluids (examples)
    • -O2 moves from lungs into blood, into interstitial spaces, into cells
    • -CO2 moves from cells into interstitial spaces, into blood, out through lungs
    • -Water moves across epithelium of digestive tract into body tissues
    • -Anesthetics diffuse into cells
  13. Do membranes need to be permeable to the substance for diffusion to occur?
  14. Diffusion: Lipid Bilayer of cell membranes
    • -permeable to O2, CO2 and most hydrophobic molecules (steroids)
    • -NOT permeable to most large molecules and most hydrophilic molecules (glucose, glycerol)
  15. What do membrane proteins provide for diffusion?
    They provide channels for passive diffusion
  16. Osmosis
    • -Diffusion of water across a semi-permeable
    • membrane in response to solute differences
    • -Concentration of water is related to total concentration of all solutes (dissolved materials) including ions, proteins,
    • monomers, polymers, etc.
    • -Water moves by diffusion down its concentration gradient
  17. Water diffuse from _____________ to ______________
    low solute concentration to high solute concentration
  18. Osmotic Pressure
    The force of water movement into a solution (pulling)
  19. Solute
    Something that is dissolved in a liquid
  20. Tonicity
    The effects of extracellular solutions on cells
  21. Isotonic solution
    No net osmosis, no net gain or loss of water (equail in and out - RBC's)
  22. Hypotonic solution
    • Net gain of water into cell
    • -Can result in cytolysis (add too much H2O to inside, overfilling cell - may burst)
  23. Hypertonic solution
    • Net flow out of the cell (way more solutes outside of cell)
    • -Can result in crenation (shrivels) - extreme dehydration
  24. Hypotonic extracellular solution (low tone)
    • Less solutes, more water than intracellular solution
    • -Water will flow INTO the cell
  25. Hypertonic extracellular solution (high tone)
    • More solutes, less water than intracellular solution
    • -Water will flow OUT of cell
  26. Factors Influencing Diffusion
    • *Distance � concentration gradients effective only over short distances � few cells are more than 125 �m from a blood vessel
    • *Diffusion is faster if
    • -Molecule is smaller
    • -Temperature is higher
    • -Concentration gradient is higher
    • *For charged ions, concentration gradient is one driving force, electrical gradient is another driving force
    • ---very fast during exercise
  27. Diffusion (in a solution or across a membrane)
    • -Passive (going down gradient)
    • -Random motion of substances down their chemical or electrical concentration gradient
    • -Channel proteins allow diffusion of some hydrophilic substances across membranes
  28. Carrier mediated transport (across membrane)
    • -Passive (down gradient) or active (across or up gradient)
    • -REquires transport protein in membrane
  29. Carrier mediate transport
    • -Membrane proteins biund and transport specific molecules or ions
    • -Many carrier proteins transport one substance, one way only; some fo two at same time
  30. Specificity
    Carrier proteins are generally specific for a particular substance
  31. Saturation limits
    Rate of transport subject to number of transport proteins available
  32. Regulation
    Various control factors exist that affect activity of carrier proteins
  33. Cotransport
    • Both go same directions across membrane
    • -uses less ATP
  34. Counter-Transport
    • Go opposite directions across membrane
    • -Restores balance
  35. Facilitated Diffusion (across membrane)
    • -Substance moves DOWN conc. gradient (E supplied, no ATP)
    • -Requires transport proteins (diff transport proteins for diff substances)
    • -Differs from simple diffusion b/c of transport proteins (maximum rate is dependent on availability of transport proteins-can reach saturation)
  36. Facilitated Diffusion (w/ co-transport against conc. gradient)
    • -One substance moves down its conc. gradient (E supplied, no ATP)
    • -Another substance moves against its conc, gradient (E supplied)
