1. Gross Anatomy of Skeletal Muscles:

     The skeletal muscles, which "flesh out" the body, can be described in anatomical language, but figures convey more information and will be used extensively. A useful description of the skeletal muscles is given in terms of their bony attachments, nerves, and functions. Accordingly, a table describing the skeletal muscles is given at the end of this book. By combining the information of the table with the figures and using a little imagination, the reader can see how parts are moved relative to each other when muscles contract.

2. Gross Anatomy of Smooth Muscles:

     The arrangement of smooth muscles depends on the part in which they are found. This arrangement will be considered in the case of each part where smooth muscle plays a role and will be discussed with the organs concerned.

3. Gross Anatomy of Cardiac Muscle:

     This muscle will be described in Chapter 10.

4. Gross Aspects of the Physiology of Muscle:

     The contraction of a muscle, regardless of its type, causes either a movement or the development of a tension. When only tension is developed, the muscle is said to have contracted isometrically, not changing in length. When there is movement without change in tension, the contraction is said to be isotonic. Most muscular movements are a combination of both isometric and isotonic contraction. Whether or not movement occurs as well as the nature of the movement, depends on the way in which the muscle is attached and what is going on around its attachments. For example, holding the fist clenched requires isometric contraction of the muscles of the forearm and hand; pushing a piano is primarily an isometric exercise until the piano moves, after which the muscular movement is partially isotonic. In doing push-ups the arm and chest muscles contract almost isotonically, but those which hold the back and legs stiff are in isometric contraction.

5. General Anatomy of Skeletal Muscle:

     In order to understand how muscle contracts, we will need to know how muscle cells are arranged in a typical muscle. In general, the muscle is enveloped by a membrane. Within this membrane, paral1el muscle fibers, each consisting of a group of cells surrounded by its own membrane, extend from the beginning to the ends of the muscle. The internal and external membranes fuse to form a tendon which may attach to a small thickened part of the membrane which surrounds the bone, the periosteum. The arrangement is illustrated in Figure 29.

6. General Anatomy of Smooth Muscle:

     Smooth muscle consists of arrays of spindle-shaped cells. Their arrangement is very variable, occurring in flat sheets, in bands, and as single fibers. Figure 30a illustrates the arrangement of the smooth muscles of the stomach, of an artery, and of a hair, respectively.

7. General Anatomy of Cardiac Muscle:

     The heart muscle is divided into four chambers. Two of them, the atria, are made of one muscle. The other two, the ventricles, also made of one muscle, are separated from the atria by a ring of fibrous tissue. The anatomy of the heart is illustrated schematically in Figure 31. It will be considered in more detail in Chapter 10.

8. Microscopic structure of the Skeletal Muscle Fiber:

     Skeletal muscle fibers are made of muscle fibrils. Both show characteristic cross striations (Figure 3b) with light and dark bands alternate in regular fashion. Each light band shows a dark line which divides it in two, while each dark band has a light area between its ends (see below). The unit of structure of the muscle fibril is from one dark line to the next, sarcomere.

9. Physiology of Muscle:

a. Microscopic Aspects:

     The mechanism by which muscles change their length and tension has long been intensively investigated. The problem is not altogether solved, but the solution appears to be within sight.

     When a myofibril from a striated muscle cell is examined microscopically, it is seen to consist of alternating dark and light areas. Each light area is divided by a cross membrane, the Z line). The dark areas contain light bands (Figure 37). Contraction occurs by shortening the distance between the Z lines. The light areas shorten and the light bands in the middle of the dark areas also shorten, though the dark areas do not change in length. Some of the molecular changes which underly these changes are described in the sliding filament theory.

     According to this theory, a sarcomere contains two types of protein molecules. Some are thin, actin, and are attached to the Z bands. Others are thick, myosin, and lie between the filaments. The relationship between the myosin and actin molecules is shown in two dimensions in Figure 38. The relaxed state is shown in Figure 39, and the arrangement after contraction is shown in the Figure 38d. Note that the light bands correspond to the actin filaments, while the dark bands are related to myosin. Where both myosin and actin are present, the dark band becomes darker, and when myosin is present without actin, the dark band has a light zone.

