types of skeletal fibers

10.6 Types of Skeletal Muscle Fibers

OBJECTIVE

Compare the structure and function of the three types of skeletal muscle fibers.

Skeletal muscle fibers are not all alike in composition and function. For example, muscle fibers vary in their content of myoglobin, the red-colored protein that binds oxygen in muscle fibers. Skeletal muscle fibers that have a high myoglobin content are termed red muscle fibers and appear darker (the dark meat in chicken legs and thighs); those that have a low content of myoglobin are called white muscle fibers and appear lighter (the white meat in chicken breasts). Red muscle fibers also contain more mitochondria and are supplied by more blood capillaries.

Skeletal muscle fibers also contract and relax at different speeds, and vary in which metabolic reactions they use to generate ATP and in how quickly they fatigue. For example, a fiber is categorized as either slow or fast depending on how rapidly the ATPase in its myosin heads hydrolyzes ATP. Based on all these structural and functional characteristics, skeletal muscle fibers are classified into three main types: (1) slow oxidative fibers, (2) fast oxidative–glycolytic fibers, and (3) fast glycolytic fibers.

Slow Oxidative Fibers

Slow oxidative (SO) fibers appear dark red because they contain large amounts of myoglobin and many blood capillaries. Because they have many large mitochondria, SO fibers generate ATP mainly by aerobic respiration, which is why they are called oxidative fibers. These fibers are said to be “slow” because the ATPase in the myosin heads hydrolyzes ATP relatively slowly, and the contraction cycle proceeds at a slower pace than in “fast” fibers. As a result, SO fibers have a slow speed of contraction. Their twitch contractions last from 100 to 200 msec, and they take longer to reach peak tension. However, slow fibers are very resistant to fatigue and are capable of prolonged, sustained contractions for many hours. These slow-twitch, fatigue-resistant fibers are adapted for maintaining posture and for aerobic, endurance-type activities such as running a marathon.

Fast Oxidative–Glycolytic Fibers

Fast oxidative–glycolytic (FOG) fibers are typically the largest fibers. Like slow oxidative fibers, they contain large amounts of myoglobin and many blood capillaries. Thus, they also have a dark red appearance. FOG fibers can generate considerable ATP by aerobic respiration, which gives them a moderately high resistance to fatigue. Because their intracellular glycogen level is high, they also generate ATP by anaerobic glycolysis. FOG fibers are “fast” because the ATPase in their myosin heads hydrolyzes ATP three to five times faster than the myosin ATPase in SO fibers, which makes their speed of contraction faster. Thus, twitches of FOG fibers reach peak tension more quickly than those of SO fibers but are briefer in duration—less than 100 msec. FOG fibers contribute to activities such as walking and sprinting.

Fast Glycolytic Fibers

Fast glycolytic (FG) fibers have low myoglobin content, relatively few blood capillaries, and few mitochondria, and appear white in color. They contain large amounts of glycogen and generate ATP mainly by glycolysis. Due to their ability to hydrolyze ATP rapidly, FG fibers contract strongly and quickly. These fast glycolytic fibers are adapted for intense movements of short duration, such as weight lifting or throwing a ball, but they fatigue quickly. Strength training programs that engage a person in activities requiring great strength for short times increase the size, strength, and glycogen content of fast glycolytic fibers. The FG fibers of a weight lifter may be 50% larger than those of a sedentary person or an endurance athlete because of increased synthesis of muscle proteins. The overall result is muscle enlargement due to hypertrophy of the FG fibers.

Distribution and Recruitment of Different Types of Fibers

Most skeletal muscles are a mixture of all three types of skeletal muscle fibers; about half of the fibers in a typical skeletal muscle are SO fibers. However, the proportions vary somewhat, depending on the action of the muscle, the person’s training regimen, and genetic factors. For example, the continually active postural muscles of the neck, back, and legs have a high proportion of SO fibers. Muscles of the shoulders and arms, in contrast, are not constantly active but are used briefly now and then to produce large amounts of tension, such as in lifting and throwing. These muscles have a high proportion of FG fibers. Leg muscles, which not only support the body but are also used for walking and running, have large numbers of both SO and FOG fibers.

Within a particular motor unit, all of the skeletal muscle fibers are of the same type. The different motor units in a muscle are recruited in a specific order, depending on need. For example, if weak contractions suffice to perform a task, only SO motor units are activated. If more force is needed, the motor units of FOG fibers are also recruited. Finally, if maximal force is required, motor units of FG fibers are also called into action with the other two types. Activation of various motor units is controlled by the brain and spinal cord.

Table 10.4 summarizes the characteristics of the three types of skeletal muscle fibers.

Checkpoint

Why are some skeletal muscle fibers classified as “fast” and others are said to be “slow”?

In what order are the various types of skeletal muscle fibers recruited when you sprint to make it to the bus stop?

10.7 Exercise and Skeletal Muscle Tissue

OBJECTIVE

Describe the effects of exercise on different types of skeletal muscle fibers.

The relative ratio of fast glycolytic (FG) and slow oxidative (SO) fibers in each muscle is genetically determined and helps account for individual differences in physical performance. For example, people with a higher proportion of FG fibers (see Table 10.4) often excel in activities that require periods of intense activity, such as weight lifting or sprinting. People with higher percentages of SO fibers are better at activities that require endurance, such as long-distance running.

TABLE 10.4 Characteristics of the Three Types of Skeletal Muscle Fibers

An L M micrograph at 440 times magnification shows a transverse section of three types of skeletal muscle fibers. The dark cells are slow oxidative fibers, the pale cells are fast glycolytic fibers, and the gray cells are fast oxidative-glycolytic fibers.

Slow Oxidative (SO) Fibers

Fast Oxidative–Glycolytic (FOG) Fibers

Fast Glycolytic (FG) Fibers

STRUCTURAL CHARACTERISTIC

Myoglobin content

Large amount.

Small amount.

Mitochondria

Many.

Few.

Capillaries

Many.

