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GRCC BI121 lec #3
GRCC BI 121 muscles Exam 3
| Question | Answer |
|---|---|
| Types of muscles | Skeletal, cardiac and smooth |
| Muscle functions | contract, thermoregulate and protection from trauma |
| e.g. of how muscles protect from trauma | major nerves and vessels |
| Skeletal muscles | movement of skeleton |
| What type of muscle has rapid contraction and rapids fatigue | Skeletal muscles |
| Skeletal muscles are attached to ? | Usually attached to bone (except rectus abdominis) |
| Are skeletal muscles involuntary or voluntary? | They are voluntary |
| Muscles that enable movement withing hollow organs | Smooth muscles |
| e.g. of smooth muscles | Intestines, stomach, vessels, bronchioles |
| Which mucsle is slow contraction and slow fatigue? | Smooth muscle |
| Think birth contractions | Smooth muscle moves slow, so its good they fatigue slow too because this can be a long drawn out situation |
| are smooth muscles voluntary? | No, they are involuntary...think uterus contractsion and menstral cramping. |
| where would you find smooth muscles? | organs, vessels, and dermis |
| Cardiac muscles | help with circulation |
| Are cardiac involuntary or voluntary? | Involuntary |
| These muscles are rapid contraction and no fatigue | Cardiac muscles |
| A muscles with no fatigue? | Cardiac...it is constantly contracting....if it stops we die....so it can't fatigue. |
| skeletal muscle connective tissue anatomy | Think layers of cylinders within cylinders |
| First layer of muscle tissue - very thing covering | fascia |
| fasica | connect tissue covering individual muscles |
| Tendon | Extends from fascia to the end of perimysium, that attaches bone to muscle. |
| Aponeuroses | Broadsheets of CT that attach adjoining skeletal muscles. |
| Epimysium | irregular CT on surface of muscles. |
| Perimysium | CT that seperates fascicles |
| Endomysium | CT that seperates fibers (cells) within fasciae. |
| fascia - epimysium - perimysium - _____________ | endomysium |
| ________ - epimysium - perimysium - endomysium | fascia |
| fascia - ______________ - Perimysium - endomysium | epimysium |
| fascia - epi- ______________- endo | Perimysium |
| CT muscle layers | fascia- epimysium - perimysium - endomysium |
| Muscle Heiarchy preview | whole muscle - fascicle - fiber - myofibrils - sarcomeres |
| whole muscle - _____________ - fiber - myofibrils - sarcomeres | fascicle |
| Whole muscle - fascicle - _________ - myofibrils - sarcomeres | fiber |
| ________- fascicle- fiber - myofibrils - sarcomeres | whole muscles |
| Whole muscles - fasicles - fibers - myofibrils - ________ | sarcomeres |
| Whole muscles - fasicles - fibers - ____________ - sarcomeres | myofibrils |
| Whole muscles | made up of fasicles |
| e.g. of whole muscle | sartorius |
| Fasicicles | Bundles of muscle fibers (cells) |
| a fusion of muscle nuclei making a bundle of fibers | fasicles |
| muscle fibers | within a fascicle and are muscle cells |
| Components of muscle fibers | sarcaolema, sarcoplasm, myofibrils |
| Sarcolema | Component of a muscle fiber; it is the cell membrane of muscle cells |
| Sarcoplasm | Component of the muscle fiber; it is the cell cytoplasm of muscle cells |
| myofibrils | component of muscle fibers; contractile units |
| this plays a fundamental role in muscle contraction mechanism | myofibrils is a component of muscle fibers. |
| muscle fibers are torn= | muscle strain |
| torn fascia and torn fibers = | damage cell membrane (sarcolema) and fascia, etc |
| Torn muscle fibers result in what? | minor muscle strain. |
| If many fibers and fascia tears, then what results? | severe muscle strain. |
| Dystrophin | duct tape that holds muscles together and keeps them from tearing apart |
| What prevents tearing of sarcolema during contraction? | Dystrophin |
| A skeletal muscle protein dysrtophin prevents what | prevents tearing of sarcolema during contraction. |
| Duchenne MD does what | it does not produce dystrophin. |
| What happens without dystrophin | sarcolemas tear or burst- muscle cells die |
| What do people with skeletal muscles usually die from? | suffocation- cuz the lungs are protected by rib cage....surrounded by skeletal muscle. |
| sarcomeres | Repeating segments of myosin and actin. The actual site of contraction. |
| what is the actual site of contraction? | sarcomeres |
| what are the components of sarcomeres? | Myosin (thick filaments), Actin (thin filaments), Sarcoplasmic reticulum, cisternae |
| Thick filament | myosin |
| myosin, a component of sarcomere | thick filamentous contractile proteins with cross bridges |
| Thin filament | actin |
