8.4: Muscle Cells

The muscles are composed primarily of muscle cells, which perform the three functions of the muscle system. Other materials in each muscle include nerve cells, collagen and elastin fibers, fat, and blood vessels (Figure 8.2).

Figure 8.2 Components of a skeletal muscle. (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

Structure and Functioning

The main activity of muscle cells is contraction, which produces both the force needed for movement and support and most of the heat derived from the muscle system. Muscle cells have many specializations that permit them to perform contraction.

Muscle cells are very long and thin, reaching lengths of up to several centimeters. Usually, these cells are as long as the muscle in which they are contained. Because of their shape, muscle cells are also called muscle fibers (Figure 8.2).

Cell Membrane (Sarcolemma)

The muscle cell membrane (sarcolemma) is modified in three ways (Figure 8.3a, Figure 8.3b). First, the spot on the membrane that receives stimulatory messages from a somatic motor neuron is highly convoluted. This modified area (motor end plate) apparently provides more surface area and receptor molecules to receive and respond to molecules of acetylcholine from the somatic motor neuron. Second, the cell membrane can carry messages in the form of action potentials, just as axons do. Third, the membrane has many penetrating indentations (T tubules), which deliver action potentials deep within the cell.

Figure 8.3a Components of a muscle cell. (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.

Figure 8.3b Neuromuscular junction. (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

Myoglobin, Oxygen, and Energy

The muscle cell cytoplasm (sarcoplasm) contains a protein called myoglobin, which is found only in muscle cells and causes muscles to appear red in color. Myoglobin attracts oxygen from the blood into the muscle cells and stores oxygen. As soon as a muscle cell uses some of the oxygen, its myoglobin quickly attracts more (Figure 8.4).

Figure 8.4 Obtaining energy in muscle cells. (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

The muscle cell uses the oxygen to obtain energy from sugar and other nutrient molecules. As long as the cell has enough oxygen, it can obtain much energy from nutrients while producing only carbon dioxide (CO₂) and water as waste products. The CO₂ and water are easily removed from the cell and can be eliminated from the body by the respiratory and urinary systems, respectively.

When a person engages in vigorous activity, the amount of oxygen required to produce the energy needed by a muscle cell often rises above the supply of oxygen to the cell. The cell can continue to work because some energy can be obtained by breaking nutrients down partially. One of the main waste products from this process is lactic acid (Figure 8.4), which tends to accumulate in muscle cells and causes them to become acidic. A result of lactic acid accumulation is weakening of the muscle cell's contractions. The affected person experiences fatigue in the forms of muscle weakness and muscle pain. The person also feels out of breath.

If activity decreases, the circulatory and respiratory systems can again deliver oxygen to the muscle cell faster than oxygen is consumed. The extra oxygen is used to complete the breakdown of lactic acid into CO₂ and water; this not only eliminates the lactic acid but also makes a large amount of energy available to the muscle cell. The affected person's sensation of fatigue subsides and he or she may claim, "I have caught my breath." The oxygen used to eliminate the lactic acid produced by vigorous exercise is called the oxygen debt.

Much of what has just been said is also true of cardiac muscle cells. For example, when cardiac or skeletal muscle cells accumulate lactic acid, they become weak. However, unlike cardiac muscle cells, skeletal muscle cells are rarely seriously injured or killed by lactic acid. These cells can continue to work with lactic acid present as long as the acid concentration does not become too severe. Still, exceedingly high levels of lactic acid will prevent skeletal muscle cells from contracting.

Contraction

The membranes of the endoplasmic reticulum within muscle cells are arranged in the form of lacy tubes that extend over the length of the cell (Figure 8.3). These membranes are called sarcoplasmic reticulum and regulate the movement of calcium ions needed for contraction.

The region in the cell surrounded by each tube of sarcoplasmic reticulum contains an array of tiny fibers called myofilaments. Clusters of thick myofilaments alternate with clusters of thin myofilaments (Figure 8.5). The alternating clusters overlap to form units called sarcomeres, which extend from one end of the cell to the other like links in a chain. Each chain of sarcomeres is surrounded by sarcoplasmic reticulum and is called a myofibril.

Figure 8.5 Myofilaments and the process of contraction. (Copyright 2020: Augustine G. DiGiovanna, Ph.D., Salisbury University, Maryland. Used with permission.)

When the cell is stimulated and action potentials pass over the sarcolemma, the sarcoplasmic reticulum releases calcium, which causes the thick myofilaments to pull on the thin myofilaments and slide farther among them. The pulling and sliding cause the muscle cell to become shorter; contraction has occurred. The contraction applies a pulling force to the bone or other structure to which the muscle is attached, and the structure is either moved or held in place.

Recall that energy for contraction comes from the breakdown of nutrient molecules. Only some of the energy released from these molecules is converted into movement of the myofilaments; the remainder is converted into heat. This is why muscles produce so much heat when they contract.

