Describe the structure and function of skeletal muscle fibers It starts with a signal from the nervous system. So it starts with a signal from your brain. The signal passes through your nervous system to your muscle. Your muscles contract and your bones move. And all of this happens incredibly fast. • Calcium ions and the proteins tropomyosin and troponin control muscle contractions The relaxation of skeletal muscle fibers and finally skeletal muscle begins with the motor neuron, which stops releasing its chemical signal, ACh, into the synapse at the NMJ. The muscle fiber will repolarize, which closes the doors in the SR where Ca++ has been released. ATP-controlled pumps will move Ca++ from the sarcoplasm to the SR. This leads to a “shielding” of the actin binding sites on thin filaments.
Without the ability to form transverse bridges between thin and thick filaments, the muscle fiber loses its tension and relaxes. Figure 6.9. This diagram shows the excitation-contraction coupling in a skeletal muscle contraction. The sarcoplasmic reticulum is a specialized endoplasmic reticulum found in muscle cells. When all the sarcomeres in a muscle fiber shorten, the fiber contracts. A muscle fiber contracts completely or does not contract at all. The number of fibers that contract determines the strength of muscle strength. If more fibers contract at the same time, the force is greater. Skeletal muscle is made up of cells collectively called muscle fibers. Each muscle fiber is multinucleated with its nuclei located along the periphery of the fiber. Each muscle fiber is further divided into myofibrils, which are the basic units of the muscle fiber.
These myofibrils are surrounded by the muscular cell membrane (sarkolemma), which forms deep intussusceptions called transverse tubules (T-tubules) in the myofibrillus. Each myofibril contains contractile proteins, described as thick, thin filaments, arranged longitudinally in units called sarcomeres. DMD is an inherited disease caused by an abnormal X chromosome. It mainly affects men and is usually diagnosed in early childhood. DMD usually occurs first as a difficulty with balance and movement, and then develops into an inability to walk. It progresses higher in the body from the lower limbs to the upper body, where it affects the muscles responsible for breathing and circulation. It eventually causes death due to respiratory failure, and sufferers usually do not live beyond the age of 20. Muscles cannot contract on their own.
They need a stimulus from a nerve cell to “tell” them to contract. Let`s say you decide to raise your hand in class. Your brain sends electrical messages to nerve cells called motor neurons in your arm and shoulder. Motor neurons, in turn, stimulate the muscle fibers in your arm and shoulder to contract, causing your arm to rise. Involuntary contractions of the heart and smooth muscles are also controlled by the nerves. To enable muscle contraction, tropomyosin must alter conformation, expose the myosin binding site to an actin molecule, and allow the formation of transverse bridges. This can only occur in the presence of calcium, which is maintained in the sarcoplasm at extremely low concentrations. When present, calcium ions bind to troponin, resulting in conformational changes in troponin that allow tropomyosin to move away from myosin binding sites on actin. Once tropomyosin is eliminated, a transverse bridge can form between actin and myosin, triggering contraction.
Transverse cycling will continue until Ca2+ ions and ATP are no longer available and tropomyosin again covers actin binding sites. In the relaxed muscle, the site of binding to myosin on actin is blocked by _________. When a muscle is at rest, actin and myosin are separated. To prevent actin from binding to the active center of myosin, regulatory proteins block molecular binding sites. Tropomyosin blocks myosin binding sites to actin molecules, prevents the formation of transverse bridges, and prevents contraction in a muscle without nerve input. Troponin binds to tropomyosin and helps position it on the actin molecule; It also binds calcium ions. When an event changes the permeability of the membrane for Na+ ions, they enter the cell. It changes the tension. This is an electrical event called action potential that can be used as a cellular signal. Communication between nerves and muscles is via neurotransmitters. The action potentials of neurons cause the release of neurotransmitters from the synaptic terminal into the synaptic cleft, where they can then diffuse through the synaptic cleft and bind to a receptor molecule on the motor end plate. The end plate of the motor has connecting folds – folds in the sarcolemma that create a large area for the neurotransmitter to bind to the receptors.
Receptors are actually sodium channels that open to allow Na+ to pass into the cell when they receive a neurotransmitter signal. The deadly nerve gas sarin irreversibly inhibits acetylcholinesterase. What effect would sarin have on muscle contraction? After depolarization, the membrane returns to its resting state. This is called repolarization, in which voltage-dependent sodium channels close. Potassium channels remain at 90% conductivity. Since the sodium-potassium atPase plasma membrane always carries ions, the resting state (negatively charged inside relative to the outside) is restored. The period immediately after the transmission of an impulse into a nerve or muscle, in which a neuron or muscle cell regains its ability to transmit another impulse, is called the refractory period. During the refractory period, the membrane can no longer generate action potential. The refractory period allows voltage-sensitive ion channels to return to their resting configurations. Sodium-potassium ATPase continuously moves Na+ out of the cell and K+ into the cell, and K+ exits, leaving a negative charge. Very quickly, the membrane repolarizes so that it can be depolarized again.
Each muscle fiber contains hundreds of organelles called myofibrils. .