Few.

Color

Red.

Red-pink.

White (pale).

FUNCTIONAL CHARACTERISTIC

Capacity for generating ATP and method used

High, by aerobic respiration.

Intermediate, by both aerobic respiration and anaerobic glycolysis.

Low, by anaerobic glycolysis.

Rate of ATP hydrolysis by myosin ATPase

Slow.

Fast.

Contraction velocity

Slow.

Fast.

Fatigue resistance

High.

Intermediate.

Low.

Creatine kinase

Lowest amount.

Intermediate amount.

Highest amount.

Glycogen stores

Low.

Intermediate.

High.

Order of recruitment

First.

Second.

Third.

Location where fibers are abundant

Postural muscles such as those of neck.

Lower limb muscles.

Extraocular muscles.

Primary functions of fibers

Maintaining posture and aerobic endurance activities.

Walking, sprinting.

Rapid, intense movements of short duration.

Although the total number of skeletal muscle fibers usually does not increase with exercise, the characteristics of those present can change to some extent. Various types of exercises can induce changes in the fibers in a skeletal muscle. Endurance-type (aerobic) exercises, such as running or swimming, cause a gradual transformation of some FG fibers into fast oxidative–glycolytic (FOG) fibers. The transformed muscle fibers show slight increases in diameter, number of mitochondria, blood supply, and strength. Endurance exercises also result in cardiovascular and respiratory changes that cause skeletal muscles to receive better supplies of oxygen and nutrients but do not increase muscle mass. By contrast, exercises that require great strength for short periods produce an increase in the size and strength of FG fibers. The increase in size is due to increased synthesis of thick and thin filaments. The overall result is muscle enlargement (hypertrophy), as evidenced by the bulging muscles of body builders.

A certain degree of elasticity is an important attribute of skeletal muscles and their connective tissue attachments. Greater elasticity contributes to a greater degree of flexibility, increasing the range of motion of a joint. When a relaxed muscle is physically stretched, its ability to lengthen is limited by connective tissue structures, such as fasciae. Regular stretching gradually lengthens these structures, but the process occurs very slowly. To see an improvement in flexibility, stretching exercises must be performed regularly—daily, if possible—for many weeks.

Clinical Connection

Anabolic Steroids

Anabolic steroids (an-a-BOL-ik = muscle building) are synthetic variations of testosterone, the sex hormone responsible for the development of male sexual characteristics. Common names for anabolic steroids are “raids,” “juice,” “gear,” and “stackers.” Specifically, anabolic steroids increase muscle size by increasing protein synthesis in muscles, which increases strength. Although anabolic steroids can be prescribed to build muscle mass in patients with medical conditions such as cancer and AIDS and to treat delayed puberty, athletes and bodybuilders can abuse the drugs to improve physical appearance or enhance performance. Individuals who use anabolic steroids typically take them orally, by injection directly into the muscles, or by application to the skin. When anabolic steroids are abused, they are usually taken in doses that range from 10 to 100 times those needed to treat medical conditions.

The large doses needed to produce the desired results can result in a number of side effects that range from mild to harmful to life-threatening. Among these are the following:

Cardiovascular. Changes in blood cholesterol levels, enlarged heart, high blood pressure, and blood clot formation, that can increase the risk of heart attack and stroke.

Liver. Liver cancer, liver damage, and blood-filled cysts that may rupture and result in internal bleeding.

Musculoskeletal. Short stature, stunted growth during puberty and adolescence, and tendon injury.

Integumentary. Severe acne, oily hair and skin, baldness, and jaundice (due to liver damage).

Infections. Non-sterile injection techniques and shared needles can lead to HIV infection and hepatitis B and C.

Behavioral problems. Aggression, increased irritability, extreme mood swings, delusions, and impaired judgment.

Anabolic steroids also have gender-specific side effects:

Males. Atrophy of the testes, decreased testosterone levels, low sperm count, development of breasts, and increased risk of prostate cancer.

Females. Atrophy of the breasts and uterus, menstrual irregularities, enlarged clitoris, sterility, growth of facial hair, and deepening of the voice.

Effective Stretching

Stretching cold muscles does not increase flexibility and may cause injury. Tissues stretch best when slow, gentle force is applied at elevated tissue temperatures. An external source of heat, such as hot packs or ultrasound, may be used, but 10 or more minutes of muscular contraction is also a good way to raise muscle temperature. Exercise heats muscle more deeply and thoroughly than external measures. That’s where the term “warm-up” comes from. Many people stretch before they engage in exercise, but it’s important to warm up (for example, walking, jogging, easy swimming, or easy aerobics) before stretching to avoid injury.

Strength Training

Strength training refers to the process of exercising with progressively heavier resistance for the purpose of strengthening the musculoskeletal system. This activity results not only in stronger muscles, but in many other health benefits as well. Strength training also helps to increase bone strength by increasing the deposition of bone minerals in young adults and helping to prevent, or at least slow, their loss in later life. By increasing muscle mass, strength training raises resting metabolic rate, the amount of energy expended at rest, so a person can eat more food without gaining weight. Strength training helps to prevent back injury and other injuries from participation in sports and other physical activities. Psychological benefits include reductions in feelings of stress and fatigue. As repeated training builds exercise tolerance, it takes increasingly longer before lactic acid is produced in the muscle, resulting in a reduced probability of muscle spasms.

Checkpoint

On a cellular level, what causes muscle hypertrophy?

10.8 Cardiac Muscle Tissue

OBJECTIVE

Describe the main structural and functional characteristics of cardiac muscle tissue.

