CH 09 Sliding Filament Mechanism

Exam 3 Review: Chapter 09: Sliding Filament Mechanism

excitation-contraction coupling - The arrival of a nerve impulse (action potential) at the axon terminal of the neuro-muscular junction leads to acetylcholine release; acetylcholine then binds with gated sodium channels to initiate the depolarization of the sarcolemma; that depolarization leads to depolarization of the sarcoplasmic reticulum permitting the second messenger, calcium ions, to diffuse into the sarcoplasm and trigger the sliding filament contraction of the myofibrils; the cause-and-effect chain of motor neuron depolarization, synaptic neurotransmitter release, nerotransmitter binding, sarcolemma depolarization, sarcoplasmic reticulum depolarization, calcium outflow, and myofibril contraction.

sliding filament mechanism - The specific interactions between myosin and actin, triggered by calcium ions and using the energy of ATP hydrolysis, which include a repetitive covalent binding of the myosin head to the actin filament, the power stroke of the myosin head, the movement of the actin filament toward the M line of the sarcomere, and then the breaking of covalent link between actin and myosin so that the myosin head may bind to the next actin in the "ratchet action" which ultimately shortens each sarcomere and thus causes the muscle cell to contract; this "unit action" is repeated thousands of times since each sarcomere contains many myosin and actin filaments.

cross-bridges - The temporary covalent linkages between myosin heads and myosin-binding sites on acting during muscle contraction; energy for the covalent bond comes from hydrolysis of the ATP bound to the myosin head.

power stroke - The conformational change in a myosin head, using the energy of ATP hydrolysis, after it has covalently bound to actin, which pulls the thin filament a small molecular distance in the direction of the M line at the center of the sarcomere.

all-or-none response - The type of response by any regulated system, upon stimulation to either perform a complete response or to have a total lack of response or effect; e.g., a muscle cell contraction or a nerve impulse (action potential) generated by a weak stimulus, just minimally above the threshold limit, is just as strong as one generated by a strong stimulus well beyond the threshold value.

ATP = adenosine tri-phosphate - A nucleotide [C₁₀H₁₆N₅O₁₃P₃] which contains the purine adenine, a pentose sugar (ribose or deoxyribose) and three high-energy phosphate groups; the potential chemical energy in the bonds connecting the phosphate groups is used to transport energy within cells for biochemical processes (including muscle contraction and enzymatic metabolism) through its hydrolysis; the mitochondrion is the primary cell organelle synthesizing this compound using energy derived from the final oxidation of nutrient molecules.

List:

4. The sequence of biochemical events, starting with a nerve impulse, and ending with depolarization of the sarcolemma of a muscle fiber (i.e., excitation-contraction coupling). Name all the chemicals and cell parts involved.

          a. a nerve impulse (action potential = depolarization event) is transmitted along the motor neuron axon to the axon end bulb.
          b. a nerve impulse (action potential = depolarization event) causes Na⁺ and Ca⁺⁺ ions to enter the axon end bulb through voltage-gated Na⁺ and Ca⁺⁺ ion channels.
          c. the entry of Na⁺ and Ca⁺⁺ ions triggers cytoskeletal elements to move neurotransmitter = acetyl choline (ACh), stored in vesicles, to the axon end bulb cell membrane (neurolemma).
          d. the neurotransmitter vesicles merge with the axon end bulb cell membrane (neurolemma), releasing neurotransmitter = acetyl choline (ACh) molecules into the synapse of the neuromuscular junction.
          e. the acetyl choline (ACh) molecules diffuse throughout the synaptic cleft, eventually reaching neurotransmitter receptor molecules on the skeletal muscle sarcolemma at the motor end plate; the resting state of the sarcolemma is polarized (the membrane charge polarity is positive outside and negative inside as a result of the action of the Na⁺- K⁺- ATPase pumps).
          f. the acetyl choline (ACh) molecules bind non-covalently (reversibly) with the neurotransmitter receptor molecules on the skeletal muscle sarcolemma at the motor end plate.
          g. the Ach receptor molecules at the motor end plate are chemically-gated Na⁺ ion channels which have been closed, but now open in response to binding with ACh, allowing Na⁺ ions to diffuse into the sarcoplasm at the motor end plate.
          h. the Na⁺ ions influx into the sarcoplasm at the motor end plate initiates the depolarization of the sarcolemma at the motor end plate.
          i the depolarization of the sarcolemma at the motor end plate (the reversal of the membrane charge polarity, now negative outside and positive inside) destabilizes adjacent voltage-gated Na⁺ ion channels which have been closed, but now open in response to the nearby depolarization.
          j. the opening of these adjacent voltage-gated Na⁺ ion channels in response to the nearby depolarization allows additional Na⁺ ions to diffuse into the sarcoplasm creating a spreading wave of depolarization across the entire sarcolemma and simultaneously depolarizing the T-tubules by the same mechanism.

5. The sequence of biochemical events in the skeletal muscle beginning with the depolarization of the T-tubules and ending with the start of the sliding filament mechanism, the "power stroke" of muscle contraction (i.e., sliding of actin past myosin). Name all the chemicals and cell parts involved.

          a. the opening of the voltage-gated Na⁺ ion channels in the general sarcolemma (in response to the nearby depolarization of chemically-gated Na⁺ ion channels at the motor end plate) allows additional Na⁺ ions to diffuse into the sarcoplasm creating a spreading wave of depolarization across the entire sarcolemma and simultaneously depolarizing the T-tubules by the same mechanism.
          b. a spreading wave of depolarization (the Na⁺ ions influx into the sarcoplasm) passes along the entire system of T-tubules which penetrate the sarcoplasm.
          c. the influx of Na⁺ ions into the sarcoplasm destabilizes the sarcoplasmic reticulum membrane wherever it is located near a T-tubule.
          d. the destabilization of the sarcoplasmic reticulum membrane causes the opening of the voltage-gated Ca⁺⁺ ion channels in the sarcoplasmic reticulum membrane; calcium and phosphate ions are stored within the lumen of the sarcoplasmic reticulum in a gel state.
          e. the opening of the voltage-gated Ca⁺⁺ ion channels in the sarcoplasmic reticulum allows Ca⁺⁺ ions to diffuse rapidly into the sarcoplasm.
          f. when the Ca⁺⁺ ions to diffuse into the sarcoplasm they quickly enter the sarcomeres of the myofibrils, which allows them to act as second messengers to interact with myosin and actin to trigger the sliding filament mechanism, the "power stroke" of muscle contraction (i.e., sliding of actin past myosin).

