I this lab we used the ADAM CD rom to learn about different aspects of the Muscular system. The CD had six different parts: muscle anatomy review, the neuromscular junction, the sliding filament theory, muscle metabolism, motor unit contraction, and whole muscle contraction.
Muscle anatomy review: The three different types of muscle cells are smooth, skeletal and cardiac. They are contrasted nicely in this diagram. Skeletal muscles, in particular, have important 'investments' in connective tissue. Not only is the entire muscle surrounded by connective tissue, each bundle of muscle cells as well as each fascicle is also. As the muscle fibers end the connective tissue extends to anchor the muscle to the bone. The internal anatomy of the muscle is important in understanding how the muscle works. All the intricate parts work together to create what we experience as muscle contrractions. One of the smallest parts invoved in the action is the sarcomere. Myofilaments are made up of many of these.
The Neuromuscular Junction: The neuromuscular junction is where the action potential transfers from the neuron to the muscle cell. This occurs in a series of steps. As the wave of depolarization arrives at the axon terminal, the voltage change causes voltage-gated channels to open allowing calcium to rush in. This calcium causes several synaptic vescicles to fuse with the membrane of the axon terminal. The The neurotransmitter, Actylcholine, is liberated from the vescicles by exocytosis and moves into the synaptic cleft. Meanwhile, calcium is pumped back out of the cell. The Acetylcholine diffuses away from the receptor site and the ion channels close. Then, the ACh is broken down by Acetylcholinesterase. This causes a depolarization of the motor end plate which initiates an action potential. This propagates along the sarcolemma and down the T-tubules. As this action potential passes by, it causes the release of calcium from the ternimal cisternae, of the sarcoplasmic reticulum, into the cytosol. The calcium causes the contraction of the muscle cells which is discussed in detail in the section on the sliding filament theory.
Sliding Filament Theory: In this section we learned how certain molecules within the muscle cell work together to make the muscle contract. There are five participants invoved: myosin, actin, troponin, tropomyosin, ATP, and calcium. A key part in understanding the sliding filament theory is knowing the relationship of actin, tropomyosin, troponin and calcium. The actin molecules join together to form a helix. On each of these molecules there is a myosin binding site. These sites are covered by a strand of tropomyosin. The tropomyosin strands have a molecule called troponin on them in various places along the complex. When calcium is released from the terminal cisternae of the sarcoplasmic reticulum, it binds to troponin molecules causing a change in the conformation of the complex. The tropomyosin moves away from the myosin binding site allowing myosin to bind there. Knowing this, we can go on to look at the six steps of cross-bridge cycling. 1) Influx of calcium exposes myosin binding sites on actin 2) myosin bunds to actin 3) the power stroke of the cross-bridge causes sliding of the thin filaments 4) ATP binds to the cross-bridge causing it to disconnect from the actin 5) hydrolysis of ATP which leads to the re-energizing and repositioning of the cross-bridges 6) calcium ions ar etransported back into the sarcoplasmic reticulum. In a whole muscle contraction, many of these cross-bridges bind and release to have a cumulative effect.
Muscle Metabolism: This section was largely about Adenosine Triphosphate (ATP) in relation to muscular contractions. ATP is made a few different ways, using glucose as the starting molecule. Glucose is first converted to Pyruvic Acid which yields 2 ATP as a biproduct. Pyruvic Acid can then be further converted either anaerobically or aerobically. Anaerobically it is converted to lactic acic and no ATP is yielded. Aerobically, ATP is converted to Acetyl Co-A which goes through oxidative phosphorylation in the Kreb's Cycle. This yields CO2, H2O and 36 ATP. These ATP molecules are used in three ways during a muscle contraction. One is used to unbind the cross-bridge from the actin molecule, one energizes the power stroke of the myosin cross-bridges, and one is used to actively pump calcium back into the sarcoplasmic reticulum. We also learned other things in this section, for instance, the sources of oxygen for muscle cells. They get the oxygen either from the blood or from myoglobin in red muscle cells. Red muscle fibers are about half the diameter of white muscle cells and contain many mitochondria. They also have a rich blood capillary supply allowing them to restore their oxygen debts quickly. As a result, they fatigue much less rapidly than white muscle cells. These white muscle fibers have a larger diameter, less mitochondria, less myoglobin which gives it a lighter color, and a less sufficient blood capillary supply. This makes it much harder for them to supply their oxygen need and so they tire fairly rapidly. Because white muscle cells have so much less oxygen available, they use the anaerobic method of getting ATP which doesn't require any. Red muscle fibers use ATP from the Kreb's Cycle for their oxygen supply.
Contraction of Motor Units: A motor unit is a motor neuron and all of the muscle cells it stimulates. The stimulation of more motor units produces increased muscle tension. Control of the muscle depens on the size of the motor unit. The fewer muscles controlled by each neuron, the more precise the movement. Tone of a muscle is maintained by random, asynchronous muscle contractions causing a nearly constant state of low level contraction.
Contraction of Whole Muscle: There are three phases in a single twitch: latent, contraction, and relaxation. During the latent phase, the sarcolemma and T-tubules release calcium into the cytosol, and the cross-bridges begin to cycle but there is not yet shortening of the muscle. In contraction, sarcomeres shorten as a result of cross-bridge cycling. During relaxation, calcium is actively transported back into the terminal cisternae, cross-bridge cycling decreases and ends, tension is reduced and the muscle returns to its original state. Temporal summation of two stimuli (of equal intensity) looks like this. It occurs when the second contraction happens before the first has fully relaxed so there is an increased amplitude. If the stimuli occur further apart, there will be no summation. The stages of multiple stimuli are treppe, temporal summation, incomplete tetanus, tetanus, and fatigue. Treppe occurs during the first few contractions. Each subsequent muscle twitch shows a very slight increase in strength but relaxation is still complete. As the frequency increases there is temporal summation because there is not adequate time for full muscle relaxation. As the frequency of contraction continues to increase and the contraction-relaxation cycles get shorter the muscle enters the incomplete tetanus stage. Here, there is still a slight relaxation. Once this relaxation is completely absent the contractions fuse into a smooth, continuous total contraction. There is an abundance of calcium in the muscle cell at this point which provides for many cross-bridge cycles. Eventually, the muscle will gradually elongate as it fatigues. This is due to a build up of acidic compounds that affect protein functions, relative lack of ATP and ionic imbalances resulting from membrane activity. One last thing worth noting is that the contraction force of a muscle is strongest when it begins while the muscle is moderately stretched. It is not as effective when it begins while the muscle is unstretched or overstretched.
