Skeletal Muscle Cells
Much of what scientists know about cell movement has been learned from studying the contraction of muscle cells. Vertebrate animals are able to move via the contraction of skeletal muscles, which in turn can occur only through contractions initiated at the cellular level. For example, when skeletal muscle cells contract, the skeletal muscle tissue as a whole contracts. As a result of this, a bone moves. Then the organism moves. In essence, an organism's complex movement can only be initiated through movement of the tiniest cell.
Skeletal muscles move bones by contracting and shortening. Each muscle is composed of long fibers that run along the length of it. Each individual fiber is considered a single muscle cell called a myocyte. Components of muscle fibers include:
- Myofibril - a bundle of thick and thin filaments that make up muscle fibers. Within a myofibril are thin filaments called actin, and thick filaments called myosin.
- Actin - also called G-actin, is a protein found in all eukaryotic cells. Its monomeric form is the subunit of actin filaments. Alternating with the actin filaments are thick filaments of myosin.
- Myosin - a motor protein that uses ATP to drive movements along actin filaments. Each myosin fiber has a bulbous head region and a long tail. This tail attaches to the tails of other myosin fibers, creating the thickness of myosin.
Muscle Fiber Structure
- The start of a muscle contraction induces the release of calcium ions.
- This calcium binds to troponin, the protein associated with the actin filaments, which causes tropomyosin to move away from and expose the active myosin-binding site of the actin filament. This myosin-binding site is the site of origin of the muscle contraction.
- The head of the myosin fiber, which is bound to ATP, interacts with the active site of actin. Once the actin and ATP are bound together, a cross bridge is formed. A cross bridge is the structure formed when the myosin head is bound to the actin.
- The myosin heads pull the actin molecule, called the power stroke, causing it to slide past the myosin filament and thereby shorten the muscle. while releasing then returns to a lower energy state because of the release of the phosphate from the ATP.
- The myosin releases ADP. New ATP binds to the myosin heads, thereby breaking the actin-myosin bond at the myosin binding site.
- The actin moves toward the center of the sarcomere with each myosin cycle. As a result, the myosin head attaches at a site farther along the actin fiber, shortening the muscle each time.
The arrival of an action potential at the end of a motor neuron causes the release of the neurotransmitter acetylcholine, which stimulates the muscle to shorten. As the muscle shortens, it pulls on the tendon (a strong fibrous tissue), which pulls on the bone. This process occurs repeatedly until the muscle has shortened enough to the move the bone as required, causing the nerve signal to stop. Muscles can only pull on bone; they cannot push. In order for the bone to move back the other way, a different muscle must contract while the original muscle relaxes. A muscle contraction requires multiple binding and release events between actin and myosin filaments.
Myosin has approximately 300 active heads in each filament, which can form approximately five cross bridges per second. It is this rapid attachment and release that makes actin and myosin slide past each other. A protein called troponin attaches itself to another protein called tropomyosin, which is found in the grooves along the actin fibers. When the muscle is relaxed, the tropomyosin blocks the attachment of the myosin, thereby preventing cross bridges from forming.
When skeletal muscle cells are at rest, sufficient ATP is readily available for only a few muscle contractions. When muscle cells need to contract more than once, or for longer periods of time, creatine phosphate and glycogen are used to generate additional ATP to energize the contraction. Creatine phosphate releases a phosphate molecule to adenine diphosphate (ADP) so it can hydrolyze into ATP. Additionally, glycogen breaks down into glucose, which enters into the cellular respiration pathway to generate more ATP.Sliding Filament Model
Muscle Contraction and Relaxation
Smooth Muscle Cells
The cells of smooth muscle differ in structure from skeletal muscle cells but also rely on actin and myosin to contract. Smooth muscle, which is involuntary in its action, differs from skeletal muscle in that it lacks visible striations (stripes) and its muscle fibers are attached to structures called dense bodies. A dense body serves as an anchor point for the sarcomere as the fibers contract. Smooth muscle contractions are slow. Like striated muscle, smooth muscle depends upon the concentration of calcium ions (Ca2+) but uses different pathways. The calcium in smooth muscle activates an enzyme called a kinase, which transfers a phosphate group from ATP to another molecule. This changes the shape of myosin heads in order to form cross bridges.
Unlike a skeletal muscle contraction that pulls the myosin and actin past each other, a smooth muscle contraction clasps the cell from all directions. This is because the myofibrils are not aligned along the main axis of the cell in a uniform pattern. When the stimulus is received to initiate a contraction, calcium is released into the cytoplasm of the cell. This calcium binds to a calcium-binding protein, which attaches to an enzyme that phosphorylates, or changes the structure of through the addition of a phosphate group, the myosin head. This action causes a release of additional neurotransmitters, or chemicals that bind to receptors and excite or inhibit cells that come after the gaps between nerve cells. When the neurotransmitter reaches the smooth muscle cell membrane, it activates a special protein that, along with a series of enzymes, allows the myosin to form a cross bridge with the actin filament. The phosphorylated myosin head has a high affinity for the active sites on the actin filaments. As long as the levels of calcium remain stable, the smooth muscle fibers will remain contracted. Lowering of the calcium levels induces the relaxation of the muscle. Smooth muscle has no troponin, and its tropomyosin does not cover the active sites.
Various neurotransmitters have effects on smooth muscle - some inhibitory, others excitatory -depending on the location of and types of receptors on the smooth muscle tissue. Acetylcholine, which is released from parasympathetic neurons and intrinsic nerves of the gastrointestinal tract, directly causes contraction of smooth muscle via muscarinic receptors. Also released from the intrinsic nerves of the gastrointestinal system is the neurotransmitter nitric oxide, or NO, which serves as the major inhibitory neurotransmitter of smooth muscle in the gastrointestinal tract. As a result, smooth muscle relaxes in response to NO.
Cardiac Muscle Cells
Cardiac muscle cells are found only in the tissues that make up the heart. These cells create a striated appearance in the heart tissue but are considered involuntary. They can produce their own contractions without the input of the nervous system. This is because of the specialized cells that act to initiate the contraction. Each of these pacemaker cells sends a signal throughout the heart by way of an intercalated disk, which is a structure that connects cardiac muscle cells and supports cardiac muscle contraction. The electrical signals from the pacemakers are transported through the intercalated disks to generate the action potentials needed to contract the muscle tissue.
Cardiac excitation-contraction coupling is the contraction and immediate relaxation of the heart muscle. This occurs when there is an influx of calcium and sodium ions into the cytoplasm of the cardiac muscle cells. These calcium and sodium ions trigger action potentials to travel down the sarcomere and change the structure of the myosin heads. Similar to skeletal muscle tissue, the myosin within cardiac muscle binds to the actin to form a cross bridge with the input of ATP. Myosin and actin pull on each other, shortening the length of the muscle. The muscle stays contracted as long as the calcium and sodium levels are high, but because the stimulus is short lived, the cardiac muscle relaxes quickly in order to contract again almost immediately. This keeps blood moving through the heart.