| actin, a component of sarcomere | protein back bone of thin filaments |
| Components of actin | tropomyosin, troponin |
| tropomyosin | blocks cross bridge binding sites action and |
| Troponin a component of actin | controls position of tropomysin |
| Troponin in blood | Death of tissue due to MI- death tissue decomposes into blood |
| if troponin is found in blood | then pt had an MI |
| sarcoplasmic reticulum and cisternae | Modified endoplasmic reticulum with increased levels of Calcium ions |
| cisternae | stores calcium ions which are essential for muscle contractions. |
| Sliding filament theory | sacromere shortens, but the thick & thin filaments do not change length, instead they slide past one another |
| Thin filaments movement towards ? | center of the sarcomere...from each end. |
| what happens when there is a motor impulse to motor neuron | thin filaments move towards center of sarcomere and the muscle shortens (aka sliding filament theory) |
| do thick and thin filaments shorten? | no, the slide on top of one another...think about intertwining fingers from left and right hand..bring them close to gether, the length is shorter..not the fingers |
| Nueromuscular junction | Motor neuron, motor end plate, synaptic cleft |
| motor nueron, motor end plate, synaptic cleft | known as a motor unit (all three are components make up neuromuscular junction) |
| Disease of motor neuron | Poliomyelitis |
| poliomyelitis | a viral infection of the motor neuron resulting in paralysis of the infected muscles |
| What are thick filaments responsiblity? | It grabs thin filaments and brings them together. |
| Muscle impulse transmission | ACh released from motor neuron & recived by motor end plate & then muscle impulse relayed to muscle contracts |
| Threshold stimulus | the minimum chemical stimulates to cause contraction |
| An autoimmune disorder that attacks ACh | Myasthenia gravis (MG) |
| MG | An autoimmune disorder that attacks ACh receptors on muscle cells resulting in muscle weakness and possible death. |
| with MG, ACh recepters are killed by autoimmune results in what? | ACh has nothing to attach to so they cant work |
| MG and Polimyelitis could lead to what type of demise? | suffocation |
| How does nerve gas affect ACh recepters | they are blocked causing muscle weakness and possible death via suffocation. |
| What does nerve gas do to prevent ACh from working properly? | Mimics ACh shape and docks with receptors instead of ACh |
| Calcium is stimulated by? | ACh |
| Details of contraction | ACh released- attaches to ACh receptors - muscle impulse releases Ca from cisternae- Ca binds with tropinin-altering position of tropomyosin - actin moves to center |
| Step 1: what happens sfter ACh is released & is recieved by it's recepter triggering a muscle impulse | Muscle impulse releases Ca from cisternae |
| Step 2: what happens to Ca after it is released from muscle impulses? | Ca binds to troponin, therefore, altering tropomysin and exposing binding sites on actin |
| Step 3: what happens after the binding sites on actin are exposed | myosin cross bridges attach to actin and pull, moving the actin to the center of the sacromere and shortening muscle |
| Step 4: what happens after the actin is moved towards the center of the sacromere and shortens muscle? | Cross bridges release |
| How long does the process of contraction work? | As long as ATP, Ca and ACh are present. |
| Details of relaxation | ACh stops, Ca pumps move back to sarcoplasmic reticulum, cross bridges break and tropomyosin moves back into position |
| Step 1 of relaxation | Nervous release of ACh is stopped (AChase breaks down remaining ACh) |
| Step 2 of relaxation | Ca pumps move back calcium back to sarcoplasmic reticulum |
| Step 3 of relaxation | Cross bridges break and tropomyosin moves back into postion (blocking binding sites) |
| What happens several hours post-mortem | cisternae releases Ca and triggers contraction, but crossbridges that release contraction do not release since remaining ATP was used in contraction. |
| Rigor Mortis | Ca Ions are released, inititating cross bridges to attach to actin and pulls (contraction)- due to NO ATP, cross bridges can not release from actin therefore contraction continues |
| what do insecticides do? | Inhibit acetylocholinestrase, without this enzyme, ACh is not broken down = increase ACh leading to uncontrolled muscle contractions. |
| Inhibits AChase, which causes uncontrolled muscle contractions and death | Insecticides lead to too much ACh due to what? |
| How is excess ACh broken down? | by ACh ase |
| ATP is necessary for what? | for both muscle contraction and muscle relaxation. |