The principal tissue in the heart wall is cardiac muscle tissue (described in more detail in Chapter 20 and illustrated in Figure 20.9). Between the layers of cardiac muscle fibers (the contractile cells of the heart) are sheets of connective tissue that contain blood vessels, nerves, and the conduction system of the heart. Cardiac muscle fibers have the same arrangement of actin and myosin and the same bands, zones, and Z discs as skeletal muscle fibers. T tubules of cardiac muscle are wider but less abundant than those of skeletal muscle; there is one T tubule per sarcomere, located at the Z disc. The sarcoplasmic reticulum of cardiac muscle fibers is somewhat smaller than the SR of skeletal muscle fibers. However, intercalated discs (in-TER-ka-lāt-ed; intercal- = to insert between) are unique to cardiac muscle fibers. These microscopic structures are irregular transverse thickenings of the sarcolemma that connect the ends of cardiac muscle fibers to one another. The discs contain desmosomes, which hold the fibers together, and gap junctions, which allow muscle action potentials to spread from one cardiac muscle fiber to another (see Figure 4.2e). Cardiac muscle tissue has an endomysium and perimysium, but lacks an epimysium.

In response to a single action potential, cardiac muscle tissue remains contracted 10 to 15 times longer than skeletal muscle tissue (see Figure 20.11). The long contraction is due to prolonged delivery of Ca2+ into the sarcoplasm. In cardiac muscle fibers, Ca2+ enters the sarcoplasm both from the sarcoplasmic reticulum (as in skeletal muscle fibers) and from the interstitial fluid that bathes the fibers. Because the channels that allow inflow of Ca2+ from interstitial fluid stay open for a relatively long time, a cardiac muscle contraction lasts much longer than a skeletal muscle twitch.

We have seen that skeletal muscle tissue contracts only when stimulated by acetylcholine released by a nerve impulse in a motor neuron. In contrast, cardiac muscle tissue contracts when stimulated by its own autorhythmic muscle fibers. Under normal resting conditions, cardiac muscle tissue contracts and relaxes about 75 times a minute. This continuous, rhythmic activity is a major physiological difference between cardiac and skeletal muscle tissue. The mitochondria in cardiac muscle fibers are larger and more numerous than in skeletal muscle fibers. This structural feature correctly suggests that cardiac muscle depends largely on aerobic respiration to generate ATP, and thus requires a constant supply of oxygen. Cardiac muscle fibers can also use lactic acid produced by skeletal muscle fibers to make ATP, a benefit during exercise. Like skeletal muscle, cardiac muscle fibers can undergo hypertrophy in response to an increased workload. This is called a physiological enlarged heart and it is why many athletes have enlarged hearts. By contrast, a pathological enlarged heart is related to significant heart disease.

Checkpoint

What are the similarities and differences among skeletal and cardiac muscle?

10.9 Smooth Muscle Tissue

OBJECTIVE

Describe the main structural and functional characteristics of smooth muscle tissue.

Like cardiac muscle tissue, smooth muscle tissue is usually activated involuntarily. Of the two types of smooth muscle tissue, the more common type is visceral (single-unit) smooth muscle tissue (Figure 10.16a). It is found in the skin and in tubular arrangements that form part of the walls of small arteries and veins and of hollow organs such as the stomach, intestines, uterus, and urinary bladder. Like cardiac muscle, visceral smooth muscle is autorhythmic. The fibers connect to one another by gap junctions, forming a network through which muscle action potentials can spread. When a neurotransmitter, hormone, or autorhythmic signal stimulates one fiber, the muscle action potential is transmitted to neighboring fibers, which then contract in unison, as a single unit.

The second type of smooth muscle tissue, multi-unit smooth muscle tissue (Figure 10.16b), consists of individual fibers, each with its own motor neuron terminals and with few gap junctions between neighboring fibers. Stimulation of one visceral muscle fiber causes contraction of many adjacent fibers, but stimulation of one multi-unit fiber causes contraction of that fiber only. Multi-unit smooth muscle tissue is found in the walls of large arteries, in airways to the lungs, in the arrector muscles of the hair that attach to hair follicles, in the muscles of the iris that adjust pupil diameter, and in the ciliary body that adjusts focus of the lens in the eye.

Microscopic Anatomy of Smooth Muscle

A single relaxed smooth muscle fiber is 30–200 µm long. It is thickest in the middle (3–8 µm) and tapers at each end (Figure 10.16c). Within each fiber is a single, oval, centrally located nucleus. The sarcoplasm of smooth muscle fibers contains both thick filaments and thin filaments, in ratios between 1:10 and 1:15, but they are not arranged in orderly sarcomeres as in striated muscle. Smooth muscle fibers also contain intermediate filaments. Because the various filaments have no regular pattern of overlap, smooth muscle fibers do not exhibit striations (see Table 4.9), causing a smooth appearance. Smooth muscle fibers also lack T tubules and have only a small amount of sarcoplasmic reticulum for storage of Ca2+. Although there are no T tubules in smooth muscle tissue, there are small pouchlike invaginations of the plasma membrane called caveolae (kav′-ē-Ō-lē; cavus = space) that contain extracellular Ca2+ that can be used for muscular contraction.

In smooth muscle fibers, the thin filaments attach to structures called dense bodies, which are functionally similar to Z discs in striated muscle fibers. Some dense bodies are dispersed throughout the sarcoplasm; others are attached to the sarcolemma. Bundles of intermediate filaments also attach to dense bodies and stretch from one dense body to another (Figure 10.16c). During contraction, the sliding filament mechanism involving thick and thin filaments generates tension that is transmitted to intermediate filaments. These in turn pull on the dense bodies attached to the sarcolemma, causing a lengthwise shortening of the muscle fiber. As a smooth muscle fiber contracts, it rotates as a corkscrew turns. The fiber twists in a helix as it contracts, and rotates in the opposite direction as it relaxes.

A three-part diagram shows the structure of smooth muscle tissue. Diagram (a) in visceral, or single unit, smooth muscle tissue the spindle-shaped nucleated cells are joined closely together in cords innervated by autonomic neurons. Diagram (b) in multi-unit smooth muscle tissue, the long, tapering muscle fibers are spread out and connected by branching autonomic neurons. Diagram (c) microscopic anatomy of a relaxed smooth muscle fiber and a contracted smooth muscle fiber. The relaxed muscle fiber shows a diamond pattern of intermediate filaments connected by dense bodies. Sarcolemma with their thick and thin filaments are shown. When relaxed, the muscle fiber is long and tapered. The contracted fiber appears shorter and wider.