    • -Requires transport protein
  37. Active transport (across membrane)
    • -Consumes ATP
    • -Independent of Conc. gradient
    • Examples: Ion pumps, secondary active transport
  38. Trans-membrane potential
    • -Difference in electrical potential between inside and outside a cell
    • --Outside more (+), inside more (-) -->resting membrane potential
  39. Electro-chemical gradient
    • -Sum of forces of all chemical and electrical gradients acting across the cell membrane
    • --->work together to make ONE gradient
  40. Bio-electricity in nerve and muscle cells
    • -Ion flow is a form of electrical current
    • -Ions move across the membrane through protein channels
    • --Driving force is diffusion along electrochemical gradient (trans-membrane potential is equivalent of a battery)
  41. Gated channels
    Open in response to various stimuli
  42. Chemically regulated (gated) channels
    Open or close when they BIND specific chemicals
  43. Voltage regulated (gated) channels
    • Open of close in response to level of trans-membrane potential
    • --only open if change in chemical charge
  44. Acetylcholine (ACh) gated sodium ion channel
    • -Neuromuscular junction � synapse between nerve cell and muscle cell
    • -Nerve cell process releases acetylcholine by exocytosis
    • -ACh binds to receptor on gated sodium channels in muscle membrane, causing sodium channel to open
  45. Ex. of Voltage regulated gated channel
    • -Found in excitable membranes, those capable of having action potentials, closed at resting potential
    • -Nerve cells and muscle cells are excitable
  46. Voltage regulated ion channels
    -Change in level of trans-membrane potentialopens or closes voltage regulated ion channels
  47. Depolarization
    Trans-membrane potential becomes LESS NEGATIVE (inside of cell becomes more positive)
  48. Hyperpolarization
    Trans-membrane potential becomes MORE NEGATIVE
  49. Repolarization
    Trans0membrane potential returns toward resting potential after being depolarized
  50. Skeletal Muscle
    • Attached to bone
    • -Striated, voluntary
  51. Cardiac Muscle
    • Found in the heart
    • -Striated Involuntary
  52. Smooth Muscle
    • Lines hollow organs, blood vessels, iris of eye, GI tract, uteris and ureter
    • -Nonstriated, invlountary
  53. Skeletal Muscle functions
    • -Produce skeletal movement
    • -Maintain posture and body position
    • -Support soft tissues
    • -Guard entrances and exits
    • -Maintain body temperature
    • -Nutrient Reserves
  54. Origin and Insertion
    • (attached to bone by tendon)
    • O-attached to bone that remains relatively stationary during movement
    • I-attached to bone that moves
  55. Synergistic muscles
    Muscles that work together for movement
  56. Antagonistic muscles
    • Muscles that work opposite (have opposite effect)
    • -Flexors AND extensors
  57. Endomysium
    Covers individual muscle fibers (plasma membrane)
  58. Perimysium
    • Sheathes bundles of muscle fibers (muscle fasicles)
    • -contain blood vessels and nerves
  59. Epimysium
    • Surrounds a muscle
    • -contains blood vessels and nerves
  60. Deep fascia
    • Wrap groups of cooperating muscles together
    • -Fascicles separated by Connective TIssue
  61. Muscle cell = ___________
    muscle fiber
  62. Each muscle cell is as long as _____________
    • the muscle
    • -Multinucleate, very long cell
  63. Skeletal muscle cells are formed during _______
    -embryogenesis (by end-to-end fusion of uni-nucleate myoblasts)
  64. Myoblasts
    Fuse together to make one long muscle with mulit-nuclei
  65. Adult muscle repair is _________
    • limited
    • -New skeletal muscle cells come from stemm cells called SATELLITE CELLS
  66. Satellite cells
    • Stem cells for muscle repair
    • -Will divide and try to repair muscle injuries BUT doesn't repair quickly and scar tissue may form faster
  67. Myofilaments
    Protein filaments. Large quantities of myofilaments compose the muscle fiber
  68. Myofibrils
    • Bundles of myofilaments (proteins)
