I. Types and Characteristics of Muscle Tissue (p. 420; table 12.1)

A. Universal Characteristics of Muscle (p. 420)

1. All muscle tissue exhibits responsiveness (excitability), conductivity, contractility, extensibility, and elasticity.

B. Skeletal Muscle (p. 420)

1. Skeletal muscle is voluntary striated muscle usually attached to bone.

2. A typical muscle cell (fiber) is about 100 µm long, but can be up to 30 cm long. (fig. 12.1)

3. Skeletal muscle exhibits striations, reflecting the overlapping nature of the internal contractile proteins.

C. Series-Elastic Components (p. 420)

1. The series-elastic components of muscular tissue include the stretched endomysium, perimysium, epimysium, fascia, and tendon, all of which are not excitable but do stretch and recoil.

2. During muscle contraction, the muscle generates internal tension, followed by external tension that moves the load.

II. Microscopic Anatomy of Skeletal Muscle (p. 421)

A. The Muscle Fiber (p. 421; fig. 12.2; TR 422)

1. The plasma membrane of the muscle fiber is the sarcolemma. It has transverse (T) tubules.

2. The cytoplasm (sarcoplasm) contains myofibrils made up of myofilaments.

3. Sarcoplasmic reticulum (a reservoir for calcium ions) joins with T tubules to form terminal cisternae.

4. The sarcoplasm contains abundant glycogen and myoglobin.

B. Myofilaments (p. 421; fig. 12.3; TR 423)

1. Myofilaments are central to muscle contraction. Three kinds exist: thick filaments, thin filaments, and elastic filaments.

2. Thick myofilaments are made of myosin and shaped somewhat like a golf club.

3. Thin myofilaments are made up of fibrous actin with beadlike subunits of globular actin, each of which has an active site that can bind the head of a myosin molecule.

4. Elastic filaments are made of titin and run through the thick filament, connecting it to the Z disc.

5. Within the fibrous actin lies another protein called tropomyosin, which itself has smaller proteins called troponin. Tropomyosin and troponin are the regulatory proteins of muscle contraction.

C. Striations (p. 423; fig. 12.4; TR 424)

1. Striated muscle has dark A bands (thick filaments) alternating with lighter I bands. In the middle of the A band is a lighter region called the H band, into which the thin filaments do not extend.

2. Each I band has a narrow dark line called the Z disc. Each segment of myofibril from one Z disc to the next is the sarcomere, the unit of contraction of a muscle fiber.

III. The Nerve-Muscle Relationship (p. 424)

A. Motor Neurons (p. 424)

1. Skeletal muscle is innervated by somatic motor neurons whose cell bodies are in the brainstem and spinal cord.

2. The axons of motor neurons are called somatic motor fibers, and their distal branches lead to the fibers of skeletal muscle. (fig. 12.5)

3. Each muscle fiber is supplied by only one motor neuron.

B. The Motor Unit (p. 424; fig. 12.6; TR 425)

1. A motor unit consists of one nerve fiber and all the muscle fibers it innervates.

2. A motor unit behaves as a single functional unit and contracts as one.

3. Motor units vary in size. Muscles for eye movement have 23 muscle fibers per motor unit, whereas the large thigh muscles have 500–1,000 fibers per motor unit.

4. Multiple motor units within a muscle are able to "work in shifts."

C. The Neuromuscular Junction (p. 425; fig. 12.7; TR 426; table 12.2)

1. The point of contact between a neuron and its target cell is called a synapse. When the target cell is a muscle cell, the synapse is called a neuromuscular junction.

2. At the neuromuscular junction, the neurons expand into a synaptic knob. Where the muscle cell receives the message from the neuron is the motor end plate. There is a tiny gap between the two cells called the synaptic cleft.