     The transition from the relaxed to the contracted state must involve the bringing together of the ends of the actin filaments. This is an energy consuming process. The exact way in which energy is used to pull the thin filaments together is not known: it seems certain, however, that organically bound phosphate is involved, adenosine triphosphate or ATP. ATP is formed when foodstuffs are broken down in the body. It is consumed when muscle contracts, and is also involved in other energy transformations to be considered later. The thick filaments, myosin, seem to be involved in breaking ATP down. The energy released when ATP is destroyed is somehow used to bring the thin filaments, actin, together. When ATP is no longer produced, the thin filaments separate again and the muscle relaxes. A remarkable demonstration that actin and myosin are the essential components required for muscular contraction can be made. After mild extraction of muscle with cold glycerine, actin and myosin alone remain and the cells, are to all intents, destroyed. Yet addition of ATP to the solution now causes contraction of the "dead" muscle.

b. The Twitch:

     When a muscle removed from the body is stimulated, either directly or by way of its nerve, it responds in a characteristic way. For a short time--about 3/1000 of a second--no mechanical event can be observed, and is called the latent period. It is probable that during the latent period, the stimulating impulse is spread to the sarcomeres, and myosin begins the breakdown of ATP. With ATP breakdown, the filaments of actin are pulled together. The muscle shortens increasingly as more sarcomeres become involved. Contraction lasts about 30 thousandths of a second (0.030 s). If the stimulus is not continued, the previous condition is restored, and the muscle relaxes. Complete relaxation occurs after 70-100 thousandths of a second. These events are summarized in Figure 39.

c. Refractory Period:

     When a muscle is stimulated, a train of events is set into motion during the latent period and in early contraction. A second stimulus during this time encounters a muscle already prepared to contract and indifferent to any new stimulus. For a second stimulus to be effective, the muscle must have restored some of the conditions which were abolished during latency. This takes a significant amount of time, referred to as the refractory period. The length of the refractory period varies with the muscle. In the heart, the refractory period is unusually long, lasting throughout contraction, meaning the heart will not respond to a second stimulus offered while it is contracting.

d. Summation, Clonus, and Tetanus:

     Most muscles have very short refractory periods. A second stimulus applied after the refractory period produces a second response even though the muscle is already contracting. This second response adds to the first one, producing the phenomenon called summation. Repetitive stimuli, so spaced that each new stimulus comes to the muscle just after it has begun to relax, produce a state of sustained, but somewhat jerky, contraction, called clonus. Increasing the frequency of stimulation further produces a less jerky contraction, in which relaxations are hardly detectable. This is called tetanus. Summation, clonus and tetanus are illustrated in Figure 40.

e. Contraction in the Body:

     In the living body, summation, clonus, and tetanus can all be observed. In addition, however, the strength of a muscular contraction can be varied by changing the amount of muscle involved. Other circumstances, such as the resting length of the muscle and its chemical surroundings, also influence the strength of contraction. Each muscle, though it appears an anatomical entity, is actually a collection of motor units, each with its own nerve fiber. Motor units contain from 10 to 1000 muscle cells. The strength of contraction of any motor unit depends on the frequency with which its nerve fiber discharges. The strength of contraction of the whole muscle, however, depends on the number of motor units involved as well as the resting length of the muscle and the number of chemical circumstances, which are poorly understood. Some of these factors are considered later in this chapter and in Chapter 10.

     Usually, a muscle contracting in the body uses a fraction of its motor units. These relax and are replaced by other motor units, which in turn relax and are replaced by still other motor units. Thus, in a muscle contracting weakly, most of the muscle is at rest.

f. Fatigue:

     The exact cause of fatigue is not known. However, it is clear that a motor unit which is called on intermittently and relaxed when not called on will fatigue slowly. Thus extraordinary feats of endurance are possible. Holding the erect posture for a few hours at a time may be very boring, but it does not generate muscular fatigue because the muscle units are rotated through periods of rest and activity. On the other hand, when maximal activity is demanded of a muscle, so that all its motor units must be continuously operative, fatigue occurs quickly. One may see such fatigue in, for example, an individual holding a 20 pound weight at arm's length to one side. The tension needed to perform this simple task requires the activity of all the motor units of the involved muscles, and in a short time it becomes impossible to support the weight.