    • -Can actively shorten; anchored to inner surface of sarcolemma at either end of cell
  69. Actin has _______ myofilaments
    thin, skinny strands
  70. Myosin has _________ myofilaments
  71. Sarcoplasm is the ______________ and is _______ to the muscle
    muscle cell membrane, specific
  72. Sarcolemma is the ______________
    cell membrane (it's very excitable)
  73. Sarcoplasmic REticulum (SR) holds __________
    Calcium reserves (it's a modified ER)
  74. Sarcolemma's T-tubules
    • -Make muscle contract quickly together
    • -NArrow tubes of sarcolemma that extend into cell at right angles to cell surface
    • -Conduct action potential deep into cell
    • -COmes in close contact with SR
  75. SR=Lots of _____________; forms a ____________________ around each myofibril
    • -Calcium (stores high conc. of ions needed for contraction);
    • -tubular network (completely surrounds actin and myosin. Terminal cisternae form triads with T-tubules)
  76. Sarcomeres
    • Repeating units of myofilaments in myofibril
    • -Arrangements of actin and myosin in fiber/cell
  77. Striated sarcomeres
    -Differences in distribution of thick and thin myofilaments gives banded appearance
  78. I-bands
    • lIght bands
    • -contain only thin filaments
  79. A-bands
    • dArk bands
    • -contain thick filaments, and some overlap with thin filaments
    • -H band contains only thick filaments
  80. Z disk (line)
    border between sarcomeres
  81. Muscles shorten during contraction because:
    The mysoin and actin filaments slide between each other to shorten each sarcomere
  82. How do you make muscles bigger?
    Adding/producing more myofibrils
  83. What are responsible for muscle contraction?
    Interactions between thin and thick sarcomere filaments (actin and myosin)
  84. Thin filaments slide over thick filaments shortening the _____________
  85. Myofibrils consist of thousands of ____________ end to end
  86. Shortening occurs in every ___________ in the myofibril, thus shortens the __________
    sarcomere, myofibril
  87. When is the sarcomere at maximum shortening?
    • When it is the width of the A band, no I band or H band is visible
    • --Actin has maximally overlapped myosin
  88. Thin actin filaments are attached to __________
    Z disk
  89. What occurs as actin filaments move toward center of sarcomere
    • -Thin filaments slide over thick filaments (myosin)
    • -Z lines are pulled closer together
    • -I bands and H bands are narrow
    • -A band stays the same width
    • ----The area with no myosin gets really small
  90. What causes thin and thick myofilaments to slide across each other?
    -Cross bridges are formed and pull the actin over the mysoin
  91. Cross bridges
    • -When myosin heads bind to the active site of actin
    • -Once formed, they change the sahpe pulling actin past the myosin
    • -Use ATP to change shape and pull the actin - convert chemical energy to mechanical energy
  92. Molecular anatomy of Myosin
    • -Have elongated tail, globular head - golf club shape
    • -arrayed with half facing each end, center is just tails
    • -Heads form cross bridges during CONTRACTION
    • -Interactions between myosin and actin prevented by tropomysin during rest
  93. Tropomyosin
    • Protein that sits on top of active sites of actin, prevents cross bridges
    • -Attached by troponin (protein)
  94. Molecular anatomy of Actin
    • -Twisted strand composed of two rows of individual globular actin molecules
    • -Each actin molecule in twisted strand has active site to which myosin head can attach (only attracted to head)
    • -Strands of tropomyosin cover the actin active site during rest
  95. Calcium is the _______that binds to ____________to unlock ___________, revealing the active site of actin
    key, troponin, tropomyosin
  96. Sliding filament theory
    • -Cyclic process beginning with CALCIUM release from SR
    • --Calcium binds to troponin
    • --Troponin moves, moving tropomyosin and exposing actins active site
    • --Mysoin head forms cross bridge to actin, bends toward center of sarcomere, pulling the actin closer to the M-line
