Chapter 10

 

  1. The myofilaments in muscle are both actin and myosin. Actin is present as monomers of G-actin that polymerize to form F-actin. F-actin is the filamentous actin that myosin binds to. Myosin is a long filament that has both a head and a tail region. The head region consists of two myosin heavy chains and multiple light chains. The heavy myosin twists around itself to give rise to the tail. Many myosin give rise to each other to form the thick filaments. Myofibrils are the long extensions of repeating sarcomeres (that are all attached to each other) and extend in parallel to each other. They exist in groups within an individual fiber. Muscle fibers are individual cells that contain many nuclei and they contain many bundles of myofibrils. Fibers can be extremely long and are under the control of one individual neuron. A muscle is an aggregate of many muscle fibers. Muscle can contain multiple types of individual fibers, which will give it its individual functional strengths and weaknesses.
  2. They proposed this theory after studying the length of I –Bands and H-zones. In a stretched muscle the I-band in long and the H-zone is wide. They are both reduced in the contracted muscle.
  3. Figures 10-1 and 10-2.
  4. The troponin molecules in the muscle fibers will bind up calcium as the calcium concentrations increase. When this occurs the troponin will undergo a conformational change inducing a change in the tropomyosin molecule. The tropomyosin will then rotate and allow actin and myosin to bind. From here myosin will contract. Myosin then goes through its motions to produce the shortening of the sarcomere and then the release of the actin from the myosin.
  5. Fig 10-9b
  6. When an individual dies they are unable to make more ATP. Without ATP Ca will leak into the cytoplasm from the smooth ER and from outside the cell. When this happens the Ca will induce the troponin/tropomyosin changes and allow myosin and actin to bind. And as we learned in class, ATP is required to release myosin from the actin molecule. Since the ATP stores are depleted the myosin is unable to be released from the actin. Ultimately, the myosin and actin are degraded due to the changing conditions and the muscles relax.
  7. Myosin is normally (after the hydrolysis of ATP) in the energized state. Thus when myosin binds to actin it has the energy to drive the shortening. This occurs because myosin has a high affinity to actin and is in a lower energy state when it is head region has shortened. Therefore, the ATP gets the myosin ready to shorten with the actin simply by letting myosin go back down to its resting energy state. Cross-bridges are elastic, as the myosin head rocks through its positions the cross-bridges stretch and then pull myosin and actin past each other to relieve the stretch.
  8. Vmax is defined as the velocity at which a muscle can contract when there is no weight attached. So there is no force generated. Power is also zero. When considering this, remember that there is no load on the muscle.
  9. The velocity will decrease because the muscle is approaching the limit to the amount of work that can be produced by the muscle (isometric contractions). The limit to the amount of force that can be produced is defined at the point where shortening of the muscle no longer occurs.
  10. Troponin is a protein made of 3 distinct subunits. When Ca binds to troponin C then the complex roles out of the way. When troponin moves myosin is able to bind. In invertebrate systems the Ca has its main effect on myosin as opposed to troponin.
  11. Acetylcholine (ACh) binds to the receptors on the surface of the fiber at the synapse and elicits a depolarization. This depolarization will sweep down the length of the fiber (synapse is usually in the center) in both directions and through t-tubules. There the dyhydropyridine receptors can sense the change in voltage and undergo a change in conformation. This change in conformation induces another change in conformation in the ryanodine receptor. This receptor is located on the smooth ER (same thing as the sarcoplasmic reticulum) rather than the plasma membrane and is thus been shown to open calcium channels. Or rather the conformational change in the ryanodine receptor lifts its inhibitory role on the channels. Ca then floods the cell and contraction starts. Relaxation occurs when the membrane returns to normal and the Ca is actively pumped into the smooth ER.
  12. The depolarization is physically coupled to the release of calcium as described previously. The dihydropyridine receptor senses the voltage change and this is transmitted to the ryanodine receptors. This occurs because these two receptors are touching. Only these two receptors are involved, Ca is not. Although, Ca has been implicated to open ryanodine receptors that are not bound to voltage censors on the plasma membrane.
  13. Ca pumping in to the smooth ER and ATP hydrolysis by the myosin heavy chains.
  14. The number of actin/myosin cross-bridges in tension forming position limits myofibril tension. The number of myofibrils limits a muscle fiber to the amount of tension it may form. Fiber types and series elastic components limit the amount of tension a muscle can form.
  15. During tetanus the Ca is at its highest concentration in the cytoplasm and the muscle has already taken up all of the slack in the filaments.
  16. Power is equal to work per unit time. In both these examples no work is being down. During isometric contractions the muscle is not shortening and thus can not do any work. No work... no power. At Vmax there is no load. Similarly, if there is no load then there is no force. No force... no work.
  17. I am not certain what I am being asked here. With locomotion you would want to balance speed and power with fatigue. A slow fiber may not be fast enough or provide enough power for the job. Conversely, the fast fiber may wear out too easily.
  18. The main feature here is the presence of different muscles in the fish. For the slow swim with little curvature in the spine the fish uses red muscle (slow). For the fast swim with a large curvature, the fish will use a white muscle (fast). Another feature is the anatomical location of the muscles. The white muscles are helical in the fish allowing for optimal curvature of the spine with a reduced shortening of the sarcomere ( as opposed to a muscle running parallel to the spine).
  19. These muscles need to relax quickly because the frequency of contraction will produce the sound. If they relax slowly then the frequency of the contractions will decrease. Many optimal conditions must be met for this to occur. First off the Ca must be released and reabsorbed (by the smooth ER) extremely fast. This includes the idea that troponin must let go of Ca quickly. Speed of myosin/actin release is also important in producing the fast excitation and relaxation.
  20. The large energetic cost stems from the increased number of calcium pumps in the smooth ER. The bugs are able to avoid this added cost because the increase in calcium is not the only stimulus for contraction in these muscles. These muscle need to be stretched in the presence of high calcium to elicit a contraction. Therefore pumping up all the calcium between contractions id not necessary.
  21. Action Potentials tell the wings when to contract. They do not determine the frequency. Both the mechanical resonance of the parts and the length of the wings determine the frequency.
  22. Too many to list (which is why I graded a different question on your homework). Check out table 10-2. J