The Role Of Calcium In Muscle Contraction – The human body is a beautiful thing. It is incredible how a complex set of mechanisms combine different processes, including biochemical reactions, to complete a task. For example, have you ever taken a moment to think about what happens behind muscle movement? Let’s analyze it further…

Muscle tissue is composed of many sarcomeres, which are the smallest contractile units of a muscle. These sarcomeres are composed of smaller myofilaments, such as myosin and actin. A thick filament has lots of myosin heads and tails and a thin filament has actin. This is where the basic elements of body muscle movement occur.

The Role Of Calcium In Muscle Contraction

The mechanism behind the movement of these myofilaments is fairly complex. It is a cycle that begins with an energy source constantly present in our body known as adenosine triphosphate (ATP). As the name suggests, ATP has three phosphates. Myosin heads from the thick filament remove a phosphate from ATP, converting it to adenosine diphosphate (ADP), which contains only two phosphates. From this, the myosin head is rebuilt and gains more strength. Then, the myosin heads bind to a thin filament of actin. By binding, these are now called “cross-bridges”. Later, this cross-bridge opens and ADP is released. Eventually, the myosin head and actin will detach from each other. All these events lead to a contraction of the skeletal muscles.

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, and is used in the contraction and relaxation of muscles. Ionized calcium is found in the sarcoplasmic reticulum of skeletal muscle, which stores and releases calcium in muscle cells. Muscle contraction begins when calcium is present in muscle cells. Muscle cell membranes contain calcium pumps that allow calcium to be rapidly transported back into the sarcoplasmic reticulum. When the amount of calcium in the muscle cell decreases, the myosin heads close, causing the muscle to relax. Calcium works in cooperation with the myofilaments of muscle tissue to coordinate muscle contraction and relaxation.

The nervous system also contributes to muscle movement because many nerves involve impulses and communicate directly with muscles. Initially, nerve impulses arriving at the synaptic end bulb stimulate voltage gate channels to open. Calcium then flows inward because its concentration is higher outside the cell. As calcium arrives, acetylcholine (a neurotransmitter) is released. It diffuses across the synaptic cleft between the motor neuron and the motor end plate. Whenever acetylcholine binds to motor end plate receptors, an ion channel opens. This allows small positively charged ions, such as sodium ions, to flow across the membrane. This influx of sodium ions causes the interior of the muscle fiber to become more positively charged and creates an action potential. This action potential releases stored ionized calcium, causing muscle contraction. Acetylcholine secretion is controlled by releasing an enzyme called acetylcholinesterase, which breaks down acetylcholine.

The description of these processes has hopefully left you in awe as it was when I first discovered it. The human body deserves to be admired for all its beautiful intricacies and functions. Just as Julien Afroy de la Metre once said: “The human body is a machine that winds its own springs”. The binding of myosin heads to muscle actin is a highly regulated process. When a muscle is at rest, actin and myosin separate. To prevent actin from binding to the active site of myosin, regulatory proteins block molecular binding sites. Tropomyosin blocks the myosin binding sites on actin molecules, preventing cross-bridge formation, which prevents contraction in muscles without nerve input. The protein complex troponin binds to tropomyosin, helping to position it on actin molecules.

To enable muscle contraction, tropomyosin must change conformation and expose the myosin-binding site on an actin molecule, thereby allowing cross-bridge formation. Troponin, which regulates tropomyosin, is activated by calcium, which is kept in extremely low concentrations in the sarcoplasm. If present, calcium ions bind to troponin, causing a conformational change in troponin that allows tropomyosin to move away from the myosin-binding site on actin. Once tropomyosin is removed, a cross-bridge can form between actin and myosin, triggering contraction. Cross-bridge cycling continues until Ca

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Figure (PageIndex): Muscle contraction: Calcium remains in the sarcoplasmic reticulum until released by a stimulus. Calcium then binds to troponin, causing troponin to change shape and remove tropomyosin from the binding site. Cross-bridge clinging continues until calcium ions and ATP are no longer available.