FIGURE 10.16 Smooth muscle tissue. (a) One autonomic motor neuron synapses with several visceral smooth muscle fibers, and action potentials spread to neighboring fibers through gap junctions. (b) Three autonomic motor neurons synapse with individual multi-unit smooth muscle fibers; stimulation of one multi-unit fiber causes contraction of that fiber only. (c) Relaxed and contracted smooth muscle fiber. A photomicrograph of smooth muscle tissue is shown in Table 4.9.

Visceral smooth muscle fibers connect to one another by gap junctions and contract as a single unit. Multi-unit smooth muscle fibers lack gap junctions and contract independently.

Q Which type of smooth muscle is more like cardiac muscle than skeletal muscle, with respect to both its structure and function?

Physiology of Smooth Muscle

Although the principles of contraction are similar, smooth muscle tissue exhibits some important physiological differences from cardiac and skeletal muscle tissue. Contraction in a smooth muscle fiber starts more slowly and lasts much longer than skeletal muscle fiber contraction. Another difference is that smooth muscle can both shorten and stretch to a greater extent than the other muscle types.

An increase in the concentration of Ca2+ in the sarcoplasm of a smooth muscle fiber initiates contraction, just as in striated muscle. Sarcoplasmic reticulum (the reservoir for Ca2+ in striated muscle) is found in small amounts in smooth muscle. Calcium ions flow into smooth muscle sarcoplasm from both the interstitial fluid and sarcoplasmic reticulum. Because there are no T tubules in smooth muscle fibers (there are caveolae instead), it takes longer for Ca2+ to reach the filaments in the center of the fiber and trigger the contractile process. This accounts, in part, for the slow onset of contraction of smooth muscle.

Several mechanisms regulate contraction and relaxation of smooth muscle cells. In one such mechanism, a regulatory protein called calmodulin (cal-MOD-ū-lin) binds to Ca2+ in the sarcoplasm. (Recall that troponin takes this role in striated muscle fibers.) After binding to Ca2+, calmodulin activates an enzyme called myosin light chain kinase. This enzyme uses ATP to add a phosphate group to a portion of the myosin head. Once the phosphate group is attached, the myosin head can bind to actin, and contraction can occur. Because myosin light chain kinase works rather slowly, it contributes to the slowness of smooth muscle contraction.

Not only do calcium ions enter smooth muscle fibers slowly, they also move slowly out of the muscle fiber, which delays relaxation. The prolonged presence of Ca2+ in the cytosol provides for smooth muscle tone, a state of continued partial contraction. Smooth muscle tissue can thus sustain long-term tone, which is important in the digestive canal, where the walls maintain a steady pressure on the contents of the canal, and in the walls of blood vessels called arterioles, which maintain a steady pressure on blood.

Most smooth muscle fibers contract or relax in response to nerve impulses from the autonomic nervous system. In addition, many smooth muscle fibers contract or relax in response to stretching, hormones, or local factors such as changes in pH, oxygen and carbon dioxide levels, temperature, and ion concentrations. For example, the hormone epinephrine, released by the suprarenal medulla, causes relaxation of smooth muscle in the airways and in some blood vessel walls (those that have so-called β2 receptors; see Table 15.2).

Unlike striated muscle fibers, smooth muscle fibers can stretch considerably and still maintain their contractile function. When smooth muscle fibers are stretched, they initially contract, developing increased tension. Within a minute or so, the tension decreases. This phenomenon, which is called the stress–relaxation response, allows smooth muscle to undergo great changes in length while retaining the ability to contract effectively. Thus, even though smooth muscle in the walls of blood vessels and hollow organs such as the stomach, intestines, and urinary bladder can stretch, the pressure on the contents within them changes very little. After the organ empties, the smooth muscle in the wall rebounds, and the wall retains its firmness.

Checkpoint

What are the differences between visceral and multi-unit smooth muscle?

How are skeletal and smooth muscle similar? How do they differ?

10.10 Regeneration of Muscular Tissue

OBJECTIVE

Explain how muscle fibers regenerate.

Because mature skeletal muscle fibers have lost the ability to undergo cell division, growth of skeletal muscle after birth is due mainly to hypertrophy (hī-PER-trō-fē), the enlargement of existing cells, rather than to hyperplasia (hī-per-PLĀ-zē-a), an increase in the number of fibers. Satellite cells divide slowly and fuse with existing fibers to assist both in muscle growth and in repair of damaged fibers. Thus, skeletal muscle tissue can regenerate only to a limited extent.

Until recently it was believed that damaged cardiac muscle fibers could not be replaced and that healing took place exclusively by fibrosis, the formation of scar tissue. New research described in Chapter 20 indicates that, under certain circumstances, cardiac muscle tissue can regenerate. In addition, cardiac muscle fibers can undergo hypertrophy in response to increased workload. Hence, many athletes have enlarged hearts.

Smooth muscle tissue, like skeletal and cardiac muscle tissue, can undergo hypertrophy. In addition, certain smooth muscle fibers, such as those in the uterus, retain their capacity for division and thus can grow by hyperplasia. Also, new smooth muscle fibers can arise from cells called pericytes, stem cells found in association with blood capillaries and small veins. Smooth muscle fibers can also proliferate in certain pathological conditions, such as occur in the development of atherosclerosis (see Disorders: Homeostatic Imbalances in Chapter 20). Compared with the other two types of muscle tissue, smooth muscle tissue has considerably greater powers of regeneration. Such powers are still limited when compared with other tissues, such as epithelium.

Table 10.5 summarizes the major characteristics of the three types of muscular tissue.

TABLE 10.5 Major Features of the Three Types of Muscular Tissue

Characteristic

Skeletal Muscle

Cardiac Muscle

Smooth Muscle

Microscopic appearance and features

Long cylindrical fiber with many peripherally located nuclei; unbranched; striated.

