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Figure 6-12

Isotonic and isometric systems for recording muscle contractions.

Duration of isometric contractions for different types of mammalian skeletal muscles, showing a latent period between the action potential (depolarization) and muscle contraction.

secondary importance. (5) Fewer mitochondria, also because oxidative metabolism is secondary.

Slow Fibers. (1) Smaller fibers. (2) Also innervated by smaller nerve fibers. (3) More extensive blood vessel system and capillaries to supply extra amounts of oxygen. (4) Greatly increased numbers of mitochondria, also to support high levels of oxidative metabolism. (5) Fibers contain large amounts of myoglobin, an iron-containing protein similar to hemoglobin in red blood cells. Myoglobin combines with oxygen and stores it until needed; this also greatly speeds oxygen transport to the mitochondria. The myoglobin gives the slow muscle a reddish appearance and the name red muscle, whereas a deficit of red myoglobin in fast muscle gives it the name white muscle.

Mechanics of Skeletal Muscle Contraction

Motor Unit. Each motoneuron that leaves the spinal cord innervates multiple muscle fibers, the number depending on the type of muscle. All the muscle fibers innervated by a single nerve fiber are called a motor unit. In general, small muscles that react rapidly and whose control must be exact have more nerve fibers for fewer muscle fibers (for instance, as few as two or three muscle fibers per motor unit in some of the laryngeal muscles). Conversely, large muscles that do not require fine control, such as the soleus muscle, may have several hundred muscle fibers in a motor unit. An average figure for all the muscles of the body is questionable, but a good guess would be about 80 to 100 muscle fibers to a motor unit.

The muscle fibers in each motor unit are not all bunched together in the muscle but overlap other motor units in microbundles of 3 to 15 fibers. This interdigita-tion allows the separate motor units to contract in support of one another rather than entirely as individual segments.

Muscle Contractions of Different Force—Force Summation.

Summation means the adding together of individual twitch contractions to increase the intensity of overall muscle contraction. Summation occurs in two ways: (1) by increasing the number of motor units contracting simultaneously, which is called multiple fiber summation, and (2) by increasing the frequency of contraction, which is called frequency summation and can lead to tetanization.

Multiple Fiber Summation. When the central nervous system sends a weak signal to contract a muscle, the smaller motor units of the muscle may be stimulated in preference to the larger motor units. Then, as the strength of the signal increases, larger and larger motor units begin to be excited as well, with the largest motor units often having as much as 50 times the contractile force of the smallest units. This is called the size principle. It is important, because it allows the gradations of muscle force during weak contraction to occur in small steps, whereas the steps become progressively greater when large amounts of force are required. The cause of this size principle is that the smaller motor units are driven by small motor nerve fibers, and the small motoneurons in the spinal cord are more excitable than the larger ones, so they naturally are excited first.

Rate of stimulation (times per second)

Figure 6-13

Frequency summation and tetanization.

Another important feature of multiple fiber summation is that the different motor units are driven asynchronously by the spinal cord, so that contraction alternates among motor units one after the other, thus providing smooth contraction even at low frequencies of nerve signals.

Frequency Summation and Tetanization. Figure 6-13 shows the principles of frequency summation and tetanization. To the left are displayed individual twitch contractions occurring one after another at low frequency of stimulation. Then, as the frequency increases, there comes a point where each new contraction occurs before the preceding one is over. As a result, the second contraction is added partially to the first, so that the total strength of contraction rises progressively with increasing frequency. When the frequency reaches a critical level, the successive contractions eventually become so rapid that they fuse together, and the whole muscle contraction appears to be completely smooth and continuous, as shown in the figure. This is called tetanization. At a slightly higher frequency, the strength of contraction reaches its maximum, so that any additional increase in frequency beyond that point has no further effect in increasing contractile force. This occurs because enough calcium ions are maintained in the muscle sarcoplasm, even between action potentials, so that full contractile state is sustained without allowing any relaxation between the action potentials.

