What Is the Contraction Cycle

• The contraction of skeletal muscles is achieved by sliding actin and myosin filaments The cycle of muscle contraction is triggered by calcium ions that bind to the troponin protein complex and expose the active binding sites on actin. Once the actin binding sites are exposed, the high-energy myosin head closes the gap and forms a transverse bridge. Once the myosin binds to the actin, the pi is released and the myosin undergoes a conformational change at a lower energy state. When myosin consumes energy, it moves through the “force snap” and pulls the actin filament towards the M line. When the actin is pulled about 10 nm in the direction of the M line, the sarcomere shortens and the muscle contracts. At the end of the strength race, the myosin is in a low-energy position. Excitation-contraction coupling: This diagram shows the excitation-contraction coupling in a skeletal muscle contraction. The sarcoplasmic reticulum is a specialized endoplasmic reticulum found in muscle cells. The release of calcium ions triggers muscle contractions. Watch this video to learn more about the role of calcium. a) What are “T-tubules” and what role do they play? (b) Please describe how actin binding sites are provided for cross-bridging with myosin heads during contraction. Muscle contraction usually stops when motor neuron signaling ends, which repolarizes the sarcolemma and T tubules and closes the voltage-controlled calcium channels in the SR.

The Ca++ ions are then pumped into the SR, allowing tropomyosin to protect (or cover) the binding sites on the actin strands. A muscle can also stop contracting when it lacks ATP and fatigue (Figure 10.9). The sequence of events that leads to the contraction of a single muscle fiber begins with a signal – the neurotransmitter ACh – from the motor neuron, which innervates that fiber. The local membrane of the fiber depolarizes when positively charged sodium ions (Na+) enter, triggering an action potential that propagates to the rest of the membrane that depolarizes, including the T tubules. This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then triggers a contraction maintained by the ATP (Figure 10.8). As long as Ca++ ions remain in the sarcoplasm to bind to troponin, which keeps actin binding sites “unshielded,” and as long as ATP is available to drive the cross-bridge cycle and myosin pulling of actin strands, the muscle fiber will continue to shorten to an anatomical limit. ATP is crucial for muscle contractions because it breaks the myosin-actin transverse bridge and releases myosin for the next contraction.

ACh is broken down into acetyl and choline by the enzyme acetylcholinesterase (AChE). AChE is located in the synaptic cleft and breaks down ACh so that it does not remain bound to ACh receptors, which would lead to prolonged unwanted muscle contraction. Because DMD is caused by a mutation in the gene that codes for dystrophin, it was thought that introducing healthy myoblasts into patients could be an effective treatment. Myoblasts are the embryonic cells responsible for muscle development and, ideally, they would carry healthy genes that could produce the dystrophin needed for normal muscle contraction. This approach has been largely unsuccessful in humans. A more recent approach was to increase the production of utrophin in muscle, a dystrophin-like protein that could potentially play the role of dystrophin and prevent cell damage. The process of muscle contraction occurs through a number of key stages, including: When a neurotransmitter binds, these ion channels open and Na+ ions cross the membrane into the muscle cell. This reduces the voltage difference between the inside and outside of the cell, which is called depolarization. Since the ACh binds to the engine end plate, this depolarization is called end plate potential. Depolarization then propagates along the sarcolemma and along the T tubules, creating an action potential. The action potential triggers the release of Ca2+ from the sarcoplasmic reticulum, which activates troponin and stimulates muscle contraction. The area where the thick and thin filaments overlap has a dense appearance because there is little space between the filaments.

This area, where thin and thick filaments overlap, is very important for muscle contraction because it is where the movement of the filament begins. Thin filaments anchored at their ends through the Z discs do not extend completely into the central area, which contains only thick filaments anchored to their bases in a place called the M line. A myofibril consists of many sarcomeres that run along its length; Thus, myofibrils and muscle cells contract when sarcomeres contract. The concentration of calcium in muscle cells is controlled by the sarcoplasmic reticulum, a unique form of the endoplasmic reticulum in the sarcoplasm. .

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