Branched cylindrical fiber with one centrally located nucleus; intercalated discs join neighboring fibers; striated.

Fiber thickest in middle, tapered at each end, and with one centrally positioned nucleus; not striated.

An unlabeled diagram shows a skeletal muscle tissue, as a long cylindrical fiber with numerous nuclei.

A diagram shows a cardiac muscular tissue, which is branched out in a web pattern.

A diagram shows visceral or smooth muscle tissue, which is thin and small, shaped like slivers of muscle rather than thick cords or webs.

Location

Most commonly attached by tendons to bones.

Heart.

Walls of hollow viscera, airways, blood vessels, iris and ciliary body of eye, arrector muscles of the hair.

Fiber diameter

Very large (10–100 µm).

Large (10–20 µm).

Small (3–8 µm).

Connective tissue components

Endomysium, perimysium, and epimysium.

Endomysium and perimysium.

Endomysium.

Fiber length

Very large (100 µm–30 cm = 12 in.).

Large (50–100 µm).

Intermediate (30–200 µm).

Contractile proteins organized into sarcomeres

Yes.

No.

Sarcoplasmic reticulum

Abundant.

Some.

Very little.

T tubules present

Yes, aligned with each A–I band junction.

Yes, aligned with each Z disc.

No.

Junctions between fibers

None.

Intercalated discs contain gap junctions and desmosomes.

Gap junctions in visceral smooth muscle; none in multi-unit smooth muscle.

Autorhythmicity

No.

Yes.

Yes, in visceral smooth muscle.

Source of Ca2+ for contraction

Sarcoplasmic reticulum.

Sarcoplasmic reticulum and interstitial fluid.

Regulator proteins for contraction

Troponin and tropomyosin.

Calmodulin and myosin light chain kinase.

Speed of contraction

Fast.

Moderate.

Slow.

Nervous control

Voluntary (somatic nervous system).

Involuntary (autonomic nervous system).

Contraction regulation

Acetylcholine released by somatic motor neurons.

Acetylcholine and norepinephrine released by autonomic motor neurons; several hormones.

Acetylcholine and norepinephrine released by autonomic motor neurons; several hormones; local chemical changes; stretching.

Capacity for regeneration

Limited, via satellite cells.

Limited, under certain conditions.

Considerable (compared with other muscle tissues, but limited compared with epithelium), via pericytes.

Checkpoint

Which type of muscular tissue has the highest capacity for regeneration?

10.11 Development of Muscle

OBJECTIVE

Describe the development of muscles.

Except for muscles such as those of the iris of the eyes and the arrector pili muscles attached to hairs, all muscles of the body are derived from mesoderm. As the mesoderm develops, part of it becomes arranged in dense columns on either side of the developing nervous system. These columns of mesoderm undergo segmentation into a series of cube-shaped structures called somites (SŌ-mīts) (Figure 10.17a). The first pair of somites appears on the 20th day of embryonic development. Eventually, 42 to 44 pairs of somites are formed by the end of the fifth week. The number of somites can be correlated to the approximate age of the embryo.

The cells of a somite differentiate into three regions: (1) a myotome (MĪ-ō-tōm), which, as the name suggests, forms the skeletal muscles of the trunk and limbs; (2) a dermatomal mesenchyme (der-ma-TŌM-al), which forms the connective tissues, including the dermis of the skin and subcutaneous tissue; and (3) a sclerotome (SKLE-rō-tōm), which gives rise to the vertebrae and ribs (Figure 10.17b).

Cardiac muscle develops from mesodermal cells that migrate to and envelop the developing heart while it is still in the form of endocardial heart tubes (see Figure 20.19).

Smooth muscle develops from mesodermal cells that migrate to and envelop the developing digestive canal and viscera.

A two-part diagram shows the development of muscle. Diagram (a) Dorsal view of an embryo showing somites at about 22 days. The head end and tail end are separated by a transverse plane. The head end shows the developing nervous system, including the neural plate and the two neural folds separated by the neural grove. The somites are small orbs inferior and lateral to the neural groove. Diagram (b) Transverse section through a somite showing its subdivisions. The somites on either side of the developing nervous system are made up of layers of dermatomal mesenchyme, myotome, and sclerotome. The notochord and a blood vessel that will become the aorta are inferior to the developing nervous system.

FIGURE 10.17 Location and structure of somites, key structures in the development of the muscular system.

Most muscles are derived from mesoderm.

Q Which part of a somite differentiates into skeletal muscle of the trunk and ribs?

Checkpoint

Which structures develop from myotomes, dermatomal mesenchyme, and sclerotomes?

10.12 Aging and Muscular Tissue

OBJECTIVE

Explain the effects of aging on skeletal muscle.

Between the ages of 30 and 50, humans undergo a slow, progressive loss of skeletal muscle mass that is replaced largely by fibrous connective tissue and adipose tissue. An estimated 10% of muscle mass is lost during these years. In part, this decline may be due to decreased levels of physical activity. Accompanying the loss of muscle mass is a decrease in maximal strength, a slowing of muscle reflexes, and a loss of flexibility. With aging, the relative number of slow oxidative (SO) fibers appears to increase. This could be due to either the atrophy of the other fiber types or their conversion into slow oxidative fibers. Another 40% of muscle is typically lost between the ages of 50 and 80. Loss of muscle strength is usually not perceived by persons until they reach the age of 60 to 65. At that point it is most common for muscles of the lower limbs to weaken before those of the upper limbs. Thus the independence of the elderly may be affected when it becomes difficult to climb stairs or get up from a seated position.

Assuming that there is not a chronic medical condition for which exercise is contraindicated, exercise has been shown to be effective at any age. Aerobic activities and strength training programs are effective in older people and can slow or even reverse the age-associated decline in muscular performance.

Checkpoint

Why does muscle strength decrease with aging?

Why do you think a healthy 30-year-old can lift a 25-lb load much more comfortably than an 80-year-old?

