Biology of Humans

6. The Muscular System

 

In the previous chapter we learned about bones, which support us against gravity, and about joints, which allow movement. In this chapter, we will see how muscle contraction permits movement. We will explore muscle structure and the mechanism of contraction. Then, we will see how nerves control contractions and study the energy sources that fuel muscle activity.

 

Function and Characteristics of Muscles

 

There are three kinds of muscles—skeletal, cardiac, and smooth. Each has distinct qualities and functions, but they all have four traits in common.

1. Muscles are excitable. They respond to stimuli.

2. Muscles are contractile. They have the ability to shorten (contract).

3. Muscles are extensible. They have the ability to stretch.

4. Muscles are elastic. They can return to their original length after being shortened or stretched.

This chapter focuses on skeletal muscle, the kind of muscle we usually think of when muscles are mentioned. Smooth and cardiac muscles are discussed in Chapters 4 and 12, respectively. Skeletal muscles allow you to smile with pleasure and scowl in anger. They allow you to move, some of us more gracefully than others. And they allow you to remain erect, maintaining your posture despite the pull of gravity. Besides these obvious functions of skeletal muscle, support of the internal organs is provided by muscles forming the abdominal wall and the floor of the pelvic cavity. Contraction of muscles also pushes against veins and lymphatic vessels, moving blood and lymph along. Importantly, contraction of skeletal muscles generates heat, which warms our bodies above most of the environmental temperatures we experience. If we get too warm, other mechanisms come into play to cool our bodies, as described in Chapter 4. Unlike cardiac and smooth muscle, skeletal muscle is under voluntary control—meaning we can contract it when we want to.

·       We have more than 600 skeletal muscles, most of which are attached to bones. Our muscles contract to move our body parts, so we can make our impact on the world.

 

Skeletal Muscles Working in Pairs

 

Most muscles work in pairs or groups. Muscles that must contract at the same time to cause a certain movement are called synergistic muscles. Most muscles, however, are arranged in antagonistic pairs (Figure 6.1), which produce a movement when one of the pair contracts and the other relaxes. When a muscle in an antagonistic pair contracts, it shortens and pulls on one of the bones that meet at a given joint, causing movement of the bone in one direction. Any time an antagonistic muscle contracts and pulls on a bone, its partner, which has an opposing action, must relax. For the bone to then move back to its former position, the first muscle must relax and the other muscle in the pair must contract, thus pulling the bone in the opposite direction. The biceps muscle (the muscle people like to show off), located on the top of the upper arm, cooperates in this way with the triceps muscle (the one we feel when we do push-ups), on the back of the arm. Contracting the biceps causes the arm to flex and bend at the elbow, but contracting the triceps causes the arm to extend and straighten at the elbow.

 

 

FIGURE 6.1. Antagonistic action of the triceps and biceps muscles during flexion and extension. The origins and insertions of the muscles are shown.

 

Most of the major muscles we use for locomotion, manipulation, and other voluntary movements are attached to bones. Each end of the muscle is attached to a bone by a tendon, which is a band of connective tissue. A muscle is often attached to two bones on opposite sides of a joint. The muscle's origin is the end attached to the bone that remains relatively stationary during a movement. The muscle's insertion is the end attached to the bone that moves. Thus, the bones act as levers in working with skeletal muscles to produce movement. The body has more than 600 skeletal muscles. The major ones—those most prominent in giving shape to the body—are shown in Figure 6.2.

 

 

FIGURE 6.2. Some major muscles of the body

 

In the preceding description, we said that a contracting muscle pulls a bone. In actuality, the contraction of a muscle pulls on the tendon that connects that muscle to a bone. Excessive stress on a tendon can cause it to become inflamed, a condition called tendinitis. Most tendinitis is probably due to overuse, misuse (as when lifting improperly), or age. Unfortunately, tendons heal slowly because they are poorly supplied with blood vessels. The most effective treatment is rest: if it hurts, do not use it.

The terms muscle pull, muscle strain, and muscle tear are used almost interchangeably to describe damage to a muscle or its tendons caused by overstretching. This common sports injury may also include damage to small blood vessels in the muscle, causing bleeding and pain. Treatment includes applying ice to the injured area to reduce swelling and keeping the muscle stretched.

