There are two compounds that are absolutely necessary for muscle contraction: ATP and calcium ions. Calcium ions bind to troponin, which removes tropomyosin from the binding site on actin. Only after this change occurs can myosin bind to actin and cause a contraction. ATP is hydrolyzed to alter myosin into a high energy state. This energy is released during the muscle contraction when myosin binds to actin. Even if ATP is present, the contraction cannot occur without calcium, and even if calcium is present it cannot occur without ATP.

During the contraction cycle, ATP binds to myosin in its low-energy state. ATP is converted to ADP, and the resulting energy is stored in the myosin head. The myosin then binds to actin, still carrying the ADP, and uses the energy to transition back to the low-energy state by pulling actin and shortening the sarcomere. This causes the ADP to be released from myosin. The binding of a new ATP to the myosin allows it to release actin, and the cycle begins again.

During muscle contraction thick filaments (myosin) remain stationary, while thin filaments (actin) move towards one another. In the process, the H zone and I band shorten, as the Z lines get closer together. The A band, however, never changes in length.

There are three primary types of muscle: skeletal, smooth, and cardiac.

Skeletal muscle is multinucleated and striated. Smooth muscle is mononucleated and not striated. Cardiac muscle is mononucleated and striated. If we know that the muscle type is not multinucleated, then it must be mononucleated and could be either smooth muscle or cardiac muscle.

There are seven steps involved in the signaling cascade from the initiation of contraction to the subsquent relaxation of muscle fibers.

1. Motor neurons release acetylcholine (ACh), which binds to receptors on the muscle fiber's cell membrane.
2. ACh receptor binding and activation creates an action potential that propagates along the muscle fiber membrane and down T tubules.
3. The action potential triggers the release of Ca²⁺ ions from the sarcoplasmic reticulum.
4. The released Ca²⁺ ions bind to troponin, which causes the displacement of tropomyosin, revealing the myosin-binding sites on the actin filament.
5. Myosin cross-bridges attach to actin at exposed binding sites and enter a cycle of shifts to crawl along the actin fiber. This causes the sarcomere to shorten. ATP is required for this reaction.
6. Cytosolic Ca²⁺ ions are removed and brought back into the sarcoplasmic reticulum by active transport (by a Ca²⁺ ATPase pump).
7. Tropomyosin blockage of myosin-binding sites is restored by Ca²⁺ ion removal). Contraction ends and the muscle fiber relaxes.  

The contraction of muscle cells results from the controlled interaction between actin and myosin proteins.  

Actin forms a thin filament coil structure comprised to two strands of actin and some additional regulatory proteins (troponin and tropomyosin). The actin coils are arranged above and below myosin bundles, which are also called thick filaments. One end of myosin forms a globular head shape that, in a relaxed state, is not able to bind to a site on actin. When the muscle is stimulated by a motor neuron, a signal cascade results in a conformational change that allows the myosin head to bind to actin and shift positions, allowing the muscle to shorten and contract.

While ATP is an essential component in the biochemistry of muscle contraction, it is not actually a protein. ATP is, instead, considered an amino acid derivative. Titin is the elastic protein that connects the ends of a sarcomere and allows the muscle to recoil when over-stretched.

Ca²⁺ plays a critical role in the regulation of muscle cell contraction and relaxation. Motor neuron stimulation and subsequent the action potential signals the release of Ca²⁺ from the sarcoplasmic reticulum. The ions bind to troponin—a protein found in a complex with tropomyosin and bound to actin filaments—and exposes the myosin-binding sites on the actin filament by shifting the troponin-tropomyosin complex. With the myosin-binding sites revealed, the myocyte will be able to contract.

In the absence of calcium in the cell, the binding sites on the actin filament cannot be made available and myosin will not bind. No contraction will occur.

There are three types of muscle tissue: skeletal muscle, smooth muscle, and cardiac muscle. Skeletal muscle is under voluntary control and is mainly responsible for locomotion and skeletal movement. Smooth muscle is involuntary and surrounds the viscera to aid in vascular constriction and organ movement. Cardiac muscle is found only in the heart and is responsible for pumping the blood.

The smooth muscle of the digestive tract is responsible for the wavelike movement of peristalsis. In humans, peristalsis is primarily responsible for helping move food down the digestive tract. It is important to understand that peristalisis is an involuntary movement.

The three types of muscle in the body are smooth, skeletal, and cardiac muscle. The type of muscle lining artery walls is smooth muscle, which is also present in many organs such as the intestines and the urinary bladder. Unlike skeletal muscle, smooth muscle control is involuntary and, unlike both skeletal and cardiac muscle, it is non-striated. Smooth muscle around the arteries and arterioles is important for regulating blood pressure and directing blood flow in the body.

Muscle is a major type of tissue in the human body. They contract and enable movement. The three major types of muscle tissues include skeletal, cardiac, and smooth tissues.

Skeletal muscle tissue is a categorization of muscle tissue that controls skeletal movement and posture. Skeletal muscle tissue is striated and made up of myocytes, which are organized into myofibrils. Skeletal muscle tissue can be categorized further into type I, type IIa, type IIx, and type IIb. These types include red—oxygenated—and white—deoxygenated—tissues.