Disorders: Homeostatic Imbalances

Abnormalities of skeletal muscle function may be due to disease or damage of any of the components of a motor unit: somatic motor neurons, neuromuscular junctions, or muscle fibers. The term neuromuscular disease encompasses problems at all three sites; the term myopathy (mī-OP-a-thē; - pathy= disease) signifies a disease or disorder of the skeletal muscle tissue itself.

Myasthenia Gravis

Myasthenia gravis (mī-as-THĒ-nē-a GRAV-is; mys- = muscle; -aisthesis = sensation) is an autoimmune disease that causes chronic, progressive damage of the neuromuscular junction. The immune system inappropriately produces antibodies that bind to and block some ACh receptors, thereby decreasing the number of functional ACh receptors at the motor end plates of skeletal muscles (see Figure 10.9). Because 75% of patients with myasthenia gravis have hyperplasia or tumors of the thymus, it is thought that thymic abnormalities cause the disorder. As the disease progresses, more ACh receptors are lost. Thus, muscles become increasingly weaker, fatigue more easily, and may eventually cease to function.

Myasthenia gravis occurs in about 1 in 10,000 people and is more common in women, typically ages 20 to 40 at onset; men usually are ages 50 to 60 at onset. The muscles of the face and neck are most often affected. Initial symptoms include weakness of the eye muscles, which may produce double vision, and weakness of the throat muscles that may produce difficulty in swallowing. Later, the person has difficulty chewing and talking. Eventually the muscles of the limbs may become involved. Death may result from paralysis of the respiratory muscles, but often the disorder does not progress to that stage.

Anticholinesterase drugs such as pyridostigmine (Mestinon) or neostigmine, the first line of treatment, act as inhibitors of acetylcholinesterase, the enzyme that breaks down ACh. Thus, the inhibitors raise the level of ACh that is available to bind with still-functional receptors. More recently, steroid drugs such as prednisone have been used with success to reduce antibody levels. Another treatment is plasmapheresis, a procedure that removes the antibodies from the blood. Often, surgical removal of the thymus (thymectomy) is helpful.

Muscular Dystrophy

The term muscular dystrophy (DIS-trō-fē′; dys- = difficult; - trophy= nourishment) refers to a group of inherited muscle-destroying diseases that cause progressive degeneration of skeletal muscle fibers. The most common form of muscular dystrophy is Duchenne muscular dystrophy (DMD) (doo-SHĀN). Because the mutated gene is on the X chromosome, and because males have only one X chromosome, DMD strikes boys almost exclusively. (Sex-linked inheritance is described in Chapter 29.) Worldwide, about 1 in every 3500 male babies—about 21,000 in all—are born with DMD each year. The disorder usually becomes apparent between the ages of 2 and 5, when parents notice the child falls often and has difficulty running, jumping, and hopping. By age 12 most boys with DMD are unable to walk. Respiratory or cardiac failure usually causes death by age 20.

In DMD, the gene that codes for the protein dystrophin is mutated, so little or no dystrophin is present in the sarcolemma. Without the reinforcing effect of dystrophin, the sarcolemma tears easily during muscle contraction, causing muscle fibers to rupture and die. The dystrophin gene was discovered in 1987. Treatments include steroids to reduce inflammation and strengthen muscles; eteplirsen and golodirsen, drugs that target gene mutations; creatine supplements to improve muscle strength; range of motion exercises; braces; and mobility aids.

Abnormal Contractions of Skeletal Muscle

One kind of abnormal muscular contraction is a spasm, a sudden involuntary contraction of a single muscle in a large group of muscles. A painful spasmodic contraction is known as a cramp. Cramps may be caused by inadequate blood flow to muscles, overuse of a muscle, dehydration, injury, holding a position for prolonged periods, and low blood levels of electrolytes, such as potassium. A tic is a spasmodic twitching made involuntarily by muscles that are ordinarily under voluntary control. Twitching of the eyelid and facial muscles are examples of tics. A tremor is a rhythmic, involuntary, purposeless contraction that produces a quivering or shaking movement. A fasciculation (fa-sik-ū-LĀ-shun) is an involuntary, brief twitch of an entire motor unit that is visible under the skin; it occurs irregularly and is not associated with movement of the affected muscle. Fasciculations may be seen in multiple sclerosis (see Disorders: Homeostatic Imbalances in Chapter 12) or in amyotrophic lateral sclerosis (Lou Gehrig’s disease; see Clinical Connection: Amyotrophic Lateral Sclerosis in Chapter 16). A fibrillation (fi-bri-LĀ-shun) is a spontaneous contraction of a single muscle fiber that is not visible under the skin but can be recorded by electromyography. Fibrillations may signal destruction of motor neurons.

Exercise-induced Muscle Damage

Comparison of electron micrographs of muscle tissue taken from athletes before and after intense exercise reveals considerable exercise-induced muscle damage, including torn sarcolemmas in some muscle fibers, damaged myofibrils, and disrupted Z discs. Microscopic muscle damage after exercise also is indicated by increases in blood levels of proteins, such as myoglobin and the enzyme creatine kinase, which are normally confined within muscle fibers. From 12 to 48 hours after a period of strenuous exercise, skeletal muscles often become sore. Such delayed onset muscle soreness (doms) is accompanied by stiffness, tenderness, and swelling. Although the causes of doms are not completely understood, microscopic muscle damage appears to be a major factor. In response to exercise-induced muscle damage, muscle fibers undergo repair: new regions of sarcolemma are formed to replace torn sarcolemmas, and more muscle proteins (including those of the myofibrils) are synthesized in the sarcoplasm of the muscle fibers.

Medical Terminology

Myalgia (mī-AL-jē-a; -algia = painful condition) Pain in or associated with muscles.

Myoma (mī-Ō-ma; -oma = tumor) A tumor consisting of muscle tissue.

Myomalacia (mī′-Ō-ma-LĀ-shē-a; -malacia = soft) Pathological softening of muscle tissue.