Calcium concentration within muscle cells is regulated by the sarcoplasmic reticulum, a unique variant of the endoplasmic reticulum of the sarcoplasm. Muscle contraction ends when calcium ions are pumped back into the sarcoplasmic reticulum, allowing the muscle cell to relax. During muscle cell stimulation, the motor neuron releases the neurotransmitter acetylcholine, which then binds to a post-synaptic nicotinic acetylcholine receptor.

A change in receptor conformation causes an action potential, activating voltage-gated L-type calcium channels, which are present in the plasma membrane. Inward influx of calcium from L-type calcium channels activates ryanodine receptors to release calcium ions from the sarcoplasmic reticulum. This process is called calcium-induced calcium release (CICR). Whether ryanodine receptors open due to physical opening of L-type calcium channels or due to the presence of calcium is not understood. Calcium efflux allows myosin heads access to actin cross-bridge binding sites, allowing muscle contraction. The sequence of events resulting in the contraction of an individual muscle fiber begins with a signal from the motor neuron – neurotransmitter, ACh – innervating that fiber. The local membrane of the fiber contains positively charged sodium ions (Na

) enter, triggering an action potential that spreads to the rest of the membrane and depolarizes the T-tubules. It is calcium ion (Ca

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The ions remain in the sarcoplasm to bind to troponin, which leaves the actin-binding sites “unprotected,” and as long as ATP is available for cross-bridge cycling and pulling of actin strands by myosin, the muscle fiber will continue to move. Shorten a physiological limit.

Figure (PageIndex): Contraction of a muscle fiber. A cross-bridge is formed between the actin and myosin heads which initiates contraction. As long as Ca

The ions remain in the sarcoplasm to bind to troponin, and the muscle fiber will continue to shorten as long as ATP is available.

Signaling from motor neuron endings normally results in cessation of muscle contraction, which repolarizes the sarcolemma and T-tubules and closes voltage-gated calcium channels in the SR. ca

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Ions are then pumped back into the SR, causing the tropomyosin to reposition (or reoccupy) the binding sites on the actin strand. A muscle can stop contracting when ATP is depleted and fatigued (Figure (PageIndex)).

Ions are pumped back into the SR, thereby restoring binding sites on tropomyosin actin strands. A muscle can stop contracting when it runs out of ATP and becomes fatigued.

Calcium ion release initiates muscle contraction. Watch this video to learn more about the role of calcium. (a) What are “T-tubules” and what is their role? (b) Please describe how actin-binding sites are made available for cross-bridging with myosin heads during contraction.

The molecular events of muscle fiber shortening occur within the fiber’s sarcomeres (see Figure (PageIndex)). Contraction of striated muscle fibers occurs when sarcomeres, arranged linearly within the myofibril, shorten as myosin heads pull on actin filaments.

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Areas where thick and thin filaments overlap have a dense appearance, as there is little space between the filaments. This region where the thin and thick filaments overlap is very important for muscle contraction, as this is where filament movement begins. Thin filaments anchored at their ends by Z-discs do not fully extend into the central region where only thick filaments remain, anchored at their bases at a location called the M-line. A myofibril is composed of many sarcomeres running along its length; Thus, myofibrils and muscle cells contract as sarcomeres contract.

When signaled by a motor neuron, a skeletal muscle fiber contracts as the thin filaments are pulled and then the thick filaments cross between the fiber’s sarcomeres. This mechanism is known as the sliding filament model of muscle contraction (Figure (PageIndex)). Sliding can only occur when the myosin-binding sites on actin filaments are exposed by a series of steps starting with Ca.

Figure (PageIndex): Sliding filament model of muscle contraction. When a sarcomere contracts, the Z lines move closer together and the I band shortens. A band remains the same width. During complete contraction, the thin and thick filaments overlap.

Tropomyosin is a protein that wraps around the chain of actin filaments and covers the myosin-binding sites to prevent actin from binding to myosin. Troponin binds to troponin to form a troponin-tropomyosin complex. The troponin-tropomyosin complex prevents myosin “heads” from binding to active sites.

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