6. The sequence of biochemical events in the "power stroke" of muscle contraction (i.e., sliding of actin past myosin). Name all the chemicals and cell parts involved.

          a. when Ca⁺⁺ ions, released from the sarcoplasmic reticulum, diffuse into the sarcoplasm they quickly enter the sarcomeres of the myofibrils, which allows them to act as second messengers to interact with myosin and actin to trigger the sliding filament mechanism, the "power stroke" of muscle contraction (i.e., sliding of actin past myosin).
          b. when Ca⁺⁺ ions reach the actin filament they reversibly (non-covalently) bind with the troponin "switch molecule," causing it to undergo a conformational change; that conformational change influences the adjacent tropomyosin to shift which uncovers the myosin-binding site on each G-actin monomer within the thin filaments.
          c. when Ca⁺⁺ ions reach the myosin filament, simultaneously, the Ca⁺⁺ ions reversibly (non-covalently) bind with the ATPase subunit of each myosin head, permitting the hydrolysis of the ATP which was already "loaded" into the ATPase subunit's catalytic active site.
          d. the useful energy released by the hydrolysis of the ATP allows the myosin head to make a covalent bond with a myosin-binding site on a G-actin monomer within an adjacent thin filament; the remainder of the useful energy released by the hydrolysis of the ATP allows the myosin head to make a conformational change in shape which has the effect of tugging the actin filament toward the M line, the midline of the sarcomere.
          e. the release of the ADP and P_i ion from the the ATPase subunit's active site on the myosin head, in the presence of Ca⁺⁺ ions, allows the myosin head to bind another molecule of ATP; that binding breaks the covalent bond between myosin head and the myosin-binding site on the G-actin monomer within the thin filament.
          f. the breaking of the covalent bond between myosin head and the myosin-binding site on the G-actin monomer within the thin filament allows the process to repeat, specifically, the repetition of steps b through e above.
          g. the repetition of the actions of steps b through e above cause the sliding of the actin fibers over the myosin = thick fibers, as they are pulled toward the M lines of each sarcomere; this repetitive pulling is termed the "ratchet effect."
          h. so long as the Ca⁺⁺ ions remain present in the general sarcoplasm, the sliding of actin past myosin, the "ratchet effect," will continue until each sarcomere and, therefore, each myofibril inside the skeletal muscle cell is maximally contracted, i.e., shortened; this is an "all-or-nothing" response which contracts the muscle skeletal cell.

7. The sequence of biochemical events in the skeletal muscle beginning with the end of muscle cell/myofibril/sarcomere contraction and the restoration of the resting state of the skeletal muscle cell. Name all the chemicals and cell parts involved.

          a. when no further impulses arrive at the axon end bulb, no further ACh is released into the synapse.
          b. when no further ACh is released into the synapse, the remaining ACh is soon hydrolized by acetylcholinesterase into acetate and choline groups which are recycled by the axon end bulb to re-synthesize ACh for future use.
          c. when no ACh remains in the synapse, all chemically-gated Na⁺ ion channels in the motor end plate close and the Na⁺- K⁺- ATPase pumps restore the resting membrane state, i.e., polarization, to the motor end plate membrane.
          d. when the motor end plate membrane repolarizes, the adjacent adjacent voltage-gated Na⁺ ion channels close, beginning a wave of repolarization across the sarcolemma.
          e. when the wave of repolarization crosses the sarcolemma it continues inward repolarizing the T-tubules by the same mechanism, closing adjacent adjacent voltage-gated Na⁺ ion channels; and, meanwhile, the Na⁺- K⁺- ATPase pumps restores the resting membrane state, i.e., polarization, of the T-tubules.
          f. when the T-tubules repolarize, there is no further destabilization of the sarcoplasmic reticulum, and its voltage-gated Ca⁺⁺ ion channels close; at the same time, Ca⁺⁺ - ATPase pumps begin removing Ca⁺⁺ ions from the general sarcoplasm, returning them to their storage depot inside the lumen of the sarcoplasmic reticulum.
          g. after the removal of Ca⁺⁺ ions from the general sarcoplasm, the myosin heads each bind another molecule of ATP; this binding breaks the covalent bonds between myosin heads and the myosin-binding sites on the G-actin monomer within the thin filaments; and with that, contraction ends.
          h. the skeletal muscle will still have to be stretched back out by an antagonist or by gravity, and all the stored glycogen, oxygen stored on myoglobin, and high energy phosphate bonds stored on creatine phosphate which may have been used up in the contraction will have to be restored.

Describe: (or you may sketch and label)

6. The sliding filament model of muscle contraction (shortening).

10. What is meant by "all-or-none," when referring to contraction of a muscle fiber?

When an individual skeletal muscle cell is stimulated to contract by the arrival of a nerve impulse at the neuromuscular junction of sufficient strength (threshold strength), then a complete contraction of that muscle occurs. All its sarcomeres and all of its myofibrils contract to their maximum extent.

Sketch and Label:

4. A sarcomere (including the various protein components).