The relationship between muscles, ATP, and calcium exists during the process of muscle contraction.
Muscle cells are made up of structures called sarcomeres, and these consist of two different kinds of filaments (or myofilaments): thick and thin. The thin filaments contain actin, and the thick filaments contain myosin and myosin heads.
When muscle cells are at rest, there are bunches of calcium ions located within the sarcoplasmic reticulums of the muscle cells (the SR is a special type of endoplasmic reticulum, which is the cellular organelle that produces and transports proteins).
When a nerve signal reaches a muscle cell, the action potential opens up the calcium channels, or "gates" of the sarcoplasmic reticulums, and this causes all of the calcium ions inside the sarcoplasmic reticulum to spill out. These calcium ions then spread out among the thick and thin filaments that make up muscle cells, and bind to the troponin C complex located on the actin-containing thin filaments. When this happens, the troponin changes its shape, or conformational change, and one of the proteins involved (tropomyosin) then moves out of the way so that certain binding sites for the myosin heads (on the thick filaments) are now unblocked on the thin filaments. Ordinarily, the tropomyosin protein blocks these binding sites, and prevents the binding of the myosin heads of thick filaments, but when an action potential releases calcium, the two different filaments are able to interact and bind.
After the two types of filaments bind, the myosin heads engage in something called a "power stroke," by releasing ADP and an inorganic phosphate that was originally bound to the myosin heads. This power stroke allows the myosin heads to sort of "push" the filaments together; resulting in a muscle contraction. This results in a contraction because it causes the actin filaments to be pulled closer together and shortens the overall muscle cell.
After the contraction, ATP then binds to the myosin heads, causing it to "let go" of the actin filaments, and the thick and thin filaments then unbind and the muscle relaxes. The bound ATP is converted into ADP and an inorganic phosphate again, so that it can be used again for the next muscle contraction (in which it would be released and result in another power stroke). While all of this is going on, the calcium is pumped back into the sarcoplasmic reticulum so it can be re-released during the next action potential. This is accomplished by calcium ATPase, and ATP is produced as this happens, so it can be used during the contraction process when needed.
Even though muscle fibers store some oxygen, that oxygen is quickly used up, especially during strenuous exercise. In order to convert glucose into ATP so they can continue working, muscles must receive more oxygen via the blood. That is why respiration or breathing rate increases during physical exertion. In times where work or play activities are exhausting; muscle fibers may literally run out of oxygen. If not enough oxygen is present in muscle fibers, the fibers convert glucose into lactic acid, a chemical waste product.
When lactic acid builds up in muscle fibers, it increases the acidity in the fibers. Key enzymes in the fibers are then deactivated, and the fibers can no longer function properly. As a result, muscles are not as effective, contracting less and less. This condition is known as tetany or muscle fatigue. In a state of fatigue, muscle contractions may be painful. Finally, muscles may simply stop working. Lactic acid is normally carried away from muscles by the blood. It is then transported to the liver, where it is changed back into glucose. In order to do this, however, the liver needs ATP. To produce ATP in the liver, oxygen is once again needed. This is why breathing rate remains high even after vigorous physical activity is stopped. Only after the liver produces the necessary ATP does breathing gradually return to normal.
When muscles need to create ATP, their only energy source, they combine glucose with oxygen. This reaction also creates heat as a by-product. The body uses this heat to maintain normal body temperature. When the temperature of the body drops below normal, the brain signals the muscles to contract rapidly—what we perceive as shivering. The heat generated by these rapid muscle contractions helps to raise or at least stabilize body temperature.
In death, all reactions tend to stabilize. Among the first of these processes is that of ion equilibration across all compartments of the body as ion pumps lose their energy supplies. In the case of muscle, this results in the receptacle holding fluid and extracellular calcium leaking into the sarcoplasm, raising calcium concentrations to high levels. The calcium induces conformational changes in the troponin-tropomyosin complex, exposing myosin binding sites on thin filaments. The resulting uncontrolled contractile activity hastens the total exhaustion of ATP supplies and ends with all or nearly all myosin molecules in cross-linked actomyosin complexes. The rigid state of muscles that develops shortly after death is due to this highly cross-linked state of thin and thick filaments and is known as rigor mortis.
Explain the relation between muscles, ATP energy, and the calcium ion.
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