3. A nervous impulse traveling down the neuron triggers the release of neurotransmitter from synaptic vesicles in the synaptic knob; at a neuromuscular junction, the neurotransmitter is always acetylcholine (ACh)

4. ACh receptors are present in the motor end plate within infoldings called junctional folds. Also present is acetylcholinesterase, which breaks down ACh after stimulation.

D. Electrically Excitable Cells (p. 426)

1. Muscle fibers and neurons are electrically excitable because their plasma membranes show voltage changes after stimulation.

2. The study of the electrical activity of cells is called electrophysiology.

3. Electric potential (in volts, V) is potential energy that results from a polarized state. A cell can be polarized and exhibit a resting membrane potential (RMP), which is measured in mV.

4. The RMP is maintained by the sodium—potassium pump, which removes three sodium ions from the cell for every two potassium ions it brings in, and therefore has the net effect of contributing to the negative intracellular charge.

5. When a nerve or muscle cell is stimulated, ion gates in the membrane open, sodium ions rush in, and potassium ions rush out, resulting in a change in membrane voltage called an action potential.

IV. Behavior of Skeletal Muscle Fibers (p. 429)

A. Excitation (p. 429; fig. 12.8; TR 427)

1. During excitation, action potentials in the nerve fiber give rise to action potentials in the muscle fiber.

2. Action potentials in the synaptic knob trigger the release of ACh from synaptic vesicles. ACh is released to the synaptic cleft and detected by the ligand-gated ion channels in the motor end plate.

3. Sodium ions rush into the muscle cell, which quickly reverses polarity; potassium ions rush out, and membrane polarity is reestablished. This rapid change in polarity at the motor end plate is called the end-plate potential (EPP).

4. The EPP triggers the opening of sodium and potassium channels adjacent to the motor end plate, and action potentials spread away from the plate in all directions.

B. Excitation-Contraction Coupling (p. 429; fig. 12.9; TR 428)

1. During excitation-contraction coupling, action potentials in the muscle fiber lead to activation of the myofilaments.

2. The wave of action potential reaches the T tubules and continues into terminal cisternae of the sarcoplasmic reticulum.

3. After the action potential reaches the sarcoplasmic reticulum, it releases a flood of calcium ions into the cytosol.

4. Calcium ions bind to the troponin of the thin myofilaments, causing the troponin-tropomyosin complex to shift aside, exposing the active sites on the actin filament.

5. The heads of the myosin filaments can now bind to these active sites and initiate contraction.

C. Contraction (p. 429; fig. 12.10; TR 429)

1. During the contraction phase, sliding of the thin myofilaments past the thick ones causes the muscle fiber to shorten.

2. The sliding filament theory of Hanson and Huxley suggests that thin filaments slide over thick ones, causing sarcomeres to shorten.

3. The head of each myosin molecule contains myosin ATPase that releases energy from ATP. In preparation for action, the myosin binds and hydrolyzes an ATP molecule, and is now in the "cocked" position.

4. When the active sites on the actin filament are exposed, the myosin head contacts the active site, releases energy, and performs a power stroke.

5. At the end of a power stroke, myosin binds to a new ATP, releases the actin, and returns to its original position in a recovery stroke. Many myosin heads pull of the actin at once, so the actin does not slip back into its original position.

6. The cycle of power stroke and recovery is repeated many times during muscle contraction.

D. Relaxation (p. 433; fig. 12.11; TR 430)

1. When nervous stimulation ceases, the muscle relaxes.

2. Acetylcholinesterase breaks down ACh so the muscle stops generating its action potentials.

3. Calcium is carried back to the sarcoplasmic reticulum by active transport and a protein called calsequestrin.

E. The Length-Tension Relationship and Tonus (p. 433; fig. 12.12; TR 431)

1. Muscle fibers exhibit a length-tonus relationship: The tension generated by contraction depends on how stretched or contracted the fiber was to begin with.

2. If the muscle is already mostly contracted, stimulation will cause a weak contraction.

3. Conversely, if the muscle is overly stretched, little overlap exists between actin and myosin filaments, and contraction can damage the muscle.