Maximum Strength of Contraction. The maximum strength of tetanic contraction of a muscle operating at a normal muscle length averages between 3 and 4 kilograms per square centimeter of muscle, or 50 pounds per square inch. Because a quadriceps muscle can have as much as 16 square inches of muscle belly, as much as 800 pounds of tension may be applied to the patellar tendon. Thus, one can readily understand how it is possible for muscles to pull their tendons out of their insertions in bone.

Changes in Muscle Strength at the Onset of Contraction—The Staircase Effect (Treppe). When a muscle begins to contract after a long period of rest, its initial strength of contraction may be as little as one half its strength 10 to 50 muscle twitches later. That is, the strength of contraction increases to a plateau, a phenomenon called the staircase effect, or treppe.

Although all the possible causes of the staircase effect are not known, it is believed to be caused primarily by increasing calcium ions in the cytosol because of the release of more and more ions from the sarcoplasmic reticulum with each successive muscle action potential and failure of the sarcoplasm to recapture the ions immediately.

Skeletal Muscle Tone. Even when muscles are at rest, a certain amount of tautness usually remains. This is called muscle tone. Because normal skeletal muscle fibers do not contract without an action potential to stimulate the fibers, skeletal muscle tone results entirely from a low rate of nerve impulses coming from the spinal cord. These, in turn, are controlled partly by signals transmitted from the brain to the appropriate spinal cord anterior motoneurons and partly by signals that originate in muscle spindles located in the muscle itself. Both of these are discussed in relation to muscle spindle and spinal cord function in Chapter 54.

Muscle Fatigue. Prolonged and strong contraction of a muscle leads to the well-known state of muscle fatigue. Studies in athletes have shown that muscle fatigue increases in almost direct proportion to the rate of depletion of muscle glycogen. Therefore, fatigue results mainly from inability of the contractile and metabolic processes of the muscle fibers to continue supplying the same work output. However, experiments have also shown that transmission of the nerve signal through the neuromuscular junction, which is discussed in Chapter 7, can diminish at least a small amount after intense prolonged muscle activity, thus further diminishing muscle contraction. Interruption of blood flow through a contracting muscle leads to almost complete muscle fatigue within 1 or 2 minutes because of the loss of nutrient supply, especially loss of oxygen.

Lever Systems of the Body. Muscles operate by applying tension to their points of insertion into bones, and the bones in turn form various types of lever systems. Figure 6-14 shows the lever system activated by the biceps muscle to lift the forearm. If we assume that a large

Figure 6-14

Lever system activated by the biceps muscle.

biceps muscle has a cross-sectional area of 6 square inches, the maximum force of contraction would be about 300 pounds. When the forearm is at right angles with the upper arm, the tendon attachment of the biceps is about 2 inches anterior to the fulcrum at the elbow, and the total length of the forearm lever is about 14 inches. Therefore, the amount of lifting power of the biceps at the hand would be only one seventh of the 300 pounds of muscle force, or about 43 pounds. When the arm is fully extended, the attachment of the biceps is much less than 2 inches anterior to the fulcrum, and the force with which the hand can be brought forward is also much less than 43 pounds.

In short, an analysis of the lever systems of the body depends on knowledge of (1) the point of muscle insertion, (2) its distance from the fulcrum of the lever, (3) the length of the lever arm, and (4) the position of the lever. Many types of movement are required in the body, some of which need great strength and others of which need large distances of movement. For this reason, there are many different types of muscle; some are long and contract a long distance, and some are short but have large cross-sectional areas and can provide extreme strength of contraction over short distances. The study of different types of muscles, lever systems, and their movements is called kinesiology and is an important scientific component of human physioanatomy.

"Positioning" of a Body Part by Contraction of Agonist and Antagonist Muscles on Opposite Sides of a Joint—"Coactivation" of Antagonist Muscles. Virtually all body movements are caused by simultaneous contraction of agonist and antagonist muscles on opposite sides of joints. This is called coactivation of the agonist and antagonist muscles, and it is controlled by the motor control centers of the brain and spinal cord.