 

Contraction of Muscles

 

Now we'll look at the brawny bulk that gives shape to the body, gradually delving deep into the fine structure forming the mechanism responsible for muscle contraction. An entire, intact muscle is formed from individual muscle fibers grouped in increasingly larger bundles, each wrapped in a connective tissue sheath (Figure 6.3). Each individual muscle, the biceps brachii for instance, is covered by a membrane made of fibrous connective tissue. The muscles themselves are formed of smaller bundles called fascicles, each wrapped in its own connective tissue sheath. The connective tissue sheaths merge and condense at the ends of the muscles to form the tendons that attach the muscle to bone.

 

 

FIGURE 6.3. The structure of a skeletal muscle

 

Inside the fascicles are the muscle fibers themselves, the actual muscle cells. Skeletal muscle cells can be several centimeters long, which is enormously long compared to most of the body's other cells. Muscle cells in the thigh can be 30 cm (1 ft) in length. The fine structure of these cells provides numerous clues to the mechanism responsible for muscle contraction.

Skeletal muscle is also called striated (striped) muscle, because under the microscope, the muscle cells are seen to have pronounced bands that look like stripes (Figure 6.3). The striations are caused by the orderly arrangement of many elongated myofibrils, which are specialized bundles of proteins within the muscle cell. Each myofibril contains two types of the long protein filaments called myofilaments: the thicker myosin filaments and a greater number of the thinner actin filaments. The bundles of myofilaments make up about 80% of the cell volume.

Along its length, each myofibril has tens of thousands of contractile units called sarcomeres. The ends of each sarcomere are marked by dark bands of protein, called Z lines. Within each sarcomere, the actin and myosin filaments are arranged in a specific manner. One end of each actin filament is attached to a Z line. Myosin filaments lie in the middle of the sarcomere, their ends partially overlapping with surrounding actin filaments. The degree of overlap increases when the muscle contracts.

 

Sliding Filament Model

According to the sliding filament model of muscle contraction, a muscle contracts when the actin filaments slide along the myosin filaments, increasing the degree of overlap between actin and myosin and thus shortening the sarcomere. When many sarcomeres shorten, the muscle as a whole contracts.

To understand the sliding of the actin and myosin filaments, let's look at their molecular structures. A thin, actin myofilament is made up of two chains of spherical actin molecules resembling two strings of beads twisted around each other to form a helix. A thick, myosin filament is composed of myosin molecules shaped like two-headed golf clubs. In a myosin filament, the "shafts" of several hundred myosin molecules lie along the filament's length, and the "heads" protrude along each end of the bundle in a spiral pattern. The club-shaped myosin heads are the key to the movement of actin filaments and, therefore, to muscle contraction (Figure 6.4).

 

 

FIGURE 6.4. Each myofibril is packed with actin filaments and myosin filaments. When a muscle contracts, actin filaments slide past myosin filaments. Movements of the heads of myosin filaments pull actin filaments toward the center of a sarcomere.

 

The sliding filament model holds that muscle contraction results from the following cycle of interactions between myosin and actin:

• Resting sarcomere. At the start of each cycle, the myosin heads have already split a molecule of adenosine triphosphate (ATP) to adenosine diphosphate (ADP) and inorganic phosphate (P;). The energy released from splitting the ATP causes the myosin heads to swivel in a way that extends them toward the Z lines at the ends of the sarcomere. This step is analogous to cocking a pistol so it is poised and ready to fire.

• Step 1: Cross-bridge attachment. The myosin heads attach themselves to the nearest actin filament. When the myosin head is bound to an actin molecule, it acts as a bridge between the thick and thin filaments. For this reason, myosin heads are also called cross-bridges.

• Step 2: Bending of myosin head (the power stroke). When myosin heads bind to actin, the energy previously stored from breaking down ATP to ADP and inorganic phosphate is released, causing the myosin heads to swing forcefully back to their bent positions. The actin filaments, still bound to the myosin heads, are therefore pulled toward the midline of the sarcomere. This so-called power stroke is analogous to pulling the trigger on a pistol. During the power stroke, the ADP and inorganic phosphate are released from the myosin head.

• Step 3: Cross-bridge detachment. New ATP molecules now bind to the myosin heads, causing the myosin heads to disengage from the actin.

• Step 4: Myosin reactivation. The myosin heads split the ATP into ADP and P; and store the energy, causing the contraction cycle to begin again.

This cycle of events is repeated hundreds of times in a second.