| where do muscles get energy from that requires to connect and diconnect the cross bridges? | ambient ATP |
| Ambient ATP | the source of initial contraction and relaxation |
| Supplies energy to recycle ADP into ATP | Creatinine phosphate |
| Is there enough ATP and creatinine phosphates in skeletal muscles to support the muscle activity? | the maximum support of muscle activity is no more than 10 seconds. |
| Once Creatinine phosphates and ATP energy sources are used up, then where does muscle fibers get its energy from next? | Muscle fibers utilize cellular respiration of glucose to synthesize ATP. |
| As ambient ATP and creatinine decrease, cells depend on what? | Depend upon cellular respiration for ATP (from breakdown of glycogen) |
| Hemoglobin (protein) | Oxygen binds to this and transports to the body; in regions of the body where oxygen is low, oxygen is released allowing aerobic respiration |
| Hgb hands of oxygen to where? | Myoglobin (a protein that temporarily stores oxygen in the muscle tissue) |
| Muscle energetics- oxygen comes from where? | Myoglobin (this has a greater oxygen storage than Hgb) |
| what happens when oxygen decreases? | Aerobic respiration stops and anaerobic respiration begins. |
| Energy source overview | Ambient ATP - creatinine phosphate - aerobic respiration - anaerobic resp |
| ______________- creatinine phosphate - aerobic resp - anaerobic resp | ambient atp |
| ambient ATP - creatinine phosphate - ___________ - anaerobic resp | aerobic resp |
| ambient atp - _____________- aerobic resp - anaerobic resp | creatinine phosphate |
| ambient atp - creatinine phosphate- aerobic resp - _____________ | anaerobic resp |
| causes of fatigue | decreased blood flow, decreased Ca ions, perception of fatigue, increase of lactic acid |
| Decreased blood flow | causes Hypoxia and hypoglyemia (low oxygen and glucose) leads to muscle fatigue |
| Decrease calcium ions levels is caused by? | repeated stimualtion/ persistent use of a muscle for a prolonged period of time |
| Perception of fatigue | Psych loss of the desire to continue exercising (nothing has changed...just your perception) |
| Most likelycause of muscle fatigue | Increase lactic acid |
| what does increase lactic acid do? | It decrease Ph (acidity) accumulating in muscles and blood stream leading to stoping contractions. |
| How do muscle cramps occur? | Electrolytes in the extracellular fluid become imbalanced leading to uncontrolled muscle stimulation. |
| An electrolyte imbalance in the extracellular fluid may lead to what? | Uncontrolled muscle stimulation (AKA muscle cramps) |
| Motor unit activation | all or nothing, fibers respond at same time, all motor units may not respond at same time, motor units are recruited as stim levels increase |
| A muscle fiber contracts with same intensity regardless of stimulation level, some of the time, most of the time or all of the time? | All; These always contract regardless; its the all or nothing response. |
| How do muscles fibers of a motor unit respond? | They respond at the same time. |
| How do all motor units respond? | They may not all respond at once |
| What happens when stimulation is increased? | more motor units respond or recruited |
| think weight lifting and motor units | 1st lift is harder- motor units are recruited, the 2nd lift is a bit easier. |
| A single muscle fiber that responds with one complete contraction and relaxation. | muscle twitch |
| Increase of stimulation results in only partial relaxation and increase force of contraction. | summation |
| Think labor and summation | As labor proceeds, the body forces baby out by increased contractions, it can fully relax or the baby will never come out. |
| staircase effect (Treppe) | Increase of contraction force with each stimulus...contractions levels increase- looks like a staircase. |
| tetanus | sustained contractions without relaxation; continous contraction. |
| Anaerobic bacteria (clostridium tetani) | may cause sustained/continous spasms of skeletal muscles resulting in paralysis and death. |
| Colstridium tetani can be introduced via | puncture wound (not a rusty nail) |
| muscle fibers vary in what type of speed? | contraction speed- referred as slow or fast twitches. |
| Type 1 -Slow twitch/red fiber | resistance to fatigue due to increase myoglobin and increased mitochondria there fore aerobic respiration. |
| What is an example of a muscle that is type 1 - slow twitch/red fiber | The back muscles- we use these all day long- they need to be resistant to fatigue to sustain a full day. |
| Type 2a- fast twitch/white fiber | glyco |
Created by:
Wends1984
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