Myositis (mī′-ō-SĪ-tis; -itis = inflammation of) Inflammation of muscle fibers.

Myotonia (mī′-ō-TŌ-nē-a; -tonia = tension) Increased muscular excitability and contractility, with decreased power of relaxation; tonic spasm of the muscle.

Volkmann’s contracture (FŌLK-manz kon-TRAK-chur; contra- = against) Permanent shortening (contracture) of a muscle due to replacement of destroyed muscle fibers by fibrous connective tissue, which lacks extensibility. Typically occurs in forearm flexor muscles. Destruction of muscle fibers may occur from interference with circulation caused by a tight bandage, a piece of elastic, or a cast.

Chapter Review

Review

Introduction

1. Motion results from alternating contraction and relaxation of muscles, which constitute 40–50% of total body weight.

2. The prime function of muscle is changing chemical energy into mechanical energy to perform work.

10.1 Overview of Muscular Tissue

1. The three types of muscular tissue are skeletal, cardiac, and smooth. Skeletal muscle tissue is primarily attached to bones; it is striated and voluntary. Cardiac muscle tissue forms the wall of the heart; it is striated and involuntary. Smooth muscle tissue is located primarily in internal organs; it is nonstriated (smooth) and involuntary.

2. Through contraction and relaxation, muscular tissue performs four important functions, producing body movements, stabilizing body positions, moving substances within the body and regulating organ volume, and producing heat.

3. Four special properties of muscular tissues are (1) electrical excitability, the property of responding to stimuli by producing action potentials; (2) contractility, the ability to generate tension to do work; (3) extensibility, the ability to be extended (stretched); and (4) elasticity, the ability to return to original shape after contraction or extension.

10.2 Structure of Skeletal Muscle Tissue

1. The subcutaneous tissue separates skin from muscles, provides a pathway for blood vessels and nerves to enter and exit muscles, and protects muscles from physical trauma. Fascia lines the body wall and limbs that surround and support muscles, allows free movement of muscles, carries nerves and blood vessels, and fills space between muscles.

2. Connective tissues surrounding skeletal muscles are epimysium, covering the entire muscle; perimysium, covering muscle fascicles; and endomysium, covering muscle fibers. Fascia covers all muscles of a region and separates muscle from the skin. Tendons and aponeuroses are extensions of connective tissue within the muscle belly beyond the muscle fibers that attach muscle to bone or to other muscle.

3. Tendons and aponeuroses are extensions of connective tissue beyond muscle fibers that attach the muscle to bone or to other muscle. A tendon is generally ropelike in shape; an aponeurosis is wide and flat.

4. Skeletal muscles are well supplied with nerves and blood vessels. Generally, an artery and one or two veins accompany each nerve that penetrates a skeletal muscle.

5. Somatic motor neurons provide the nerve impulses that stimulate skeletal muscle to contract.

6. Blood capillaries bring in oxygen and nutrients and remove heat and waste products of muscle metabolism.

7. The major cells of skeletal muscle tissue are termed skeletal muscle fibers. Each muscle fiber has 100 or more nuclei because it arises from the fusion of many myoblasts. Satellite cells are myoblasts that persist after birth. The sarcolemma is a muscle fiber’s plasma membrane; it surrounds the sarcoplasm. T tubules are invaginations of the sarcolemma.

8. Each muscle fiber contains hundreds of myofibrils, the contractile elements of skeletal muscle. Sarcoplasmic reticulum surrounds each myofibril. Within a myofibril are thin and thick filaments, arranged in compartments called sarcomeres.

9. The overlapping of thick and thin filaments produces striations. Darker A bands alternate with lighter I bands. Table 10.1 summarizes the components of the sarcomere.

10. Myofibrils are composed of three types of proteins: contractile, regulatory, and structural. The contractile proteins are myosin (thick filament) and actin (thin filament). Regulatory proteins are tropomyosin and troponin, both of which are part of the thin filament. Structural proteins include titin (links Z disc to M line and stabilizes thick filament), myomesin (forms M line), nebulin (anchors thin filaments to Z discs and regulates length of thin filaments during development), and dystrophin (links thin filaments to sarcolemma). Table 10.2 summarizes the different types of skeletal muscle fiber proteins. Table 10.3 summarizes the levels of organization within a skeletal muscle.

11. Projecting myosin heads contain actin-binding and ATP-binding sites and are the motor proteins that power muscle contraction.

10.3 Contraction and Relaxation of Skeletal Muscle Fibers

1. Muscle contraction occurs because cross-bridges attach to and “walk” along the thin filaments at both ends of a sarcomere, progressively pulling the thin filaments toward the center of a sarcomere. As the thin filaments slide inward, the Z discs come closer together, and the sarcomere shortens.

2. The contraction cycle is the repeating sequence of events that causes sliding of the filaments: (1) Myosin ATPase hydrolyzes ATP and becomes energized; (2) the myosin head attaches to actin, forming a cross-bridge; (3) the cross-bridge generates force as it rotates toward the center of the sarcomere (power stroke); and (4) binding of ATP to the myosin head detaches it from actin. The myosin head again hydrolyzes the ATP, returns to its original position, and binds to a new site on actin as the cycle continues.

3. An increase in Ca2+ concentration in the sarcoplasm starts filament sliding; a decrease turns off the sliding process.

4. The muscle action potential propagating into the T tubule system stimulates voltage-gated Ca2+channels in the T tubule membrane. This causes opening of Ca2+ release channels in the SR membrane. Calcium ions diffuse from the SR into the sarcoplasm and combine with troponin. This binding causes tropomyosin to move away from the myosin-binding sites on actin.

5. Ca2+ active transport pumps continually remove Ca2+ from the sarcoplasm into the SR. When the concentration of calcium ions in the sarcoplasm decreases, tropomyosin slides back over and blocks the myosin-binding sites, and the muscle fiber relaxes.