 

Calcium Ions and Regulatory Proteins

Muscle contractions are controlled by the availability of calcium ions. How? Muscle cells contain the proteins troponin and tropomyosin, which together form a troponin-tropomyosin complex (Figure 6.5). During muscle relaxation, the actin-myosin-binding sites where the myosin heads would otherwise attach to the actin filaments are covered over by the troponin-tropomyosin complex. Contraction occurs when calcium ions enter the sarcomere and bind to troponin, causing it to change shape. This change causes tropomyosin to shift position, which pulls the tropomyosin molecule away from the myosin-binding sites on the actin. The exposed binding sites enable actin to bind to myosin.

 

 

FIGURE 6.5. Calciumions initiate muscle contraction.

 

Where do the calcium ions come from? Calcium ions are stored in the sarcoplasmic reticulum, an elaborate form of smooth endoplasmic reticulum found in muscle cells. The sarcoplasmic reticulum can be pictured as a sleeve of thick lace surrounding each myofibril in a muscle cell. (Recall that a myofibril is a bundle of actin and myosin.) Also scattered through the cell are a number of transverse tubules (T tubules), which are tiny, cylindrical pockets in the muscle cell's plasma membrane. The T tubules carry signals from motor neurons deep into the muscle cell to virtually every sarcomere.

As we have seen, it takes an ATP molecule to break the cross-bridges so that new ones may be formed. This dependency explains why muscles become stiff within a few hours after death, through a phenomenon known as rigor mortis. Soon after death, calcium ions begin to leak out of the sarcoplasmic reticulum, initiating muscle contraction. Muscle contraction will occur as long as ATP is present. However, after a person dies, ATP is no longer being produced and the supply runs out. Without ATP, cross-bridges cannot be broken, and within 3-4 hours after death the muscles becomes stiff. The muscles' proteins actin and myosin gradually break down, allowing the muscles to relax again after 2-3 days.

 

Stop and think

How would the degree of rigor mortis help a forensic scientist determine the approximate time of death of a corpse?

 

Role of Nerves

The stimulus that ultimately leads to the release of calcium ions, and therefore to muscle contraction, is a nerve impulse from a motor neuron (described in Chapter 7). The junction between the tip of a motor neuron and a skeletal muscle cell is called a neuromuscular junction. When a nerve impulse reaches a neuromuscular junction, it causes the release of the chemical acetylcholine (a neurotransmitter) from small packets in the tip of the motor neuron. Acetylcholine then diffuses across a small gap onto the surface of the muscle cell, where it binds to special receptors on the muscle cell membrane. Acetylcholine causes changes in the membrane's permeability, thus creating an electrochemical message similar to a nerve impulse. The message travels along the muscle cell's plasma membrane, into the T tubules, and then to the sarcoplasmic reticulum, causing channels there to open and release calcium ions. The calcium ions then combine with troponin, the myosin-binding sites on actin are exposed, and the muscle contracts. This is the chain of events that must happen in order for you to absentmindedly scratch your head, and it happens a lot faster than it takes to describe.

When the nerve impulse stops, membrane pumps quickly clear the sarcomere of calcium ions, and the troponin-tropomyosin complexes move to where they again block the binding sites, causing the muscle to relax. The contraction of other muscles then stretches the sarcomere back to its original length (Figure 6.6).

 

 

FIGURE 6.6. The connection between a motor neuron and a muscle cell is called a neuromuscular junction.

 

Low blood levels of calcium, magnesium, or potassium are possible causes of muscle cramps, also called muscle spasms, which are forceful, involuntary muscle contractions. Muscle cramps can usually be relieved by stretching or gently rubbing the affected muscle.

 

Stop and think

Curare is a poison used in South America on poison arrow darts. It prevents acetylcholine from binding to muscle. The diaphragm is a voluntary skeletal muscle necessary for breathing. How do poison arrows cause death?

 

Muscular Dystrophy

We have seen that calcium ions must enter the cell for muscle contraction to occur. However, if too many calcium ions enter the cell, those ions can destroy proteins within the cell, causing it to die. If this cell death occurs on a large scale, muscles become increasingly damaged and weak. That is, in fact, what happens in muscular dystrophy, which is a general term for a group of inherited conditions. One of the most common forms, Duchenne muscular dystrophy, is caused by a defective gene for production of the protein dystrophin. The lack of dystrophin allows excess calcium ions to enter the muscle cell and rise to levels that destroy other important proteins and kill the cell. Dead muscle cells are replaced by fat and connective tissue, so the skeletal muscles become progressively weaker. (The mode of inheritance of Duchenne muscular dystrophy is described in Chapter 20.)

