Musculoskeletal systems

  1. We say muscle fiber because fiber is really multiple muscle cells aka ______ that fused _______. So a muscle fiber is the unit of control that we move/control limbs with on a ______ level
    • myoblasts
    • embryonically
    • neuronal
  2. bone to bone = ________
    muscle to bone = _______
    • ligaments 
    • tendons
  3. When we move limbs, what we are really doing is contracting skeletal muscle that is using _____ to pull bone.  Muscles are covered with connective tissue like _______ Muscles have a lot of ______within them. They are a bunch of individual muscle fibers, grouped together.
    • tendons
    • epimysium
    • fascicles
  4. Around fascicles we have another layer of connective tissue called _______. Around the individual layer of muscle fibers, we have _______.
    • perimysium
    • endomysium
  5. At the muscle fiber level, we don’t call it plasma membrane, we call it ______. Inside of cells we have cytoplasm and inside of muscle fibers we have______. Within muscle fibers, we have______.
    • sarcolemma
    • sarcoplasm
    • myofibrils
  6. Muscle fibers are multinucleate because of their ____ the need multiple nuclei to maintain them.
    length
  7. Muscle contraction story
    • Quadriceps (any skeletal muscle) will have axon terminals on them from axons leading back to motor neurons.
    • For example, the quadriceps would an axon fed to it from motor neurons in the lumbar region through the femoral nerve.
    • So when the motor neuron fires an action potential the axon terminal would release transmitter (Ach) where it is connected to the quadriceps (on muscle fibers). Then we get a contraction.
    • Take note that we have axon terminals making contact with more than one muscle fiber that are from the same axon. A motor neuron can only contract muscle fibers that it is connect to in this manner.
  8. When we contract, Z lines get _____. Z lines contain____. Actin is attached to the _______ and beneath actin is _____ (with globular heads) and connected to Titin. Next to myosin, toward the middle we have the ______ Areas where we have actin but no myosin, we refer to as the ____.
    • shorter 
    • titin
    • Z line
    • myosin
    • M band
    • I band
  9. Areas where we have myosin but no actin, we refer to as the _____. _____ is where there is myosin with or without actin. The M band is in the center of the ______. Titin's runs the length of the sarcomere and is one the ______ proteins in the body. As some movements demand stretching of the sarcomere, Titin's job is to _______ the structure of the sarcomere.
    • H zone
    • A band 
    • sarcomere
    • largest
    • maintain
  10. If every sarcomere along the myofibril shortens, the whole muscle fiber will ______ and we will get a contraction. Keep in mind that _____ isn’t attached to the z line so the A band remains the same length. However, myosin's globular heads will pull actin inward toward the _____
    • shorten 
    • myosin 
    • M band
  11. Sliding filament theory story:
    • Actin monomers have binding sites on them for myosin glob. heads depicted as round little dots in the lecture slides. Tropomyosin's is a rope-like structure whose job is to block those binding sites at the appropriate times. Troponin has three subunits, one is attached to the actin monomer, one for tropomyosin and the 3rd is Ca++ sensitive. When Ca++ binds to the 3rd tropinin subunit, troponin will literally change its shape (conformational change). That shape change will cause it to tug tropomyosin out of the way. This will reveal the myosin globular head binding site.
    • Motor unit: one motor neuron and every muscle fiber it has a synapse to.
    • More muscle fibers = more force for example more force in the latissimus dorsi than in the finger muscle, but the trade off is not nearly as fine motor control. The difference is more motor neurons per muscle fiber in the fingers than in the Lats.
    • We can increase the motor unit count for more demanding/ strenuous lifting by recruiting more motor neurons, therefore more motor units. The other way to do it is to fire the motor units more often aka firing more action potential.
  12. massive muscle contraction story
    • Motor neuron fires an action potential leads to the release of Ach from axon terminals to the muscle's nicotinic receptors.
    • Ach is released to what we call the end plate, the portion of the muscle (typically toward the middle of the muscle) where it has special receptors called nicotinic receptors (theyre ligand gated).
    • Ach binds and they open up allowing largely sodium in. The change in voltage is called an end plate potential (EPP).
    • Every end plate potential will be supra-threshold (meaning big enough to open up channels/ get it to threshold). So the nicotinic receptors will always sodium voltage gated channels to action potential.
    • What we will find is nicotinic recpetors facing the axon terminal of the motor neuron. On the plasma membrane of a muscle fiber, the sarcolemma, we will find volgate gated sodium channels. They will get to threshold and create action potentials that will run along the sarcolemma, up and down the muscle fiber.
    • As the action potential goes in both directions, that wave of voltage will move down inside the muscle fiber through the Transverse tubule (T tubule).
    • As the wave of depolarization goes down the t tubules, voltage gated channels/receptors, specifically dihydropyridine (DHP) receptors open, allowing Ca++ into the sarcoplasm.
    • Keep in mind the DHP receptor is physically connected to the ryanodine receptor that is expressed on the sarcoplasmic reticulum. The ryanodine receptor is also permeable to Ca++ and opens as the depolarization wave passes. Ca++ goes from high concen. to low.
    • The sarcoplasm is flooded with Ca++ and a lot more Ca++ goes from the ryanodine receptors than from the DHP. A lesser amount of Ca++ than either comes from the T tubules.
    • Next to the t tubules, we have the sarcoplasmic reticulum, it'll store Ca++ just like the endoplasmic reticulum.
    • Ca++ in our sarcoplasm must be pumped out, via uniporters, to the sarcoplasmic reticulum continuously.
    • While Ca++ is in the sarcoplasm, it'll bind to troponin subunits, this will cause a conformational change moving tropomyosin out of the way.