    • --ATP allows release of cross bridge
  97. What's the role of ATP in muscle contraction?
    • -ATP supplies the E for the movement of the mysoin head (converts chem E to mechanical E of movement)
    • -ATP bins to un-energized myosin head (ATP is split to ADP&P, mysoin head moves into energized position)
    • -Mysoin head in energized position binds to actin active site (releases ADP&P, pivots, pulling on and actin)
    • -ATP binds to un-energized myosin head (detaches mysoin from actin, Actin is split and head is energized)
  98. Role of Calcium ions in muscle contraction?
    • -Concentration of Ca2+ around sarcomere controls contraction
    • -Ca is low around sarcomere at rest
    • -Action potential in sarcolemma and T-tubules result in contraction (opens Ca channels in SR, releases Ca in sarcoplasm)
    • -Ca binds to troponin
    • -Mysoin heads bind to active site until Ca levels fall
    • -When Ca levels fall: tropomyosin covers actin ending contraction
  99. Motor neuron
    • Nerve cell that controls muscle contraction
    • --once depolarized it realeases acetyl choline
    • --action potential initiated in motor neuron in response to CNS commands
  100. Neuromuscular junction
    • Synapse between motor neuron and muscle cell
    • --every muscle fiber has it's own neural junction
  101. Action potentials travel through ______ ________ and arrives at the ______ ______.
    motor neuron, synaptic terminal
  102. Acetyl Choline (ACh) is released from ____________ and diffuses across _____________, then binds to receptors on ________ gated socium channels in muscle membrane
    motor neuron terminal, synaptic gap, chemically
  103. Sodium ions flow into muscle cells causing it to __________
    Depolarize (an action potential starts in the muscle cell)
  104. Chemically regulated gates stay open as long as ______ is present
    ACh (acetyl choline)
  105. Acetylcholine Esterase (AChE) location and function
    • -lovated in synaptic gap
    • -rapidly breaks down AcH (stops contraction by 'gobbling' up ACh and closing gates)
  106. Action Potential in muscle cell membranes are conducted intot he interior of the muscle via __________ and cause Ca2+ to be released from _____.
    T-Tubules, SR
  107. Action potential along ______ causes release of calcium from ______ of SR
    T-tubule, cisternae
  108. Excitation/contraction of muscle cycle repeats until ________ ion concentrations fall to rsting level.
    • Calcium
    • -high frequenct creates a stronger contraction
  109. How does Ca ion concentration return to resting level?
    • -AP depolarization ends, voltage gated Ca channels in SR close (Ca flow in sarcoplasm stops)
    • -Ca is actively transported out of sarcoplasm
    • ---some acros sarcolemma to outside of cell (requires ATP)
    • ---across SR to reticulum membrane into SR (requires ATP)
    • ---Requires ATP for active transport protein to function
  110. Duration of contraction depends on:
    • 1. Duration of stimulation at nerve-muscle synapse (neuromuscular junction)
    • 2. Fresence of calcium ions in sarcoplasm (contraction cycle continues until Ca ion conc. returns to resting levels)
    • 3. Availability of ATP (No ATP = contraction cycle stops no matter what)
  111. Conraction ends and relaxation occurs when:
    • 1. AP stops in motor neuron
    • 2. AChE breaks down ACh in the neuromuscular synaptic gap
    • 3. ACh gated channels close (Na is no longer diffusing into cell)
    • 4. Action potentials stop occuring in sarcolemma and T-tubules
    • 5. Ca levels in sarcoplasm return to resting levels (no new cross bridges can form)
    • 6. Relaxation requires ATP (to pump Ca into SR, to discunnect myosin heads from actin, no ATP=rigor mortis)