 

Voluntary Movement

Many of the same muscles are involved in strolling on the beach and kicking a soccer ball. However, the extent and strength of contraction is different in these two activities. How is this possible? Although an individual muscle cell contracts completely each time it is stimulated to do so, only some of the cells in a whole muscle contract at once. The combined output of these muscle cells determines the extent and strength of contraction. There are two important ways to vary the contraction of whole muscles: (1) changing the number of muscle cells contracting at a given moment and (2) changing the force of contraction in individual muscle cells by altering the frequency of stimulation. Let's see how this works.

 

Motor Units and Recruitment

As described earlier, skeletal muscles are stimulated to contract by motor neurons. Each motor neuron that brings an impulse from the brain to a muscle makes contact with a number of different muscle cells in that muscle. A motor neuron and all the muscle cells it stimulates are called a motor unit (Figure 6.7). All the muscle cells in a given motor unit contract together. On average there are 150 muscle cells in a motor unit, but this number is quite variable. Muscles responsible for precise, finely controlled movements, such as those of the fingers or eyes, have small numbers of muscle cells in each motor unit. In contrast, muscles for less precise movements, such as those of the thigh or calf, have many muscle cells in a motor unit. A single motor neuron in a motor unit in a tiny eye muscle may control only three muscle cells, making its action highly localized, whereas a single motor neuron in a motor unit in a calf muscle may control thousands of muscle cells.

 

 

FIGURE 6.7. A motor unit includes a motor neuron and the muscle cells it stimulates.

 

The nervous system increases the strength of a muscle contraction by increasing the number of motor units being stimulated, through a process called recruitment. The muscle cells of a given motor unit are generally spread throughout the muscle. Thus, if a single motor unit is stimulated, the entire muscle contracts, but only weakly. Although several of the same muscles are used to lift a table as are used to lift a fork, the number of motor units summoned in those muscles is greater when lifting the table.

Our movements tend to be smooth and graceful rather than jerky because the nervous system carefully choreographs the stimulation of different motor units, timing it so that they are not all active simultaneously or for the same amount of time. Although an individual muscle cell is either contracted or relaxed at any given instant, the muscle as a whole can consist of thousands of muscle cells, and usually only some of those cells are contracted at the same time. Even when a muscle is relaxed, some of its motor units are active (but not the same units all the time). As a result, the muscle is usually firm and solid, even when it is not being used. This state of intermediate contraction of a whole skeletal muscle is called muscle tone. A muscle that lacks muscle tone is limp.

 

Muscle Twitches, Summation, and Tetanus

If a whole skeletal muscle is artificially stimulated briefly in the laboratory, some of the muscle cells will contract, causing a muscle twitch (Figure 6.8a). The interval between the reception of the stimulus and the time when contraction begins is called the latent period. The contraction phase is quite short and is followed by a longer relaxation phase as the muscle returns to its resting state. Muscle twitches are too brief to be part of normal movements (but they can generate heat to maintain body temperature when we shiver).

 

 

FIGURE 6.8. Muscle contraction shown graphically: (a) muscle twitch, (b) summation, (c) tetanus

 

Most movements, including strolling along the beach, require sustained contraction of muscles. Sustained contractions begin when the frequency of stimulation increases. If a second stimulus is given before the muscle is fully relaxed, the second twitch will be stronger than the first. This phenomenon is described as summation, because the second contraction is added to the first (Figure 6.8b). Summation occurs because an increasing number of muscle cells are stimulated to contract.

When stimuli arrive even more frequently, the contraction becomes increasingly stronger as each new muscle twitch is added. If the stimuli occur so frequently that there is no time for any relaxation before the next stimulus arrives, the muscle goes into a sustained, powerful contraction called tetanus (Figure 6.8c). Tetanus cannot continue indefinitely. Eventually, the muscle will become unable to produce enough ATP to fuel contraction, and lactic acid will accumulate (as discussed below). As a result, the muscle will stop contracting despite continued stimulation, a condition called fatigue.

 

Energy for Muscle Contraction

 

A single contracting muscle cell can require as much as 600 trillion ATP molecules per second simply to form and break the cross-bridges producing the contraction. When we consider that even small muscles contain thousands of muscle cells, it is clear that muscle contraction requires an enormous store of energy. So where does all the ATP come from?