    • This will reveal binding sites for the myosin globular head on actin
    • On the myosin globular head there will be an ADP with an inorganic phosphate attached (a rough ATP).
    • When the binding site is revealed, myosin head will bind and the binding will cause a release of the inorganic phosphate. This is called cross-bridging
    • A power stroke (8nm) will occur, dragging actin toward the M band, in the center, and shortening the sarcomere
    • When the power stroke is completed, the ADP falls off and goes away, *maybe to the mitochondria.
    • We cannot uncross-bridge until another ATP binds, as soon as it binds we uncross-bridge
    • That ATP is hydrolyzed, creating energy for the molecule, to re-cock the head.
    • If we have decided to stop the movement, no more Ach/action potentials, nothing down t tubules, no activation of DHP or ryanodine receptors, the calcium will get pumped back in and the troponin will not move the tropomyosin and the myosin globular head will not be able to bind.
    • If we wanted to continue the contraction or make it stronger, the motor neurons would be active and we would just repeat the cycle.
  13. fatigue story:
    • When we lift weights and start to run out ATP the mitochondria take note and will sequester Ca++. So the Ca++ will no longer be cycled back into the sarcoplasmic reticulum.
    • Even though the motor neuron is releasing Ach, action potentials are occurring, the DHP receptors and ryanodine receptors are opening, the Ca++ is with the mitochondria, so nothing is coming out. This protects us from over-exerting ourselves and going into states of rigor mortis.
  14. Rigor mortis story:
    • When you die, breathing ends (no oxygen) so no ATP will be made by the mitochondria. So we will run out of ATP.
    • Uniporters will not have ATP to pump the Ca++ into the sarcoplasmic reticulum so it'll begin to leak out.
    • The Ca++ will still bind to troponin and we will get the last power stroke
    • The myosin globular head will be stuck because there will be no new ATP to uncross-bridge.
    • This occurs in every myosin globular head in the body at the point of death leaving us in a state of rigor.
    • *The myosin globular heads remain in this position until devoured by bacteria (decomposition).
  15. Muscle twitch story:
    • When you fire one motor neuron, that will give us one action potential. That is a twitch, the minimum contraction from firing of a motor neuron. Force generated in a back muscle would be huge and in finger muscle would small. Though their curves would look the same, the force would ultimately disappear because Ca++ is actively being pumped back into the sarcoplasmic reticulum. The absence of Ca++ would mean no more cross-bridging.
    • If we fire the motor neurons before the Ca++ gets pumped back in, we get a little summation so the twitch gets bigger.
    • From the muscle fiber's perspective, as we continue to fire before clearing out the Ca++, we reach the point of maximum force/ tetanus.
    • The stronger the person, the higher myofibril count, the larger the muscle fibers and the greater the amount of force generated.
  16. Slow twitch fibers are ______ (cellular respiration/ needing oxygen) and are red muscle due to _______ and _____ supply with ______. *think marathon runners
    • oxidative
    • vascularization
    • blood 
    • hemoglobin
  17. Slow twitch contains _______ which literally takes oxygen from hemoglobin/ is the oxygen reserve for muscles/slow twitch muscle fibers. Lots of _______ for cellular respiration. Lots of ____ _____ to bring glucose. Maximum tension develops slowly but more resistant to _____ because we have lots of _____ & lots of ______, so we can oxidatively produce more ATP. Lots of _____ (chains of glucose/carbohydrate for energy)
    • myoglobin
    • mitochondria
    • blood supply 
    • fatigue 
    • oxygen & mitochondria 
    • glycogen
  18. Fast twitch fiber (3)
    fewer mitochondria, fewer blood vessels, little to no myogloblin
  19. At maximum stretch, _____ does not come in contact with _____ and _____ force can be produced. You need them to overlap to create muscle tension.
    • actin 
    • myosin
    • minimal
  20. Muscle fibers have about 10 to 30 seconds of ____ & ______ ______ available (the immediate system) in the muscle fiber
    ATP and creatine phosphate
  21. Creatine phosphate is in the muscle fiber to transfer _______ to ADP to make ATP.  As we produce ______, we begin the oxidative system the efficiency with which we complete these cycles, correlates with how _____ we are
    • phophates 
    • pyruvate
    • fast
  22. Three characteristics of cardiac muscle
    unicellular, striated, can withstand high pressure by interdigitating
  23. Which are striated
    skeletal & cardiac muscle have this, in cardiac they show up in patterns (intercalated discs).
  24. Pacemaker cells found in the ___ node. All hearts are _____ and will beat outside the body. _____ muscle and _____ muscle are connected with gap junctions so their action potentials that spread. For example, when you eat and a portion of the GI tract stretches, and causes an ____ ____ that spreads and leads other portions of the GI tract contracting and stretching, this is known as _______. The connectivity of the gap junctions allow for this.
    • SA node
    • myogenic 
    • smooth muscle & cardiac muscle
    • action potential
    • peristalsis
  25. _______ is absent from smooth muscle
    troponin
  26. Smooth muscle contraction story
    • When a bolus of food stretches the GI tract, Ca++ can enter (or we can have Ach bind to g-protein receptors and cause
    • Ca++ to come out from another pathway) either way, calcium is now in the sarcoplasm Ca++ will then bind to calmodulin which will bind to/ activate another molecule, myosin kinase
    • Myosin kinase then phosphorylates making the myosin head attach to actin and we get a contraction
    • To stop this, we have myosin phosphotases to remove the phosphate, this will cause the myosin head to detach from actin.
    • When there is a lot of Ca++ present, myosin kinase wins, when they are low, myosin phosphotase wins.
Author
chikeokjr
ID
325859
Card Set
Musculoskeletal systems
Description
Musculoskeletal systems
Updated