  112. How does botulism affect ACh?
    Blockage of release of ACh
  113. Polio (Muscular system disorders)
    Loss of motor neuron
  114. Myasthenia gravis (Muscular system disorders)
    • Interference with binding of ACh to receptors
    • -muscles don't resoind
  115. Prolonged contraction (Muscular system disorders)
    Interference with ACh Esterase activity
  116. Peripheral nerve damage (Muscular system disorders)
    loss of motor neuron axon
  117. MS (Muscular system disorders)
    Reduction of AP efficiency, damage to myelin
  118. Tetanus (Muscular system disorders)
    • Excessive stimulation of motor neuron
    • -send to much ACh
  119. Tension
    • Sliding and pulling of actin and myosin filaments causes sarcomere shortening
    • -in a muscle cell, all sarcomeres shorten causing the muscle cell to shroten
    • -Pulls on CT and bone that it's attached to
  120. Tension in a muscle cell depends on:
    • -Tension that develops in individual muscle cells during contraction
    • -Number of muscle cells that contract (neighbor cells may not contract)
    • --muslce cells are grouped in motor units
  121. Amount of tension depends on number of ______ _______ formed
    • cross bridges
    • --depends on degree of everlap of actin and myosin
  122. Skeletal muscle contracts _____ forcefully over narrow ranges of resting ________
    most, lengths (overlap)
  123. Twitch (quick contraction)
    • -Cycle of contraction, relaxation produced by a SINGLE action potential in a muscle cell
    • -Not typical in normal muscle cell activity
    • --can only be seen on a dissected muscle and forcing it to twitch
  124. Latent phase (twitch)
    • Action potential occurs
    • -No contraction until Ca is released from SR
  125. Contraction Phase (twitch)
    • Tension rises to peak
    • -Ca moves tropomyosin off of actin sites
    • -Myosin cross bridges form, actin is pulled
  126. Relaxation Phase (twitch)
    • Tension fails to resting levels
    • -Ca is pumped back into SR
    • -Actin sites covered by tropomyosin
    • -No cross bridges remain
  127. Summation of tension produces ____________________
    • greater tension
    • -sum is greater than its individual parts
  128. Summation
    • Repeated stimulation produced before relaxation phase has been completed
    • -summation of tension caused by build up of Ca ions in sarcoplasm
  129. Complete tetanus
    Maximum tension production in a muscle cell-maximum cross bridge formation
  130. Atrophy
    • muscle become smaller (lack of use)
    • -decrease in diameter of a muscle
  131. Hypertrophy
    • Muscle become larger
    • -increase in diameter of muscle (adds more myofibrils)
  132. Motor units (muscle tension)
    • -All muscle fibers innervated by one motor neuron
    • -Amount of tension produced in a muscle determined by number of motor units activated (Max tension-all motor units active)
    • -Asynchronous motor unit summation for sustained contractions (allows one to relax while others are still active)
  133. Differences in number and size of motor units in different muscles determines what?
    Precision of control of movements
  134. Small motor unit=?
    • Precise control
    • -One motor neuron innervates a small number of muscle fibers - Fine motor skills
  135. Large motor unit=?
    • Gross movement control
    • -One motor neuron innervates a large number of muscle fibers
  136. Muscle Tone
    • Resting tension in a skeletal muscle
    • -In any muscle some motor units are always active, tense and firm
    • -Stabilizes bones and joints
    • -Greater resting muscle tone causes higher resting rate of metabolism
  137. Why is it difficult to contract a muscle that has been overstretched?
    Few if any mysoin-actin cross bridges can form when sarcomeres are overextended
  138. Isotonic Contracion
    Tension rises, length of muscle changes (gets shorter or longer)
  139. Concentric
    Muscle tension exceeds resistnace and muscle SHORTENS
  140. Eccentric
    Peak tension developed is less than the resistance, muscle ELONGATES
  141. Isometric Contraction
    • Tension rises, length of muscle remains constant
    • -Tension produced never exceeds resistance
    • -Muscle as a whole doesn't shorten until individual fibers shorten until internal CT and tendons are rigid
    • -Cannot shorten further b/c tension doens't exceed resistance
  142. No ______ mechanism for muscle fiber elongation
    • Active
    • -A muscle cell doens't cause itself to lengthen after contraction process ends - relaxes