Our muscles have various sources of ATP and typically use them in a certain sequence, depending on the duration and intensity of exercise. These sources include (1) ATP stored in muscle cells, (2) creatine phosphate stored in muscle cells, (3) anaerobic (without oxygen) metabolic pathways within cells, and (4) aerobic (with oxygen) respiration within cells (Figure 6.9). (Recall that cell respiration was discussed in Chapter 3.)

 

 

FIGURE 6.9. Energy sources for muscle contraction

 

Which energy source would fuel walking up a single flight of stairs?

ATP stored in muscles

 

A resting muscle stores some ATP, but this reserve is used up quickly. During vigorous exercise, the ATP reserves in the active muscles are depleted in about 6 seconds. Earlier, when the muscles were resting, energy was transferred to another high-energy compound, called creatine phosphate, that is stored in muscle tissue. Creatine phosphate has a high-energy bond connecting the creatine and the phosphate parts of the molecule. A resting muscle contains about six times as much stored creatine phosphate as stored ATP and can release its energy when needed to convert ADP to ATP. This energy supports the next 10 seconds of exercise.

Activities such as diving, weight lifting, and sprinting, which require a short burst of intense activity, are powered entirely by ATP and creatine phosphate reserves.

Once the supply of creatine phosphate is diminished, ATP must be generated from either anaerobic metabolic pathways or aerobic respiratory pathways. The primary fuel for either pathway is glucose, and the glucose that fuels muscle contraction comes mainly from glycogen, which—as you learned in Chapter 2—is stored in muscle (and liver) cells and consists of a large chain of glucose molecules. When an active muscle cell runs short of ATP and creatine phosphate, enzymes begin converting glycogen to glucose. About 1.5% of a muscle cell's total weight is glycogen. Even so, long-term activity, as in an endurance sport, may deplete a muscle's glycogen reserves. The accompanying feeling of overwhelming fatigue is known to runners as "hitting the wall," to cyclists as "bonking," and to boxers as becoming "arm weary."

The cardiovascular system can supply enough oxygen for aerobic respiratory pathways to power low levels of activity, even if continued for a prolonged time. However, anaerobic pathways produce ATP 2.5 times faster than do aerobic pathways. Therefore, during strenuous activity lasting 30 or 40 seconds, anaerobic pathways supply the ATP that fuels muscle contraction. Indeed, burstlike activities such as used in tennis or soccer rely nearly completely on anaerobic pathways of ATP production. In anaerobic respiratory pathways, the pyruvic acid produced in glycolysis is converted to lactic acid.

During more prolonged muscular activity, the body gradually switches back to aerobic pathways for producing ATP. The necessary oxygen can come from either of two sources. One is the oxygen bound to hemoglobin in the blood supply. As activity continues, the heart rate increases, and blood is pumped more quickly; moreover, it is shunted to the neediest tissues. Another oxygen source is myoglobin, an oxygen-binding pigment within muscle cells. Aerobic pathways produce more than 90% of the ATP required for intense activity lasting more than 10 minutes. These pathways also produce nearly 100% of the ATP that powers a truly prolonged intense activity, such as running a marathon.

After prolonged exercise, a person continues to breathe heavily for several minutes. Taking in extra oxygen in this way relieves the oxygen debt that was created by the muscles' using more ATP than was provided by aerobic metabolism. Most of the oxygen is used to generate ATP to convert lactic acid back to glucose. In addition, the oxygen that was released by myoglobin is replaced, and glycogen and creatine phosphate reserves are restored.

 

Stop and think

Some athletes take dietary creatine supplements to improve their performance. Creatine does seem to boost performance in sports that require short bursts of energy but not in those that require endurance. How might this difference be explained? Creatine does not increase muscle mass, yet it can enhance performance in sprint sports. How is this effect possible?

 

Slow-Twitch and Fast-Twitch Muscle Cells

 

There are two general types of skeletal muscle cells: slow-twitch and fast-twitch. Slow-twitch muscle cells contract slowly when stimulated, but with enormous endurance. These cells are dark and reddish because they are packed with the oxygenbinding pigment myoglobin and because they are richly supplied with blood vessels. Slow-twitch cells also contain abundant mitochondria, the organelles in which aerobic production of ATP occurs. Because they can produce ATP aerobically for a long time, slow-twitch cells are specialized to deliver prolonged, strong contractions.