g. Energy sources:

     It was noted above that ATP could supply the energy for muscular contraction. This can be explained in the following terms. ATP is constituted of adenine and three phosphates linked to each other, thus:

     The terminal phosphate group is extremely active, meaning it enters very readily into chemical combinations. It is sometimes called high energy phosphate. We may imagine that the terminal phosphate of ATP enters into some kind of combination with the ends of two thin filaments of actin, drawing them together.

     The ATP which has donated the phosphate to this reaction now becomes:

     or Adenosine Diphosphate, ADP.

     In relaxation, the third phosphate probably separates from the actin filaments and becomes ordinary phosphate ion. In this form it can react with small molecules, but not with actin.

     When the phosphate ions react with a small molecule and that molecule descends to a lower energy state by oxidation or by splitting, the phosphate becomes reactive with ADP so that ATP can be formed again. The new ATP can now be used to support a new muscular contraction.

h. Anaerobic Metabolism:

     For short periods muscle can contract by utilizing its stored sources of energy. No oxygen is required, and therefore no blood supply is needed. The energy developed is derived anaerobically, without air. Glycogen, a carbohydrate stored in muscle, splits to simple sugars. These combine with phosphates and split again. As indicated in the last section, this splitting makes the phosphate reactive so that it can combine with ADP to make ATP. The anaerobic process is shown in Figure 37.

     The small molecules produced in the splitting are lactic and pyruvic acids. Both are strong acids, and unless they are removed by the blood, they cause pain.

i. Requirements for Blood:

     The need for blood in muscular contraction is dramatically illustrated in a disease called intermittent claudication. In this disease, the delivery of blood to the leg muscles is considerably reduced, though not quite stopped. Persons with intermittent claudication can walk a few steps and must then stop until the lactic and pyruvic acids are washed away by the blood or broken down by oxidation.

     Most of the energy of muscular contraction is aerobic, or supported by oxidative reactions. Lactic and pyruvic acids react with inorganic phosphate. In the presence of oxygen these are broken down further, and at each step of breakdown high energy phosphate is made. Some of the high energy phosphate is used to make ATP, some is used to restore the glycogen stores of the muscle (glucose brought by the blood must also be used in this reaction), some is stored in combination with creatine as creatine phosphate. The phosphate of creatine phosphate is high energy phosphate that can be used to make ATP from ADP. The aerobic genesis of high energy phosphate is shown in Figure 38.

     The relationship between aerobic and anaerobic metabolism shows up well in athletic performance. Short, intense effort which depends primarily on stored glycogen and not at all on blood supply, can be performed at extraordinary rates compared to prolonged effort, which is dependent primarily on blood supply. Thus in running a hundred yard dash a man can reach 22 miles / hour, but in running a mile, which depends partially on stored glycogen but mostly on blood supply, only a little more than 15 miles / hour is possible. In the marathon run, (26.2 miles) which depends almost entirely on blood supply, the speed falls to 10.5 miles / hour.

     The heart and brain, which seem to depend entirely on aerobic metabolism, must continue to work whether or not oxygen is available and are peculiarly susceptible to factors which influence their blood supply. See Chapters 5 and 16 for further discussion.

j. Resting Length:

     A muscle which is overly short before it contracts contracts quite weakly. When it is slightly stretched, its contraction becomes stronger, but excessive stretching before contraction diminishes the contractility of the muscle. This relationship, illustrated in Figure 42, is extremely important in the case of the heart (Starling's Law, Chapter 10).

     This relationship is used quite unconsciously when grasping an object tightly. The muscles which flex the fingers are on the anterior surface of the forearm. By putting the wrist in a bent up position, "cocked-up", these muscles are stretched and the grip is correspondingly strengthened. One can easily break a grip by straightening the wrist, which shortens the grasping muscles.