The position of each separate part of the body, such as an arm or a leg, is determined by the relative degrees of contraction of the agonist and antagonist sets of muscles. For instance, let us assume that an arm or a leg is to be placed in a midrange position. To achieve this, agonist and antagonist muscles are excited about equally. Remember that an elongated muscle contracts with more force than a shortened muscle, which was demonstrated in Figure 6-9, showing maximum strength of contraction at full functional muscle length and almost no strength of contraction at half normal length. Therefore, the elongated muscle on one side of a joint can contract with far greater force than the shorter muscle on the opposite side. As an arm or leg moves toward its midposition, the strength of the longer muscle decreases, whereas the strength of the shorter muscle increases until the two strengths equal each other. At this point, movement of the arm or leg stops. Thus, by varying the ratios of the degree of activation of the agonist and antagonist muscles, the nervous system directs the positioning of the arm or leg.

We learn in Chapter 54 that the motor nervous system has additional important mechanisms to compensate for different muscle loads when directing this positioning process.

Remodeling of Muscle to Match Function

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

Muscle Hypertrophy and Muscle Atrophy. When the total mass of a muscle increases, this is called muscle hypertrophy. When it decreases, the process is called muscle atrophy.

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

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

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

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

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

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

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

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

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

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

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

Rigor Mortis

Several hours after death, all the muscles of the body go into a state of contracture called "rigor mortis"; that is, the muscles contract and become rigid, even without action potentials. This rigidity results from loss of all the ATP, which is required to cause separation of the cross-bridges from the actin filaments during the relaxation process. The muscles remain in rigor until the muscle proteins deteriorate about 15 to 25 hours later, which presumably results from autolysis caused by enzymes released from lysosomes. All these events occur more rapidly at higher temperatures.

References

Berchtold MW, Brinkmeier H, Muntener M: Calcium ion in skeletal muscle: its crucial role for muscle function, plasticity, and disease. Physiol Rev 80:1215, 2000.

Brooks SV: Current topics for teaching skeletal muscle physiology. Adv Physiol Educ 27:171, 2003.

Clausen T: Na+-K+ pump regulation and skeletal muscle contractility. Physiol Rev 83:1269, 2003.

Glass DJ: Molecular mechanisms modulating muscle mass. Trends Mol Med 8:344, 2003.

Glass DJ: Signalling pathways that mediate skeletal muscle hypertrophy and atrophy. Nat Cell Biol 5:87, 2003.

Gordon AM, Homsher E, Regnier M: Regulation of contraction in striated muscle. Physiol Rev 80:853, 2000.

Gordon AM, Regnier M, Homsher E: Skeletal and cardiac muscle contractile activation: tropomyosin "rocks and rolls." News Physiol Sci 16:49, 2001.

Huxley AF, Gordon AM: Striation patterns in active and passive shortening of muscle. Nature (Lond) 193:280, 1962.

Huxley HE: A personal view of muscle and motility mechanisms. Annu Rev Physiol 58:1,1996.

Jurkat-Rott K, Lerche H, Lehmann-Horn F: Skeletal muscle channelopathies. J Neurol 249:1493, 2002.

Kjœr M: Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. Physiol Rev 84:649, 2004.

Macintosh BR: Role of calcium sensitivity modulation in skeletal muscle performance. News Physiol Sci 18:222, 2003.

Matthews GG: Cellular Physiology of Nerve and Muscle. Malden, MA: Blackwell Science, 1998.

Sieck GC, Regnier M: Plasticity and energetic demands of contraction in skeletal and cardiac muscle. J Appl Physiol 90:1158, 2001.

Stamler JS, Meissner G: Physiology of nitric oxide in skeletal muscle. Physiol Rev 81:209, 2001.

Szent-Gyorgyi AG: Regulation of contraction by calcium binding myosins. Biophys Chem 59:357,1996.

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