Muscle ion

A muscle fiber contraction is a complex interaction of several cellular and chemical constituents. The final result is a movement within the myofibrils in which the filaments of actin and myosin slide past one another, shortening the sarcomeres. When this happens, the muscle fiber shortens and pulls on its attachments.

Actin, myosin, troponin, and tropomyosin are abundant in muscle cells. Scarcer proteins are also vital to muscle function. This is the case for a rod-shaped muscle protein called dystrophin. It accounts for only 0.002% of total muscle protein in skeletal muscle, but its absence causes the devastating inherited disorder Duchenne muscular dystrophy, a disease that usually affects boys. Dystrophin binds to the inside face of muscle cell membranes, supporting them against the powerful force of contraction. Without even these minute amounts of dystrophin, muscle cells burst and die. Other forms of muscular dystrophy result from abnormalities of other proteins to which dystrophin attaches.

The Sliding Filament Theory

The sarcomere is considered the functional unit of skeletal muscles. This is because contraction of an entire skeletal muscle can be described in terms of the shortening of sarcomeres within it. According to the sliding filament theory, when sarcomeres shorten, the thick and thin filaments do not themselves change length. Rather, they just slide past one another, with the thin filaments moving toward the center of the sarcomere from both ends. As this occurs, the H zones and the I bands get narrower, the regions of overlap widen, and the Z lines move closer together, shortening the sarcomere (fig. 9.8).

Neuromuscular Junction

Each skeletal muscle fiber is connected to an extension (a nerve axon) of a motor neuron (mo'tor nu'ron) that passes outward from the brain or spinal cord. Normally a skeletal muscle fiber contracts only upon stimulation by a motor neuron.

The site where the axon and muscle fiber meet is called a neuromuscular junction (myoneural junction). There, the muscle fiber membrane is specialized to form a motor end plate, where nuclei and mitochondria are abundant and the sarcolemma is extensively folded (fig. 9.9).

Myoneural Junction

Figure

Within the sarcoplasm of a skeletal muscle fiber are a network of sarcoplasmic reticulum and a system of transverse tubules.

Figure

Within the sarcoplasm of a skeletal muscle fiber are a network of sarcoplasmic reticulum and a system of transverse tubules.

A muscle fiber usually has a single motor end plate. Motor neuron axons, however, are densely branched. By means of these branches, one motor neuron axon may connect to many muscle fibers. Together, a motor neuron and the muscle fibers it controls constitute a motor unit (mo'tor u'nit) (fig. 9.10).

A small gap called the synaptic cleft separates the membrane of the neuron and the membrane of the muscle fiber. The cytoplasm at the distal ends of the nerve fiber is rich in mitochondria and contains many tiny vesicles (synaptic vesicles) that store chemicals called neurotransmitters (nu"ro-trans'mit-erz).

Stimulus for Contraction

Acetylcholine (ACh) is the neurotransmitter that motor neurons use to control skeletal muscle. ACh is synthesized in the cytoplasm of the motor neuron and is stored in synaptic vesicles near the distal end of its axon. When a nerve impulse (or action potential, described in chapter 10, page 376) reaches the end of the axon, some of these vesicles release acetylcholine into the synaptic cleft (see fig. 9.9).

Acetylcholine diffuses rapidly across the synaptic cleft, combines with ACh receptors on the motor endplate, and stimulates the muscle fiber. The response is a muscle impulse, an electrical signal that is very much like a nerve impulse. A muscle impulse changes the muscle cell membrane in a way that transmits the impulse in all directions along and around the muscle cell, into the transverse tubules, into the sarcoplasm, and ultimately to the sar-coplasmic reticulum and the cisternae. Clinical Application 9.1 discusses myasthenia gravis, in which the immune system attacks certain neuromuscular junctions.

In the summer months of the early 1950s, parents in the United States lived in terror of their children contracting poliomyelitis, a viral infection that attacks nerve cells that stimulate skeletal muscles to contract. In half of the millions of affected children, fever, headache, and nausea rapidly progressed to a stiffened back and neck, drowsiness, and then the feared paralysis, usually of the lower limbs or muscles that control breathing or swallowing. Today, many a middle-aged person with a limp owes this slight disability to polio. Vaccines introduced in the middle 1950s ended the nightmare of polio—or so we thought.

Today, a third of the 1.6 million polio survivors in the United States are experiencing the fatigue, muscle weakness and atrophy, and difficulty breathing of post-polio syndrome. Researchers do not yet know whether this condition is a reactivation of the past infection, a new infection, or the effect of aging on nerve cells damaged in childhood.

Sarcomere

Sarcomere

Sarcomere

What Cause Vessels Weakness
2) Slightly contracted
Polio Victims 1950s
3) Further contracted

Sarcomere

Botulism Cell

Figure 9.8

When a skeletal muscle contracts, individual sarcomeres shorten as thick and thin filaments slide past one another (23,000x).

In September 1985, two teenage tourists from Hong Kong went to the emergency room at Montreal Children's Hospital complaining of extreme nausea and weakness. Although doctors released them when they could not identify a cause of the symptoms, the girls returned that night — far sicker. Now they were becoming paralyzed and had difficulty breathing. This time, physicians recognized symptoms of botulism.

Botulism occurs when the bacterium Clostridium botu-linum grows in an anaerobic (oxygen-poor) environment, such as in a can of food. The bacteria produce a toxin that prevents the release of acetylcholine from nerve terminals. Symptoms include nausea, vomiting, and diarrhea; headache, dizziness, and blurred or double vision; and finally, weakness, hoarseness, and difficulty swallow ing and, eventually, breathing. Fortunately, physicians can administer an antitoxin substance that binds to and inactivates botulinum toxin in the bloodstream, stemming further symptoms, although not correcting damage already done.

Prompt treatment saved the touring teens, and astute medical detective work led to a restaurant in Vancouver where they and thirty-four others had eaten roast beef sandwiches. The bread had been coated with a garlic-butter spread. The garlic was bottled with soybean oil and should have been refrigerated. It was not. With bacteria that the garlic had picked up in the soil where it grew, and eight months sitting outside of the refrigerator, conditions were just right for C. botulinum to produce its deadly toxin.

Neuron Motor End Plate

Figure 9.9

(a) A neuromuscular junction includes the end of a motor neuron and the motor end plate of a muscle fiber. (b) Micrograph of a neuromuscular junction (500x).

Motor neuron

Muscle fiber nucleus

Neuromuscular junctions

Skeletal muscle fibers

Motor neuron

Muscle fiber nucleus

Neuromuscular junctions

Skeletal muscle fibers

Neuromuscular Junctions And Motor Units

Muscle fibers within a motor unit may be distributed throughout the muscle.

Figure 9.10

Muscle fibers within a motor unit may be distributed throughout the muscle.

Motor neuron axon

Muscle fiber

Neuromuscular junction

Motor neuron axon

Neuromuscular junction

Excitation Contraction Coupling

Excitation Contraction Coupling

The sarcoplasmic reticulum has a high concentration of calcium ions compared to the cytosol. This is due to active transport of calcium ions (calcium pump) in the membrane of the sarcoplasmic reticulum. In response to a muscle impulse, the membranes of the cisternae become more permeable to these ions, and the calcium ions diffuse out of the cisternae into the cytosol of the muscle fiber (see fig. 9.7).

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Responses

  • isembard gammidge
    How does sarcomere appear when the muscle is fatigued?
    6 years ago
  • ermenegildo
    Where is myoneural junction?
    1 year ago

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