Learning Goals
By the end of this reading you should be able to:
- Describe the different types of muscle tissue
- Draw the basic structure of a skeletal muscle fiber
- Explain the sliding filament model of muscle contraction
- Describe the factors that control muscle tension
Introduction
Muscle cells are specialized for contraction. Muscles allow for motions such as walking, and they also facilitate bodily processes such as respiration and digestion. The body contains three types of muscle tissue: skeletal muscle, cardiac muscle, and smooth muscle.
Skeletal muscle tissue forms skeletal muscles, which attach to bones or skin and control locomotion and any movement that can be consciously controlled. Because it can be controlled by thought, skeletal muscle is also called voluntary muscle. Skeletal muscles are long and cylindrical in appearance; when viewed under a microscope, skeletal muscle tissue has a striped or striated appearance. The striations are caused by the regular arrangement of contractile proteins (actin and myosin). Actin is a globular contractile protein that interacts with myosin for muscle contraction. Skeletal muscle also has multiple nuclei present in a single cell.
Smooth muscle tissue occurs in the walls of hollow organs such as the intestines, stomach, and urinary bladder, and around passages such as the respiratory tract and blood vessels. Smooth muscle has no striations, is not under voluntary control, has only one nucleus per cell, is tapered at both ends, and is called involuntary muscle.
Cardiac muscle tissue is only found in the heart, and cardiac contractions pump blood throughout the body and maintain blood pressure. Like skeletal muscle, cardiac muscle is striated, but unlike skeletal muscle, cardiac muscle cannot be consciously controlled and is called involuntary muscle. It has one nucleus per cell, is branched, and is distinguished by the presence of intercalated disks.
Review Question:
Quick Review: Differences in muscle tissues
Skeletal Muscle Fiber Structure
Each skeletal muscle fiber is a skeletal muscle cell. These cells are incredibly large, with diameters of up to 100 µm and lengths of up to 30 cm. The plasma membrane of a skeletal muscle fiber is called the sarcolemma. The sarcolemma is the site of action potential conduction, which triggers muscle contraction. Within each muscle fiber are myofibrils—long cylindrical structures that lie parallel to the muscle fiber. Myofibrils run the entire length of the muscle fiber, and because they are only approximately 1.2 µm in diameter, hundreds to thousands can be found inside one muscle fiber. They attach to the sarcolemma at their ends, so that as myofibrils shorten, the entire muscle cell contracts.
The striated appearance of skeletal muscle tissue is a result of repeating bands of the proteins actin and myosin that are present along the length of myofibrils. Dark A bands and light I bands repeat along myofibrils, and the alignment of myofibrils in the cell causes the entire cell to appear striated or banded.
Each I band has a dense line running vertically through the middle called a Z disc or Z line. The Z discs mark the border of units called sarcomeres, which are the functional units of skeletal muscle. One sarcomere is the space between two consecutive Z discs and contains one entire A band and two halves of an I band, one on either side of the A band. A myofibril is composed of many sarcomeres running along its length, and as the sarcomeres individually contract, the myofibrils and muscle cells shorten.
Myofibrils are composed of smaller structures called myofilaments. There are two main types of filaments: thick filaments and thin filaments; each has different compositions and locations. Thick filaments are composed of the protein myosin and occur only in the A band of a myofibril. Thin filaments are comprised primarily of actin, attach to a protein in the Z disc and occur across the entire length of the I band and partway into the A band. Actin has binding sites for myosin but strands of tropomyosin filaments block the sites and prevent actin-myosin interactions when the muscles are at rest. The final component of the thin filaments in troponin, which is a globular protein with three subunits. One subunit binds to the topomyosin, one to the actin and the last to Ca2+ ions.
This video reviews some of the key components of skeletal muscles: https://youtu.be/XoP1diaXVCI
Review Question:
Quick Review: Filaments
Sliding Filament Model of Contraction
For a muscle cell to contract, the sarcomere must shorten. However, thick and thin filaments—the components of sarcomeres—do not shorten. Instead, they slide by one another, causing the sarcomere to shorten while the filaments remain the same length. The sliding filament theory of muscle contraction was developed to fit the differences observed in the named bands on the sarcomere at different degrees of muscle contraction and relaxation. The mechanism of contraction is the binding of myosin to actin, forming cross-bridges that generate filament movement.
The sliding filament theory of muscle contraction can be broken down into four distinct stages;
1. Muscle activation: Each skeletal muscle fiber is controlled by a motor neuron, which conducts signals from the brain or spinal cord to the muscle. The area of the sarcolemma on the muscle fiber that interacts with the neuron is called the motor end plate. Electrical signals travel along the neuron’s axon, which branches through the muscle and connects to individual muscle fibers at a neuromuscular junction. In response to a neural signal, acetylcholine (a neurotransmitter) is released from the axon terminal and binds to receptors on the sarcolemma. An action potential is generated that stimulates calcium ion release from the sarcoplasmic reticulum.