  143. Muscle returns to resting length after contraction because:
    • -Recoil in elastic components in CT
    • -Contraction of opposing muscle groups
    • -Gravity
  144. How often must cells regenerate ATP?
    Muscle cell must generate ATP at apporximately the same rate as it is used for the remainder of contraction
  145. What are Creatine Phosphate reserves for
    • -ATP isn't used for long term storage of E
    • -At rest, muscle cell makes more ATP than needed, extra ATP transfers P to creatine for storage
    • -CP reserves release stored energy to convert ADP to ATP when ATp is needed at start of contraction
  146. ________ _________ provides most ATP needed for resting muscle and for moderate levels of muscle activity
    Aerobic repsiration (PRESENCE OF O)
  147. At peak activity, alson need _______ (glycolysis) to generate additional ATP
    • Anaerobic
    • ----In addition to aerobic!!!
  148. Aerobic Metabolism
    • -Cellular Respiration (Uses O2- Releases CO2)
    • -Occurs in Mitochondria: Citric Acid Cycle (CO2 produced), ETC (ATP synthesis, O2 used)
  149. Resting muscle fibers rely on ________ metabolism of _____ ______ to generate ATP
    • Aerobic, fatty acids
    • -FAtty acids absorbed from circualtion
    • -Broken down to Acetyl CoA
    • -Excess aTP used to store glucose into GLYCOGEN, creates Creatine Phosphate
  150. Contracting muscle cell fibers rely on _____ AND ______ metabolism of glucose
    Aerobic, anaerobic
  151. Anaerobic Metabolism
    • -Produces ATP rapidly (allows muscle cell to generate extra ATP when aerobic isn't enough)
    • -Disadvantages: Inefficient use of glucose, lactic acid LOWERS intracellular pH (donates H electrons)
  152. Recovery Period
    • -Begins immediatley after activity ends
    • -Oxygen debt (excess post-exercise O consumption - panting)
    • -Rebuild ATP and CP levels
    • -Recycle lactic acid to make pyruvate
    • -Rebuild glycogen reserves
  153. People in good condition make more __________, making them able to exercise more.
  154. Fatigued muscle
    A muscle that can no longer perform a required level of activity
  155. Causes of muscle fatigue
    • -Exhaustion of E resources
    • -Build up of lactic acid and lowering of pH (acidosis)
    • -Psychological fatigue
  156. Force
    (Power, strength) Maximum amount of tension produced by a muscle or muscle group
  157. Endurance
    • Amount of time during which an individual can perform a particular activity
    • -size doesn't matter, efficiency does(amount of mitochondria)
  158. Factors that determine performance capabilities of skeletal muscle:
    • 1. Types of muscle fibers present in the muscle
    • 2. Physical conditioning or training
  159. Types of muscle fibers (3):
    • 1. Type 1-Slow fibers (Red)
    • 2. Type 2-A-Intermediate fibers
    • 3. Type 2-B-Fast fibers (white)
  160. Red fibers
    • Type 1; Slow twitch oxidative fibers
    • -Have lots of mitochondria (efficient without O)
    • -Rich blood supply (why it's red)
    • -"legs of the chicken"
    • -Low prolonged movements, marathons
  161. White fibers
    • Type 2-B; fast twitch glycolytic fibers
    • -Most efficient: anaerobic (glycolysis only)
    • -For quick movements, sprinting
    • -"Breast meat of chicken"
    • -Large in diameter
  162. Slow fibers are _____ the diameter of fast fibers
  163. Slow fibers have a high concentration of ________ and can contract for ______ periods of time
    Myoglobin (binds O in muscles-makes more red and has iron), long
  164. Slow fibers have abundant ________, and take ______ times as long to contract after stimulation
    Mitochondria (aerobic, oxidative metabolism), three
  165. Slow fibers are _______ resistant meaning they can contract for long periods of time
  166. Fast fibers have large ______ reserves and contain densely packed _______
    glycogen, myofibrils (tons of actin and myosin)
  167. Fast fibers have few _______ making them prone to _________ metabolism
    mitochondria, anaerobic (glycolytic metabolism)