Types of muscle cells The proportions of muscle cell components are different among muscle cells, so the cells have different characteristics. Type I fibers contract more slowly and can work longer before becoming fatigued. Type IIA fibers contract more quickly and resist becoming fatigued, also. Type IIB fibers contract quickly, but they become fatigued quickly. Type II fibers are intermediate between Type IIA and Type IIB. Type IIA and Type IIB fibers are most important for fast and powerful movements. Different muscles have different combinations of these types of muscle cells, and the combinations change gradually during adulthood.

Age Changes in Muscle Cells

Internal Components

As muscle cells age, the convolutions in the motor end plate decrease and the sarcolemma becomes smoother. The resulting decrease in surface area diminishes the ability of the muscle cell to be stimulated by the motor neuron. Other changes in the sarcolemma cause the action potentials that lead to contraction to become weaker, slower, and more irregular. Because of the changes in the action potentials, the cell takes longer to begin to contract and is less able to recover from one contraction and prepare for the next. Age-related slowing of calcium release and retrieval by the sarcoplasmic reticulum contribute to these effects.

The large-scale results of these cellular age changes include a longer time to respond when a person wants to move suddenly and a diminished ability to perform rapidly repeated movements such as playing fast music on a piano. Muscle composed of aging cells also has a weaker maximum strength when used for activities requiring rapid and very strong contractions, such as grasping a handrail to stop a fall.

Another change in aging muscle cells is a decrease in the substances used to supply energy for contraction (ATP, creatine phosphate, glycogen). Much of this change seems to be caused by a decrease in exercise rather than by aging. Lack of exercise also seems to cause most of the decrease in the enzymes that extract energy from nutrients. There is even a decrease in the number and size of mitochondria, which perform most of the energy extraction. Many remaining mitochondria have been damaged, so they are less efficient and produce more free radicals (*FRs). Some muscle cells seem to accumulate damaged mitochondria and become sources of *FR damage to surrounding cells. All these changes leave the cells with less energy, especially for tasks requiring a prolonged effort.

The final substantive change inside muscle cells is a decrease in the number of sarcomeres within the myofibrils. This tends to cause the cells and the muscles they compose to become shorter and have a reduced distance through which they can move. The affected person experiences stiffness and diminished freedom of movement. The loss of sarcomeres also reduces the strength of the cells and muscles.

Cell Thickness

Since muscle cells that get little exercise lose parts of their internal components, they decrease in thickness. This shrinkage is prevalent among the elderly because of the general reduction in physical activity as people age. Regularly exercised muscles show little change in cell thickness until age 70 or beyond. Even then, there is only a slight thinning of cells in muscles that receive plenty of exercise. Therefore, reduction in exercise rather than aging is the main cause of muscle cell thinning and much of the consequent decrease in muscle thickness and strength that usually accompanies advancing age.

Cell Number

Most of the decrease in the thickness of muscles with aging is caused by the death of muscle cells. Up to half the muscle cells in a muscle may be lost by late old age. This loss occurs in exercised muscles and in muscles receiving little use. Lost muscle cells are not replaced by new ones because except in very unusual circumstances, adult muscle cells cannot form new muscle cells.

Type II fibers become thinner and are lost faster than Type I fibers. The ratios of loss are different for different muscles. Some muscles may lose Type II fibers more than twice as fast as they lose Type I fibers. Type IIB fibers are lost faster than Type IIA fibers. Some of the loss of Type II fibers may be from conversion to Type I fibers. Most age-related decreases in strength and speed result from thinning and loss of Type II fibers.

In muscles receiving much regular strenuous exercise, the space left by the lost cells may be largely filled by the remaining cells. This occurs because muscle cells pulling against heavy loads on a regular basis adapt by synthesizing more internal components. The additional components increase the thickness and strength of these cells, which encroach on the vacant areas. As a result, the decline in thickness and strength of exercised muscles is slow.

Aging muscles that receive little strenuous exercise have the spaces left by lost cells filled with fibrous tissue and fat. Such muscles become thinner and considerably weaker as time passes.

Cell Repair

Though muscle cells are unable to reproduce, they can repair themselves after an injury. One common cause of injury is contracting against a load much heavier than that normally encountered by muscle cells. This type of injury can be sustained when a person who normally lifts objects weighing less than 30 pounds tries to support a 60-pound object.

A muscle containing muscle cells injured by an excessive force, such as lifting a heavy object, is weakened and causes the sensations of muscle soreness and stiffness. If the muscle is rested, the injured muscle cells will repair themselves within a few days and the soreness and stiffness will subside. As was mentioned above, the cells will adapt to the heavy demands previously placed on them by becoming thicker and stronger. They will then be more resistant to injury caused by excessive loads. For muscle cells receiving regular strenuous exercise, the ability to repair injury and recover from such weakness and soreness is not altered by aging.

It is uncertain whether muscle cells that receive little exercise can repair themselves as quickly as exercised muscle cells do. Still, muscle cells in exercised or unused muscles retain the ability to adapt to heavier loads by manufacturing internal components. Thus, the thickness and strength of muscles can be increased by strenuous exercise regardless of age. However, muscle cells in older individuals make the compensatory increase in thickness more slowly.