Mechanism of contraction

As mentioned previously, skeletal muscle fibers are very large cells with a wide diameter; the action potential is readily propagated, or transmitted, along the surface of the muscle fiber. However, a mechanism is needed to transmit the electrical impulse into the central region of the muscle fiber as well. The transverse tubules (T tubules) are invaginations of the cell membrane penetrating deep into the muscle fiber and surrounding each myofibril. (Imagine poking fingers into an inflated balloon.) As the action potential travels along the surface of the fiber, it is also transmitted into the T tubules. As a result, all regions of the muscle fiber are stimulated by the action potential.

All types of muscle require calcium for contraction. In skeletal muscle, Ca++ ions are stored within an extensive membranous network referred to as the sarcoplasmic reticulum. This network is found throughout the muscle fiber and surrounds each myofibril. Furthermore, segments of the sarcoplasmic reticulum lie adjacent to each T tubule that, with a segment of sarco-plasmic reticulum on either side of it, is referred to as a triad. As the action potential is transmitted along the T tubule, it stimulates the release of Ca++ ions from the sarcoplasmic reticulum. The only source of calcium for skeletal muscle contraction is the sarcoplasmic reticulum.

The mechanism of skeletal muscle contraction is described by the Sliding Filament Theory (see Figure 11.2). This mechanism begins with the "priming"

ATP binds

(a) Myosin

Myosin crossbridge

Myosin crossbridge

(b) High-energy myosin

Tropomyosin Troponin

(c) Binding

Tropomyosin Troponin

(d) Crossbridge cycling

(e) Detachment

ATP binds

ATP binds

Figure 11.2 Mechanism of skeletal muscle contraction. (a) Myosin — the myosin crossbridge has a binding site for ATP. (b) High-energy myosin — within the crossbridge, myosin ATPase splits ATP into ADP and inorganic phosphate (PJ. As a result, the crossbridge swivels outward and energy is stored. (c) Binding — in the presence of calcium, which binds to troponin, tropomyosin is repositioned into the groove between the two strands of actin. As a result, binding sites for myosin on the actin are uncovered and the crossbridges attach to actin. (d) Cross-bridge cycling — energy stored within the myosin crossbridge is released and the crossbridge swivels inward, pulling the actin inward. The ADP and Pj are released. (e) Detachment — binding of a new molecule of ATP to the myosin crossbridge allows myosin to detach from actin and the process begins again.

of the myosin crossbridge, a process that requires energy, which is supplied by adenosine triphosphate (ATP). Each myosin crossbridge contains myosin ATPase. When ATP attaches to its binding site on the myosin crossbridge, it is split by the myosin ATPase to yield adenosine diphosphate (ADP) and inorganic phosphate (Pi). The ADP and Pi remain tightly bound to the myosin crossbridge. Energy released by this process causes the myosin crossbridge to swivel outward toward the end of the thick filament. When the crossbridge is in this conformation, it is "primed" and referred to as the high-energy form of myosin; this form of myosin is capable of binding to actin. However, this interaction is prevented by tropomyosin, which physically covers the binding sites for myosin on the actin subunits. In order to uncover these binding sites, calcium is needed.

In a stimulated muscle fiber, Ca++ ions are released from the sarcoplasmic reticulum and bind to troponin. As a result, the troponin-actin linkage is weakened, allowing the tropomyosin to be repositioned such that the myo-sin-binding sites are uncovered. The myosin crossbridge now binds to the actin, causing the energy previously stored within the myosin to be discharged and the crossbridge to swivel inward toward the center of the thick filament. This process is referred to as crossbridge cycling. As the myosin crossbridge swivels inward, it pulls the actin inward as well. It is important to note that the interaction between actin and myosin causes the thin filaments to slide inward over the thick filaments toward the center of the sarcomere. Consequently, the sarcomeres shorten and the whole muscle shortens or contracts. It is for this reason that this process is referred to as the Sliding Filament Theory of muscle contraction.

When the myosin crossbridge binds with the actin, ADP and Pi are released from the myosin. This opens the binding site to another molecule of ATP. In fact, the myosin remains attached to the actin until another ATP molecule binds to the myosin. Binding of a new ATP causes the myosin to release the actin. This ATP is split by the ATPase and the myosin crossbridge swivels outward once again, returning the myosin to its high-energy state. As long as Ca++ ions are present and the binding sites on the actin are uncovered, crossbridge cycling continues. The crossbridges of the thick filament pull the thin filaments inward incrementally so that the sarcomeres become even shorter and the muscle contracts further.

Interestingly, the myosin crossbridges do not all cycle at the same time. At any given moment, some crossbridges remain attached to the actin and others are in the process of releasing the actin in order to cycle once again. In other words, myosin crossbridge cycling is staggered. This process maintains the shortening of the sarcomere and prevents thin filaments from slipping back to their original positions in between cycles.

In the absence of ATP, myosin crossbridges are unable to release the actin. As a result, the sarcomeres, and therefore the muscle, remain contracted. This phenomenon is referred to as rigor mortis. Following death, the concentration of intracellular calcium increases. This calcium allows the contractile process between the previously formed high-energy myosin and the actin to take place. However, the muscle stores of ATP are rapidly depleted, the myosin remains attached to the actin, and stiffness ensues.

When the action potentials in the alpha motor neuron cease, stimulation of muscle fiber is ended. Ca++ ions are pumped back into the sarcoplasmic reticulum and troponin and tropomyosin return to their original positions. As a result, the myosin-binding sites on the actin are covered once again. The thin filaments return passively to their original positions, resulting in muscle relaxation.

Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

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