In contrast, fast-twitch muscle cells contract rapidly and powerfully, but with far less endurance. Fast-twitch cells have a form of an enzyme that can split ATP bound to myosin more quickly than the same enzyme in slow-twitch cells. Because they can make and break cross-bridge attachments more quickly, fast-twitch cells can contract more rapidly. In addition, compared with their slow-twitch cousins, fast-twitch cells have a wider diameter because they are packed with more actin and myosin. This feature adds to their power. However, fast-twitch cells, rich in glycogen deposits, depend more heavily on anaerobic means of producing ATP. As a result, fast-twitch cells tire more quickly than slow-twitch cells.

The two kinds of cells are distributed unequally throughout the human body. The abdominal muscles do not need to contract rapidly, but they need to be able to contract steadily to hold our paunch in at the beach and to balance the powerful, slow-twitch back muscles so that we can stand upright. Fast-twitch cells are more common in the legs and arms, because our limbs may be called on to move quickly.

People vary in the relative amounts of slow- and fast- twitch muscle cells they possess. Whereas the leg muscles of endurance athletes, such as marathoners, are made up of about 80% slow-twitch cells, those of sprinters are about 60% fast- twitch cells. To some extent these differences are genetic, so if you are a "fast-twitch person," you can build a certain level of endurance, but only to a degree. Endurance runners, on the other hand, dread those times when, at the end of a long race, some well-trained competitor, genetically endowed with lots of fast-twitch cells, sprints past them at the finish line (Figure 6.10).

 

 

FIGURE 6.10. Slow- and fast-twitch muscle cells

 

Which type of muscle cell is best suited for cross-country skiing? Which type of muscle fiber is best suited for weight lifting?

Slow-twitch muscle cells for cross-country skiing; fast-twitch muscle cells for weight lifting.

 

Building Muscle

 

Exercise can greatly influence the further development of muscle. The hormone testosterone also builds muscle (see the Ethical Issue essay, Anabolic Steroid Abuse). Different kinds of exercise produce different results. In aerobic exercise, such as walking, jogging, or swimming, enough oxygen is delivered to the muscles to keep them going for long periods. This kind of exercise fosters the development of new blood vessels that service the muscles and development of more mitochondria to facilitate energy usage. Aerobic exercise also increases muscle coordination, improves digestive tract movement, and increases the strength of the skeleton by exerting force on the bones. It brings cardiovascular and respiratory system improvements that help muscles to function more efficiently. For example, it enlarges the heart so that each stroke pumps more blood.

Aerobic exercises, however, generally do not increase muscle size. Muscular development—the kind that helps you look good on the beach—comes mostly from resistance exercise, which can be developed by lifting heavy weights. To build muscle tone and mass, you have to make your muscles exert more than 75% of their maximum force. These exercises can be very brief. Only a few minutes of exercise every other day for a year are needed to build 50% more muscle and improve tone and strength. The bulk results from the existing muscle cells increasing in diameter, although some researchers suggest that heavy exercise splits or tears the muscle cells and that each of the parts then regrows to a larger size.

Nautilus and other muscle-building machines available at many gyms automatically adjust the resistance they offer to muscles during an exercise (Figure 6.11). This is a valuable feature because muscles are weaker at some parts of their range of motion than at others. The design of the exercise machine makes the lifting easier where the muscle is weaker and more difficult in the range the muscle can handle. "Free weights," such as barbells and dumbbells, require more training to use safely than does an exercise machine.

 

image338

 

FIGURE 6.11. Muscles get larger when they are repeatedly made to exert more than 75% of their maximum force.

 

One difficulty with building muscle is that you have to keep at it. If you train in the spring only to look good at the beach, you have an uphill battle because all the mass of muscle you built last year began to disappear 2 weeks after the training stopped.

Exercise has many health benefits in addition to those to the heart and blood vessels and an increase in strength. Exercise improves your mood. If you are having a stressful day, go for a walk or work out at the gym to calm down. Exercise even reduces depression and anxiety and improves the quality of sleep. Weight-bearing exercise strengthens bones. Are you concerned about your weight? Add exercise to your weight-loss program to burn calories faster.

Begin a fitness program slowly. If you have a medical condition, first seek medical advice. Warm up by walking and gently stretching to improve blood flow to your muscles. Increase the length of time you exercise gradually as you build stamina. While you are cooling down after exercise, walk and stretch as you did before exercise.

A day or two after intense exercise, muscles sometimes become tender and weak. This phenomenon, known as delayed onset muscle soreness (DOMS), is especially common following exercises that force a muscle to lengthen while it is contracting. For example, DOMS is more likely to occur after you run downhill than after you run on level ground. Other activities that cause a muscle to lengthen while it is contracting include walking down stairs, climbing down a mountain, skiing, and horseback riding. The cause of DOMS isn't known for certain, but researchers suggest that microscopic muscle damage or an inflammatory response in the muscle may be to blame.