10. Muscular Hypertrophy and Atrophy:

     When muscles are used heavily, they tend to hypertrophy. It is not clear what the mechanism for this hypertrophy is. Certain types of muscular exercise, for example swimming, do not produce much hypertrophy, though they may make great demands of the muscles. Weight lifting, on the other hand, produces very striking hypertrophy. It is possible that the stimulus for hypertrophy is the tension developed rather than the amount of use.

     When muscles are immobile, as, for example, after a nerve injury or around an arthritic and painful joint, they tend to waste away, to atrophy. The most marked degrees of atrophy are seen after destruction of motor neurons, as in poliomyelitis. The cause of atrophy, like the cause of hypertrophy, is unknown.

11. Disorders of Muscle:

     Very often diseases which are apparently muscular originate in the nervous system or at the neuro-muscular junction. The muscle cramps familiar to almost everyone may be caused by hyperalkalinity of the body fluids (Chapter 9). Holding one's breath, which makes the body fluids less alkaline, is often remedial.

     Muscular dystrophy is a hereditary disease in which there is progressive weakness, sometimes associated with muscular atrophy, sometimes with hypertrophy, sometimes with both. The cause is unknown.

     Myasthenia gravis is a rare disease which is characterized by very easy fatigability. It is not truly a disease of muscle, but rather of the neuromuscular junction (Chapter 4). The substance which transmits the nerve impulse to muscle, acetyl choline, is released in too small quantities, or perhaps, if released in normal amounts, it does not transmit the nerve impulse properly to the muscle. Whichever of these is the case, the disease is easily treated by the administration of drugs which prevent the destruction of acetyl choline. This destruction is accomplished by an enzyme called cholinesterase. Drugs which diminish the activity of cholinesterase, such as prostigmine and neostigmine, are to be of definite value in the treatment of this disease.

12. Guide to the Study of the Anatomy of Skeletal Muscles:

     Just as the skeleton is the framework of the body, the external form of the body is determined primarily by the skeletal muscles, the skin being an overall covering. More than half the body weight consists of skeletal muscles. These muscles are best studied by dissection, though alternatively they can be studied from diagrams. Unfortunately, these diagrams tend to obscure the relationships of these muscles to each other and to other structures. In the set of illustrations which follows (Figures 40-90) an attempt has been made to show important muscles in relation to other muscles and structures by showing all structures around a particular muscle in transparency, while the muscle in question is shown dark. In each illustration, a different muscle is emphasized.

     Knowledge of the position of each muscle must be supplemented by knowledge of its innervation and action. The table of voluntary muscles supplies this information.

a. Use of the Table of Voluntary Muscles:

     Voluntary muscles ordinarily attach to two bones. The one which remains more stable as the muscle contracts is called the origin, and the more movable bone is called the insertion. Obviously, these terms are relative; sometimes the bone of insertion remains more stationary than the bone of origin. The origins and insertions given in the Table are those accepted by custom.

     Some muscles, called sphincters, are arranged in a circle, and they work to close or open orifices. No origin and insertion are given for such muscles.

     The name of the muscle is given in the first column. Origin and insertions (when appropriate) are given in the second and third columns. The nerve supplying the muscle is given in the fourth column, and the action of the muscle is given in the fifth column. The sixth column refers to illustrations which show the muscle and its bony attachments.

     In describing the action of a muscle the following terms are used:

Flexion: The angle between the bones connected by the muscles is reduced.

Extension: The angle between the bones connected by the muscles is increased.

Adduction: The muscle brings the part toward the midline.

Abduction: The muscle brings the part away from the midline.

Pronation: The muscle turns the wrist so that the palm is down.

Supination: The muscle turns the wrist so that the palm is up.

Dorsal Plexion (applied to foot): The muscle decreases the angle between the top of the foot and leg bones.

Plantar Flexion (applied to foot): The muscle increases the angle between the top of the foot arid leg bones.

     In studying the table, the student will do well to keep the appropriate diagrams in mind. Only through understanding of these diagrams can the action of the muscle be meaningfully understood. It is also helpful to try to reason out the names of many of the muscles. The English equivalent of the Latin or Greek name of the muscle is given in parenthesis below the name of each muscle.

Continue to Chapter 4.