6. A muscle fiber develops its greatest tension when there is an optimal zone of overlap between thick and thin filaments. This dependency is the length–tension relationship.

7. The neuromuscular junction is the synapse between a somatic motor neuron and a skeletal muscle fiber. It includes the axon terminals and synaptic end bulbs of a motor neuron, plus the adjacent motor end plate of the muscle fiber sarcolemma.

8. When a nerve impulse reaches the synaptic end bulbs of a somatic motor neuron, it triggers exocytosis of the synaptic vesicles, which releases acetylcholine (ACh). ACh diffuses across the synaptic cleft and binds to ACh receptors, initiating a muscle action potential. Acetylcholinesterase then quickly breaks down ACh into its component parts.

10.4 Muscle Metabolism

1. Muscle fibers have three sources for ATP production: creatine, anaerobic glycolysis, and aerobic respiration.

2. Creatine kinase catalyzes the transfer of a high-energy phosphate group from creatine phosphate to ADP to form new ATP molecules. Together, creatine phosphate and ATP provide enough energy for muscles to contract maximally for about 15 seconds.

3. Glucose is converted to pyruvic acid in the reactions of glycolysis, which yield two ATPs without using oxygen. Anaerobic glycolysis can provide enough energy for 2 minutes of maximal muscle activity.

4. Muscular activity that occurs over a prolonged time depends on aerobic respiration, mitochondrial reactions that require oxygen to produce ATP.

5. The inability of a muscle to contract forcefully after prolonged activity is muscle fatigue.

6. Elevated oxygen use after exercise is called recovery oxygen uptake.

10.5 Control of Muscle Tension

1. A motor neuron and the muscle fibers it stimulates form a motor unit. A single motor unit may contain as few as 2 or as many as 3000 muscle fibers.

2. Recruitment is the process of increasing the number of active motor units.

3. A twitch contraction is a brief contraction of all muscle fibers in a motor unit in response to a single action potential.

4. A record of a contraction is called a myogram. It consists of a latent period, a contraction period, and a relaxation period.

5. Wave summation is the increased strength of a contraction that occurs when a second stimulus arrives before the muscle fiber has relaxed completely following a previous stimulus.

6. Repeated stimuli can produce unfused (incomplete) tetanus, a sustained muscle contraction with partial relaxation between stimuli. More rapidly repeating stimuli produce fused (complete) tetanus, a sustained contraction without partial relaxation between stimuli.

7. Continuous involuntary activation of a small number of motor units produces muscle tone, which is essential for maintaining posture.

8. In a concentric isotonic contraction, the muscle shortens to produce movement and to reduce the angle at a joint. During an eccentric isotonic contraction, the muscle lengthens.

9. Isometric contractions, in which tension is generated without a muscle changing its length, are important because they stabilize some joints as others are moved.

10.6 Types of Skeletal Muscle Fibers

1. On the basis of their structure and function, skeletal muscle fibers are classified as slow oxidative (SO), fast oxidative–glycolytic (FOG), and fast glycolytic (FG) fibers.

2. Most skeletal muscles contain a mixture of all three fiber types. Their proportions vary with the typical action of the muscle.

3. The motor units of a muscle are recruited in the following order: first SO fibers, then FOG fibers, and finally FG fibers.

4. Table 10.4 summarizes the three types of skeletal muscle fibers.

10.7 Exercise and Skeletal Muscle Tissue

1. Various types of exercises can induce changes in the fibers in a skeletal muscle. Endurance-type (aerobic) exercises cause a gradual transformation of some fast glycolytic fibers into fast oxidative–glycolytic fibers.

2. Exercises that require great strength for short periods produce an increase in the size and strength of fast glycolytic fibers. The increase in size is due to increased synthesis of thick and thin filaments.

10.8 Cardiac Muscle Tissue

1. Cardiac muscle is found only in the heart. Cardiac muscle fibers have the same arrangement of actin and myosin and the same bands, zones, and Z discs as skeletal muscle fibers. The fibers connect to one another through intercalated discs, which contain both desmosomes and gap junctions.

2. Cardiac muscle tissue remains contracted 10 to 15 times longer than skeletal muscle tissue due to prolonged delivery of Ca2+ into the sarcoplasm.

3. Cardiac muscle tissue contracts when stimulated by its own autorhythmic fibers. Due to its continuous, rhythmic activity, cardiac muscle depends greatly on aerobic respiration to generate ATP.

10.9 Smooth Muscle Tissue

1. Smooth muscle is nonstriated and involuntary.

2. Smooth muscle fibers contain intermediate filaments and dense bodies; the function of dense bodies is similar to that of the Z discs in striated muscle.

3. Visceral (single-unit) smooth muscle is found in the walls of hollow viscera and of small blood vessels. Many fibers form a network that contracts in unison.

4. Multi-unit smooth muscle is found in large blood vessels, large airways to the lungs, arrector muscles of the hair, and the eye, where it adjusts pupil diameter and lens focus. The fibers operate independently rather than in unison.

5. The duration of contraction and relaxation of smooth muscle is longer than in skeletal muscle since it takes longer for Ca2+ to reach the filaments.

6. Smooth muscle fibers contract in response to nerve impulses, hormones, and local factors.

7. Smooth muscle fibers can stretch considerably and still maintain their contractile function.

10.10 Regeneration of Muscular Tissue

1. Skeletal muscle fibers cannot divide and have limited powers of regeneration; cardiac muscle fibers can regenerate under limited circumstances; and smooth muscle fibers have the best capacity for division and regeneration.

2. Table 10.5 summarizes the major characteristics of the three types of muscular tissue.

10.11 Development of Muscle

1. With few exceptions, muscles develop from mesoderm.

2. The mesoderm segments into cube-shaped structures called somites.

10.12 Aging and Muscular Tissue

1. With aging, there is a slow, progressive loss of skeletal muscle mass, which is replaced by fibrous connective tissue and fat.

2. Aging also results in a decrease in muscle strength, slower muscle reflexes, and loss of flexibility.