Like neurons, muscle cells are excitable—that is, their cell membranes generate and conduct action potentials. Action potentials are initiated in skeletal muscle fibers by motor neurons arriving at neuromuscular junctions (see Key Concept 44.3). The axon terminals of motor neurons are generally highly branched and form synapses with hundreds of muscle fibers (Figure 47.4). A motor neuron and all of the fibers with which it synapses constitute a motor unit. The fibers contract simultaneously when the unit’s motor neuron fires. One muscle can consist of many motor units. Thus there are two ways to increase a muscle’s strength of contraction—increase the firing rate of an individual motor neuron, or recruit more motor neurons.

Question

If a motor neuron innervates only one or a few fibers, it is likely that those fibers are used in fine movements. If a single motor neuron innervates many muscle fibers of a muscle, it will be able to command strong, forceful movements.

When an action potential arrives at a neuromuscular junction, the neurotransmitter acetylcholine is released from the motor neuron terminals, diffuses across the synaptic cleft, binds to receptors in the postsynaptic membrane, and causes ion channels in the motor end plate to open (see Figure 44.11). Most of the ions that flow through these channels are Na⁺, and therefore the motor end plate is depolarized. The depolarization spreads to the surrounding cell membrane of the muscle fiber, which contains voltage-gated sodium channels. When threshold is reached, the cell membrane fires an action potential that is conducted rapidly to all points on the surface of the muscle fiber.

An action potential in a muscle fiber also travels deep within the cell. The cell membrane is continuous with a system of T tubules that descend into the muscle fiber cytoplasm (also called the sarcoplasm). The “T” stands for “transverse.” The contents of the T tubules are ouside the cell. The T tubules are like the indentations created in a water-filled balloon by poking your finger into it. The action potential that spreads over the cell membrane also spreads through this system of T tubules (Figure 47.5).

The T tubules come very close to the endoplasmic reticulum (ER) of the muscle cell. In muscle cells the ER is called the sarcoplasmic reticulum, and it is a closed compartment surrounding every myofibril. Calcium pumps in the sarcoplasmic reticulum take up Ca²⁺ from the sarcoplasm. Therefore when the muscle fiber is at rest, there is a high concentration of Ca²⁺ in the sarcoplasmic reticulum and a very low concentration of Ca²⁺ in the sarcoplasm.

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Spanning the space between the membranes of the T tubules and the membranes of the sarcoplasmic reticulum are two proteins. One protein, the dihydropyridine (DHP) receptor, is located in the T tubule membrane; it is voltage-sensitive and changes its conformation in response to an action potential spreading through the T tubule system. The other protein, the ryanodine receptor, is located in the sarcoplasmic reticulum membrane and is a Ca²⁺ channel. These two proteins are physically connected. When the DHP receptor changes its conformation due to an action potential, it causes Ca²⁺ to flow through the ryanodine receptor from the sarcoplasmic reticulum to the sarcoplasm. Ca²⁺ ions diffusing through the sarcoplasm surrounding the actin and myosin filaments trigger the interaction of actin and myosin and the sliding of the filaments. How do the Ca²⁺ ions do this?

An actin filament, as you have seen, is a helical arrangement of actin monomers. Twisted around the actin filament are two strands of the protein tropomyosin (Focus: Key Figure 47.6; see also Figure 47.3). At regular intervals, the filament also includes a globular protein, troponin. The troponin molecule has three subunits: one binds actin, one binds tropomyosin, and one binds Ca²⁺.

When the muscle is at rest, the tropomyosin strands are positioned so that they block the myosin-binding sites on the actin filaments. When Ca²⁺ is released into the sarcoplasm, it binds to troponin, changing its conformation. Because the troponin is bound to the tropomyosin, this conformational change twists the tropomyosin enough to expose the actin–myosin binding sites, and the cycle of making and breaking actin–myosin bonds is initiated. The filaments pull past each other, and the muscle fiber contracts. When the calcium pumps in the sarcoplasmic reticulum membranes remove the Ca²⁺ ions from the sarcoplasm, the conformation of the tropomyosin reverts and again blocks the binding of myosin heads to actin, and the muscle fiber returns to its resting condition. Figure 47.6 summarizes this cycle.