  168. Fast fibers produce ______, powerful contractions of ______ duration making them ________ rapidly
    rapid, short, fatigue
  169. Pink fibers
    • Fast twitch oxidative fibers - Type 2-A
    • -Fast fibers that gain greater resistance to fatigue
    • --Have additional capillary supply
    • --More mitochondria
    • --Smaller in diameter
    • --Not as dependant on anaerobic metabolism
    • -Adapt to endurance
  170. We are born with a unique amount of each of the three fibers, however, which fibers can be CONVERTED?
    -White(fast fibers) to pink (intermediate) but NONE TO WHITE
  171. Percentage of slow fibers and fast fibers are ________ determined and can vary among muscles
    • genetically
    • -Pale (white) muscles:mostly fast fibers
    • -Dark (red) muscles:dominated by slow fibers
  172. Training can change the percentage of _______ fibers that have intermediate properties to build endurance
  173. Change in muscle size is due to an increase or decrease in ________ of muscle fibers within the muscle
    • Diameter
    • -Based on activity level
  174. Muscle Fiber A is 2x the diameter of Muscle Fiber B. A can produce greater tension than B because:
    A has more myosin to actin cross bridges forming during a contraction
  175. Anaerobic Endurance
    Time period in which muscular contractions are sustained by GLYCOLYSIS after depeting ATP/CP reserves
  176. Aerobic Endurance
    Time period in which muscle can continue to contract while supported by MITOCHONDRIAL activites after depleting ATP/CP reserves
  177. How do you improve Anaerobic Endurance
    • -Frequent, brief intensive workouts
    • -Increase muscle mass
    • -Increase ATP/CP reserves
    • -Increase glycogen stores
    • -Increase ability to tolerate lactic acid buildup
  178. How do you improve Aerobic Endurance
    • -Sustained low levels of activity
    • -Increase blood supply to muscles
    • -Imporve cardiovascular activity
  179. Primary disorders
    • Result from problems with the muscular system itself
    • -Muscle trauma
    • -Muscle infections
    • -Inherited disorders
    • -Tumors
  180. Secondary disorders
    • Result of problems originating in other systems (mostly nervous system)
    • -NS disorders that affect the coordination or control of muscle contraction (MS)
    • -Nutritional or metabolic problems that affect electrolyte concentrations of the available E supply (spasms and cramps)
    • -Cardiovascular disorders that restrict or reduce blood flow to skeletal muscles
  181. Most muscle disorders are __________ disorders
  182. Muscle spasm (cramp)
    • Strong, sudden, usually painful, unwanted CONTRACTION
    • -Mostly from electrolyte imbalance
  183. Muscle spasticity
    • Excessive muscle tone
    • -Muscles contract at rest to make it look more tone
  184. Muscle flaccidity
    • Very low muscle tone
    • -Muscle doesn't contract at rest
  185. Muscle atrophy
    Deterioration or wasting due to disease, immobility, or interference with normal motor neuron innervation (of acetyl choline)
  186. Myositis
    • Muscle inflammation (swollen)
    • -Polymyositis & dermatomyositis - autoimmune
  187. Muscle Strain
    • Tears in muscle tissue
    • -Usually can repair itself
  188. Muscle sprain
    Tears in ligament or tendon or joint capsule
  189. Paralysis
    • Loss of voluntary motor control
    • -Flaccid or spastic (can be from excessive spasming)
  190. Blockage of release of Acetyl choline results in ________ paralysis (ex. botulism)
  191. Interference with binding of ACh to receptors results in _______ paralysis
  192. Interference iwth ACh Esterase activity results in _______ paralysis
  193. Loss of motor neuron results in ______ paralysis (ex. polio)
    Flaccid (increased branching of remaining motor neurons
  194. Loss of motor neuron axon results in _______ paralysis (ex. peripheral nerve damage)
  195. Excessive stimulation of motor neuron results in _______ paralysis (ex. tetanus)
  196. Muscular dystrophies
    • -Duchenne's MD-gene on X chromosome
    • -Early onset