 

Ethical Issue

Anabolic Steroid Abuse

In recent years allegations and confessions of anabolic steroid use have rocked professional sports. The prevalence of steroid use in professional sports is a reflection of the growing problem of steroid use in general, particularly among young adults. A 2007 confidential survey of high school students funded by the National Institute on Drug Abuse revealed that 1.6% of eighth-grade students, 1.8% of tenth- grade students, and 2.7% of seniors had used steroids. Of the students who admitted steroid use, 57% said that steroid use by professional athletes influenced their decision.

Anabolic steroids are a class of drugs related to the steroid hormone testosterone. These synthetic hormones mimic testosterone's ability to stimulate the body to build muscle, often leading to a dramatic increase in strength. The steroids promote these improvements by stimulating protein formation in muscle cells and by reducing the amount of rest needed between workouts.

Anabolic steroids have more than 70 possible unwanted side effects that can range in severity from acne to liver cancer. Most common and most serious are the damage to the liver, cardiovascular system, and reproductive system. Cardiovascular problems, including heart attacks and strokes, may not show up for years, but effects on the reproductive system are more immediate. The testicles of male steroid users often become smaller, and the user may become sterile and impotent (unable to achieve an erection). These effects occur because anabolic steroids inhibit natural testosterone production. Female steroid abusers develop irreversible masculine traits such as a deeper voice, growth of body hair, loss of scalp hair, smaller breasts, and an enlarged clitoris (during embryological development, the clitoris develops from the same structure that develops into the penis in a male). Among the other risks are injuries resulting from the intended effect of the drug—increased muscle strength—because that increase is not accompanied by a corresponding increase in the strength of tendons and ligaments. Injuries to tendons and ligaments may take a long time to heal.

 

 

Anabolic steroids are sometimes abused as an easy way to build muscle and strength.

 

Questions to Consider

• If you were coaching a high school football team and knew that some of your players were using anabolic steroids, would you ignore their actions?

• If you were the owner of a professional baseball team, and suspected that one of your all-star players was using anabolic steroids, what would you do?

 

 

What would you do?

The International Olympics Committee and the World Anti-Doping Agency are concerned about the future possibility of creating genetically modified athletes. Gene therapy techniques (see Chapter 21) may soon be developed for inserting genes into people to improve their athletic performance. For example, researchers exploring muscle deterioration have developed gene therapy that repairs and rebuilds muscles in old mice. Clinical trials of the technique are now under way on humans who have muscular dystrophy. If you were a competitive athlete, would you use gene therapy to repair damaged muscle tissue? Would you use gene therapy to build muscle tissue and enhance your performance? Do you think any of these uses of gene therapy should be illegal?

 

Looking ahead

In this chapter, we learned about muscles, which contract and cause movement. In the next chapter, we will consider nerve | cells and their messages that trigger muscle contraction or glandular secretion, as well as allowing communication among nerve cells.

 

Highlighting the Concepts

Function and Characteristics of Muscles (p. 103)

• There are three types of muscle: skeletal, smooth, and cardiac.

All types of muscle cells are excitable, contractile, extensible, and elastic.

Skeletal Muscles Working in Pairs (p. 104)

• Many of the skeletal muscles of the body are arranged in antagonistic pairs so that the action of one opposes the action of the other. One member of such a pair usually causes flexion (bending at the joint) and the other, extension (straightening at the joint).

• Muscles are attached to bones by tendons. The muscle origin is the end attached to the bone that is more stationary during the muscle's movement, and the insertion is the end attached to the bone that moves.

Contraction of Muscles (pp. 104-108)

• A muscle cell is packed with myofibrils, which are composed of myofilaments (the contractile proteins actin and myosin).

• A muscle contracts when myosin heads in some of its cells bind to actin, swivel, and thereby pull the actin toward the midlines of sarcomeres, causing the actin and myosin filaments to slide past one another and increase their degree of overlap.

• Contraction is controlled by the availability of calcium ions. Calcium ions interact with two proteins on the actin filament— troponin and tropomyosin—that determine whether myosin can bind to actin. Calcium ions are stored in the sarcoplasmic reticulum of muscle cells and released when a motor nerve sends an impulse.