2. Muscle contraction: Calcium floods into the muscle cell where it binds to troponin, causing conformational changes in troponin that allow tropomyosin to move away from the myosin-binding sites on actin. Once the tropomyosin is removed, a cross-bridge can form between actin and myosin. The myosin head at this point is “cocked,” it contains energy and is in a high-energy configuration. Pi is then released, allowing myosin to expend the stored energy as a conformational change. The myosin head moves toward the M line, pulling the actin along with it. As the actin is pulled, the filaments move toward the M line. This movement is called the power stroke, as it is the step at which force is produced. As the actin is pulled toward the M line, the sarcomere shortens, and the muscle contracts. After the movement, ADP is released; however, the cross-bridge formed is still in place, and actin and myosin are bound together.
3. Recharging: ATP can then attach to myosin, ATP binding causes myosin to release actin, allowing actin and myosin to detach from each other. After this happens, the newly bound ATP is converted to ADP and inorganic phosphate, Pi by an enzyme at the binding site on myosin called ATPase. The energy released during ATP hydrolysis changes the angle of the myosin head into a “cocked” position. The myosin head is then in a position for further movement, possessing potential energy, but ADP and Pi are still attached. This conformation change in myosin allows the cross-bridge cycle to start again and further muscle contraction can occur triggering contraction.
4. Relaxation: Relaxation occurs when stimulation of the nerve stops. Calcium is then pumped back into the sarcoplasmic reticulum breaking the link between actin and myosin. Actin and myosin return to their unbound state causing the muscle to relax. Alternatively, relaxation (failure) will also occur when ATP is no longer available.
This video demonstrates how all the parts of the system work together to create muscle movement. https://youtu.be/BVcgO4p88AA
Review Question:
Control of Muscle Tension
Neural control initiates the formation of actin-myosin cross-bridges, leading to the sarcomere shortening involved in muscle contraction. These contractions extend from the muscle fiber through connective tissue to pull on bones, causing skeletal movement. The pull exerted by a muscle is called tension, and the amount of force created by this tension can vary. This enables the same muscles to move very light objects and very heavy objects. In individual muscle fibers, the amount of tension produced depends on the cross-sectional area of the muscle fiber and the frequency of neural stimulation.
The number of cross-bridges formed between actin and myosin determines the amount of tension that a muscle fiber can produce. Cross-bridges can only form where thick and thin filaments overlap, allowing myosin to bind to actin. If more cross-bridges are formed, more myosin will pull on actin, and more tension will be produced.
The ideal length of a sarcomere during the production of maximal tension occurs when thick and thin filaments overlap to the greatest degree. If a sarcomere at rest is stretched past an ideal resting length, thick and thin filaments do not overlap to the greatest degree, and fewer cross-bridges can form. This results in fewer myosin heads pulling on actin, and less tension is produced. As a sarcomere is shortened, the zone of overlap is reduced as the thin filaments reach the H zone, which is composed of myosin tails. Because it is myosin heads that form cross-bridges, actin will not bind to myosin in this zone, reducing the tension produced by this myofiber. If the sarcomere is shortened, even more, thin filaments begin to overlap with each other—reducing cross-bridge formation even further and producing even less tension. Conversely, if the sarcomere is stretched to the point at which thick and thin filaments do not overlap at all, no cross-bridges are formed and no tension is produced. This amount of stretching does not usually occur because accessory proteins, internal sensory nerves, and connective tissue oppose extreme stretching.
The primary variable determining force production is the number of myofibers within the muscle that receive an action potential from the neuron that controls that fiber. When using the biceps to pick up a pencil, the motor cortex of the brain only signals a few neurons of the biceps, and only a few myofibers respond. In vertebrates, each myofiber responds fully if stimulated. When picking up a piano, the motor cortex signals all of the neurons in the biceps, and every myofiber participates. This is close to the maximum force the muscle can produce. As mentioned above, increasing the frequency of action potentials (the number of signals per second) can increase the force a bit more, because the tropomyosin is flooded with calcium.
Summary
The body contains three types of muscle tissue: skeletal muscle, cardiac muscle, and smooth muscle. Skeleton muscle tissue is composed of sarcomeres, the functional units of muscle tissue. Muscle contraction occurs when sarcomeres shorten, as thick and thin filaments slide past each other, which is called the sliding filament model of muscle contraction. ATP provides the energy for cross-bridge formation and filament sliding. Regulatory proteins, such as troponin and tropomyosin, control cross-bridge formation. The number of muscle fibers contracting determines how much force the whole muscle produces.
End of Section Review Questions:
Review: Blocking binding
Review: Muscle Structure
Review: Driving muscle contraction
References:
B
myosin
actin
A, B, C
B, D
tropomyosin
sarcolemma
