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Chapter: Medical Physiology: Membrane Physiology, Nerve, and Muscle : Contraction of Skeletal Muscle

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Remodeling of Muscle to Match Function

All the muscles of the body are continually being remodeled to match the functions that are required of them.

Remodeling of Muscle to Match Function

All the muscles of the body are continually being remodeled to match the functions that are required of them. Their diameters are altered, their lengths are altered, their strengths are altered, their vascular sup-plies are altered, and even the types of muscle fibers are altered at least slightly. This remodeling process is often quite rapid, within a few weeks. Indeed, experiments in animals have shown that muscle contractile proteins in some smaller, more active muscles can be replaced in as little as 2 weeks.

Muscle Hypertrophy and Muscle Atrophy. When the totalmass of a muscle increases, this is called muscle hyper-trophy. When it decreases, the process is called muscle atrophy.

Virtually all muscle hypertrophy results from an increase in the number of actin and myosin filaments in each muscle fiber, causing enlargement of the individ-ual muscle fibers; this is called simply fiber hypertrophy. Hypertrophy occurs to a much greater extent when the muscle is loaded during the contractile process. Only a few strong contractions each day are required to cause significant hypertrophy within 6 to 10 weeks.

The manner in which forceful contraction leads to hypertrophy is not known. It is known, however, that the rate of synthesis of muscle contractile proteins is far greater when hypertrophy is developing, leading also to progressively greater numbers of both actin and myosin filaments in the myofibrils, often increasing as much as 50 per cent. In turn, some of the myofibrils themselves have been observed to split within hypertrophying muscle to form new myofibrils, but how important this is in usual muscle hypertrophy is still unknown.

Along with the increasing size of myofibrils, the enzyme systems that provide energy also increase. This is especially true of the enzymes for glycolysis, allowing rapid supply of energy during short-term forceful muscle contraction.

When a muscle remains unused for many weeks, the rate of decay of the contractile proteins is more rapid than the rate of replacement. Therefore, muscle atrophy occurs.

Adjustment of Muscle Length. Another type of hyper-trophy occurs when muscles are stretched to greater than normal length. This causes new sarcomeres to be added at the ends of the muscle fibers, where they attach to the tendons. In fact, new sarcomeres can be added as rapidly as several per minute in newly developing muscle, illustrating the rapidity of this type of hypertrophy.

Conversely, when a muscle continually remains short-ened to less than its normal length, sarcomeres at the ends of the muscle fibers can actually disappear. It is by these processes that muscles are continually remodeled to have the appropriate length for proper muscle contraction.

Hyperplasia of Muscle Fibers. Under rare conditions ofextreme muscle force generation, the actual number of muscle fibers has been observed to increase (but only by a few percentage points), in addition to the fiber hypertrophy process. This increase in fiber number is called fiber hyperplasia. When it does occur, the mech-anism is linear splitting of previously enlarged fibers.

Effects of Muscle Denervation. When a muscle loses itsnerve supply, it no longer receives the contractile signals that are required to maintain normal muscle size. Therefore, atrophy begins almost immediately. After about 2 months, degenerative changes also begin to appear in the muscle fibers themselves. If the nerve supply to the muscle grows back rapidly, full return of function can occur in as little as 3 months, but from that time onward, the capability of functional return becomes less and less, with no further return of function after 1 to 2 years.

In the final stage of denervation atrophy, most of the muscle fibers are destroyed and replaced by fibrous and fatty tissue. The fibers that do remain are composed of a long cell membrane with a lineup of muscle cell nuclei but with few or no contractile properties and little or no capability of regenerating myofibrils if a nerve does regrow.

The fibrous tissue that replaces the muscle fibers during denervation atrophy also has a tendency to con-tinue shortening for many months, which is called con-tracture. Therefore, one of the most important problemsin the practice of physical therapy is to keep atrophying muscles from developing debilitating and disfiguring contractures. This is achieved by daily stretching of the muscles or use of appliances that keep the muscles stretched during the atrophying process.

Recovery of Muscle Contraction in Poliomyelitis: Devel-opment of Macromotor Units. When some but not allnerve fibers to a muscle are destroyed, as commonly occurs in poliomyelitis, the remaining nerve fibers branch off to form new axons that then innervate many of the paralyzed muscle fibers. This causes large motor units called macromotor units, which can contain as many as five times the normal number of muscle fibers for each motoneuron coming from the spinal cord. This decreases the fineness of control one has over the muscles but does allow the muscles to regain varying degrees of strength.

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