• Motor nerves contact muscle cells at neuromuscular junctions. When the nerve impulse reaches a neuromuscular junction, acetylcholine is released and causes a change in the permeability of the muscle cell's membrane that, in turn, causes calcium ions to be released from the sarcoplasmic reticulum.

Voluntary Movement (pp. 108-110)

• The extent and strength of contraction can be changed by altering the number of muscle cells contracting or by altering the strength of contraction of individual cells.

• A motor neuron and all the muscle cells it stimulates are collectively called a motor unit.

• The response of a muscle cell to a single brief stimulus in the laboratory is called a twitch. If a second stimulus arrives before the muscle has relaxed, the second contraction builds upon the first. This phenomenon is known as summation. Frequent stimuli cause a sustained contraction, called tetanus. Most body movements require muscle cells in tetanus.

Energy for Muscle Contraction (pp. 110-111)

• Each time an attachment between myosin and actin forms and is broken, two ATP molecules are used. The sources of ATP are (1) stored ATP, (2) creatine phosphate, (3) anaerobic metabolic pathways, and (4) aerobic respiration.

Slow-Twitch and Fast-Twitch Muscle Cells (pp. 111-112)

• Slow-twitch muscle cells contract slowly but with enormous endurance. Fast-twitch muscle cells contract rapidly and powerfully but with less endurance.

Building Muscle (pp. 112-113)

• Resistance exercise will increase muscle size. Forcing muscles to exert more than 75% of their maximal strength adds myofilaments to existing muscle cells and increases the cell diameter.

 

Reviewing the Concepts

1. Why are most skeletal muscles arranged in antagonistic pairs? Give an example illustrating the roles of each member of an antagonistic pair of muscles. p. 104

2. Describe a skeletal muscle, including descriptions of muscle cells, myofibrils, and myofilaments. p. 104

3. What is the sliding filament model of muscle contraction? pp. 105-107

4. What causes actin to move during muscle contraction? pp. 106-107

5. Explain the roles of troponin, tropomyosin, and calcium ions in regulating muscle contraction. p. 107

6. Explain how muscle contraction results from the events that occur when an impulse from a motor nerve cell reaches a neuromuscular junction and calcium ions are released from the sarcoplasmic reticulum. p. 107

7. Define a motor unit. What are the consequences of the differences in sizes of motor units? p. 109

8. Define muscle twitch, summation, and tetanus. pp. 109-110

9. List the sources of ATP for muscle contraction, and explain when each source is typically called on. pp. 110-111

10. Characterize the difference in function between slow- and fast-twitch muscle cells. pp. 111-112

11. What type of exercise can build muscles? p. 112

12. A single motor neuron and all the muscle cells it stimulates is called a

a. sarcoplasmic reticulum.

b. neuromuscular junction.

c. motor unit.

d. summation.

13. In a muscle, energy is stored in the form of

a. creatine phosphate.

b. ADP.

c. myosin.

d. glucose.

14. A muscle cell contracts when _____ filaments and _____ filaments slide past one another.

15. The contractile unit of a muscle is called a/an _____.   

 

Applying the Concepts

1. Hakeem is a 22-year-old who ate some of his Aunt Sophie's canned tomatoes for dinner last night. This morning, his speech is slurred and he is having trouble standing and walking, so his brother rushes him to the emergency room. The doctor tells Hakeem that he probably has botulism, a type of food poisoning produced by a bacterium that can grow in improperly sealed canned goods. The botulinum toxin prevents the release of acetylcholine at neuromuscular junctions. Explain how Hakeem's symptoms are related to this effect.

2. A new injury called "BlackBerry thumb" is becoming increasingly common because people send e-mails on their handheld devices and text messages on their cell phones. BlackBerry thumb is a form of tendinitis. What would cause BlackBerry thumb? What would the symptoms be? How would you treat it?

3. You are the CEO of a drug company. A research scientist approaches you with a plan to develop a new muscle-relaxing drug. The scientist explains that the drug works by flooding the muscle cell with calcium ions. Would you finance the development of this drug? Why or why not?

4. Chickens are ground-dwelling birds. They run to escape from predators, and they can fly only short distances. How do these activities explain the distribution of "white" and "dark" meat on a chicken? (Meat is skeletal muscle.)

 

Becoming Information Literate

Use at least three reliable sources (books, journals, websites) to design an exercise program for yourself. Begin by deciding on your fitness goals. Next, plan a logical progression of activity that considers the type of activities you enjoy. List each source you considered, and explain why you chose the three sources you used.