    • --Don't do transcription and translation properly
    • --Dystrophy if formed improperly affects actin, myosin, all protein for muscles
  197. Myotonic dystrophy
    • -Chromosome 19 disorder
    • -Typically onset is after puberty
    • --Don't do transcription and translation properly
    • --Dystrophy if formed improperly affects actin, myosin, all protein for muscles
  198. Compartment syndrome
    • Bleeding/inflammation in muscle
    • -Swelling damages cells in same compartment
  199. Minor trauma to muscles:
    Damage to myofibrils, sarcolemma from excessive activity
  200. Major trauma to muscles:
    Lacerations, crushing, deep bruise, muscle tear (strain)
  201. _______ problems can affect the energy supply available to the muscles from _________, like anorexia or bulimia
    Nutritional, starvation
  202. __________ problems can affect electrolyte concnetration, like dehydration or kidney disease
  203. Hyper
    to much/high
  204. Hypo
    To little
  205. Which organ systems are smooth muslces present
    • -Integument (blood vessels, arrector pili)
    • -Cardiovascular (help regulate bp)
    • -Respiratory
    • -Digestive
    • -Urinary
    • -Reproductive (uterus)
  206. Muscle ____________ moves everything
  207. Synctium
    • Fused mass of cells
    • -Most tissues
  208. Skeletal muscle is formed by ________________ cells which are formed by the fusion of many myoblasts during embryogenesis
  209. Cells are linked by _________ (endomycium) that fuse to form tendons
    connective tissue
  210. Cardiac muscle cells are linked by ________ and desmosomes into funcitonal synctium
    gap junctions
  211. Smooth muscle cells are linked by gap junctions and ____ ______ into functional synctium
    dense bodies (unique to smooth muscle, proteins where actin attache-no sarcomeres)
  212. Which muscle type DOESN'T have sarcomeres?
    Smooth muscle
  213. Smooth Muscle thick filaments are _________ throughout sarcoplasm
  214. Smooth Muscle thin filaments are attached to _____ _______
    Dense bodies
  215. Dense Bodies
    • -Some at intersections of cytoskeletal framework
    • -Some firmly attached to plasma membrane
    • -Dense bodies can link adjacent muscle cells (communicate cell-cell)
  216. Sliding of thick and thin filaments in smooth muscle causes cell to ______ and _______ (ex. stomach)
    shorten, twist
  217. Plasticity
    • Strectched muscle adapts to new length and retains ability to contract and produce tension
    • --adapts to change
  218. Smooth Muscles can undergo sustained _______ contractions
    • Tetonic
    • -All action potentials sum up and hold a HARD contraction ex. labor, vomitting
  219. Skeletal muscles are controlled by _____ _______ of voluntary nervous system
    motor neurons
  220. Cardiac muscles are controlled by _________ cells, autonomic nervous system
    • Pacemaker
    • --Can contract on own outside of body
  221. Smooth muscles are controlled by ______ cells, hormones, autonomic nervous system
  222. Rate of pacemaker cells and amount of tension can be modified by __________ nervous system
    • autonomic
    • -Innervated by motor neurons of ANS (sympathetic, parasympathetic)
  223. Visceral smooth muscle cells
    • -Connected by gap junctions into large synctia arranged in sheets or layers
    • -Automaticity-Pacesetter cells can trigger rhythmic contractions (local reflex)
    • -Stimuli from autonomic nervous system can control contraction frequency
  224. Multi-unit smooth muscle cells
    • -Not connected by gap junctions
    • -Each cell innervated by one or more motor neurons of the autonomic nervous system
  225. Skeletal muscle E source
    • -Aerobic metabolism at moderate activity
    • -Anaerobic enhances metabolism at peak activity
  226. Cardiac muscle E source
    -Aerobic metabolism ONLY (myoglobin and mitochondria content is high)
  227. Smooth muscle E source
    • -Aerobic metabolism at moderate activity (typical)
    • -Anaerobic metabolism enhances during peak activity (rare)
Card Set
Anatomy - Exam 2.txt
anatomy lecture notes for exam 2