The spread of an action potential along the sarcolemma penetrates the T tubules. For the action potential to reach the membrane of the sarcoplasmic reticulum (SR), there are periodic intussusceptions in the sarcolemma, called tubules T („T“ stands for „transverse“). The arrangement of a T-tubule with the SR membranes on both sides is called a triad (Figure (PageIndex{3})). The triad surrounds the cylindrical structure called myofibril, which contains actin and myosin. The T tubules carry the action potential inside the cell, which triggers the opening of calcium channels in the membrane of the neighboring SR, causing the diffusion of (text{Ca}^{++}) of the SR into the sarcoplasm. This is the arrival of (text{Ca}^{++}) in the sarcoplasm, which initiates the contraction of the muscle fiber through its contractile or sarcomerous units. As with all aspects of medicine, an ongoing amount of research is likely to change our future understanding of smooth muscle and its overall effects on disease. Current research on smooth muscle has shown promise for future implications, such as. B restoration of endothelial tissue, which could reveal new ways to promote revascularization in the future. Even small changes in understanding like these could have an immeasurable impact on the treatment and mortality of cardiovascular disease in the future. [4] While smooth muscle physiology remains an exceptionally profound topic, a solid understanding of its impact on healthcare, even at the most basic level, will provide healthcare professionals with tools to achieve better healthcare outcomes now and in the future.
Some smooth muscle cells also show the ability to form a spontaneous pacemaker current. This pacemaker current is maintained, for example, in the intestine by the interstitial cells of Cajal. The pacemaker current represents the repetitive oscillations of the membrane potential that occur in several cycles. These slow waves of membrane potential fluctuation are unique in that they are not responsible for the contraction of the intestine. It seems that at the potential of the membrane at rest, some calcium channels with controlled voltage become active, an influx of calcium will then propagate a slow wave to a certain threshold. When the amplitude of the slow wave is high enough, the L-type calcium channels open, causing contraction. [7] Sodium may also play a role in oscillating electrical activity. The influx of calcium stimulates the Na-Ca exchange, resulting in an influx of sodium; This will effectively increase the rate of the Na-K pump. This activity remains unique in that the oscillations of the membrane potential and the activity of slow waves are generated without the influence of the central nervous system. Slow waves are therefore able to allow smooth muscles to remain toned without having to maintain potential fires of continuous action. In 1952, the term excitation-contraction coupling was coined to describe the physiological process of converting an electrical stimulus into a mechanical response. [20] This process is fundamental to muscle physiology, with the electrical stimulus usually being an action potential and the mechanical response being a contraction.
Excitation-contraction coupling can be deregulated in many diseases. Although excitation-contraction coupling has been known for more than half a century, it is still an active area of biomedical research. The general pattern is that an action potential arrives to depolarize the cell membrane. Thanks to mechanisms specific to the muscle type, this depolarization leads to an increase in cytosolic calcium called calcium transients. This increase in calcium activates calcium-sensitive contractile proteins, which then use ATP to cause cell shortening. ATP provides the energy needed for muscle contraction. In addition to its direct role in the transverse bridge cycle, ATP also provides energy for Ca++ pumps with active transport in the SR. Muscle contraction does not occur without sufficient amounts of ATP. The amount of ATP stored in the muscle is very small and enough to cause contractions for a few seconds. Therefore, when decomposed, ATP must be rapidly regenerated and replaced to allow for prolonged contraction.
There are three mechanisms by which ATP can be regenerated: creatine phosphate metabolism, anaerobic glycolysis, fermentation, and aerobic respiration. Without reflexes, all contractions of skeletal muscle occur as a result of conscious exertion, which has its origin in the brain. The brain sends electrochemical signals through the nervous system to the motor neuron, which innervates several muscle fibers. [17] In some reflexes, the contraction signal may be caused by a feedback loop with gray matter in the spinal cord. Other actions such as locomotion, breathing and chewing have a reflex aspect: contractions can be initiated both consciously and unconsciously. In order for thin filaments to continue to slide beyond thick filaments during muscle contraction, myosin heads must pull actin to the binding sites, detach it, strain it again, attach it to other binding sites, pull it, loosen it, cover it, etc. This repeated movement is called the transverse bridge cycle. This movement of myosin heads is similar to that of rowing when a person rows a boat: pulling paddles from the oars (myosin heads) are lifted out of the water (detached), repositioned (rested), and then immersed again to shoot (Figure 4). Each cycle requires energy, and the action of myosin heads in sarcomeres that repeatedly pull on thin filaments also requires energy provided by ATP. (1) The sequence of events leading to contraction is initiated somewhere in the central nervous system, either as voluntary activity of the brain or as reflex activity of the spinal cord. (12) In living animals, an external stretching force, such as gravity or an antagonistic muscle, returns the muscle to its original length. Muscle contraction usually stops when motor neuron signaling ends, which repolarizes the sarcolemma and T tubules and closes the voltage-controlled calcium channels in the SR.
The Ca++ ions are then pumped into the SR, allowing tropomyosin to protect (or cover) the binding sites on the actin strands. .