4. The central nervous system continually monitors and adjusts the length of resting muscle to maintain a state of partial contraction called tonus.

V. Behavior of Whole Muscles (p. 436)

A. Threshold, Latent Period, and Twitch (p. 436)

1. Muscles have a threshold, or minimal voltage, necessary to produce a muscle contraction.

2. If a muscle is given a single, brief stimulation, it will show a quick cycle of contraction and relaxation called a twitch. (fig. 12.13; TR 432)

3. A very brief latent period exists between two successive twitches in which the muscle cannot contract.

B. Contraction Strength of Twitches (p. 436)

1. Muscles must be able to contract with variable strength. The strength of contraction of a whole muscle is increased as more motor units join in. (fig. 12.14; TR 433)

2. Another way to produce a stronger muscle contraction is to stimulate the muscle at a higher frequency. (fig. 12.15; TR 434)

3. Muscle cells exhibit treppe, or the staircase phenomenon, in response to a series of stimuli of the same strength. This is probably due to the inability of the muscle cells to fully return calcium to the sarcoplasmic reticulum.

4. After a twitch, a short refractory period exists during which the muscle cannot respond to another stimulus.

5. If a second stimulation arrives before the end of the refractory period, the muscle will achieve temporal summation (or wave summation) and achieve a higher level of tension.

6. If the stimuli are frequent enough that the muscle cannot relax completely in between, a state of incomplete tetanus is reached. If there is no time to relax at all between stimuli, complete tetanus is achieved.

C. Isometric and Isotonic Contraction (p. 438; figs. 12.16, 12.17; TR 435, 436)

1. Isometric contraction is tensing of the muscles—contraction without a change in length.

2. Isotonic contraction is contraction with a change in muscle length but no change in tension.

3. Isotonic contractions are of two types: concentric contraction, in which the muscle shortens as it contracts, and eccentric contraction, in which the muscle lengthens as it contracts.

VI. Muscle Metabolism (p. 439)

A. ATP Sources (p. 439)

1. During exercise, muscles use energy produced by aerobic respiration (when there is an adequate supply of oxygen) and anaerobic fermentation (when oxygen is limited, and lactic acid accumulates). (fig. 12.18; TR 437)

2. For immediate energy, muscle tissue relies on the phosphagen system to supply ATP. This includes myokinase and creatine kinase, which recruit phosphate groups. (fig. 12.19; TR 438)

3. For short-term energy, after the phosphagen system is exhausted, muscles reply temporarily on the glycogen-lactic acid system for ATP to supply energy for 30–40 seconds.

4. For long-term energy, after 40 seconds, the respiratory and cardiovascular systems catch up and deliver enough oxygen to meet the demands of aerobic respiration. Aerobic respiration can supply muscle demands for longer periods of activity.

B. Fatigue and Endurance (p. 441)

1. Muscle fatigue, the progressive weakness and loss of contractility, is due to a variety of causes: ATP synthesis declines as glycogen is consumed; the ATP shortage slows down to maintain the resting membrane potential; lactic acid lowers the pH of the sarcoplasm and impairs the action of enzymes; the accumulation of potassium ions reduces the membrane potential; motor nerve fibers use up their ACh; and the CNS fatigues for unknown reasons.

2. Physical endurance depends on the maximum oxygen uptake of the athlete and the supply of organic nutrients.

C. Oxygen Debt (p. 441)

1. Oxygen debt is the difference between the resting state of oxygen consumption and the elevated rate following an exercise.

2. Oxygen inhaled after exercise is used to replace the body's oxygen reserves, replenish the phosphagen system, oxidize lactic acid, and serve the now-elevated metabolic rate.

D. Slow- and Fast-Twitch Fibers (p. 442; tables 12.3, 12.4; TR 443, 444)

1. Slow-twitch fibers are small and produce twitches up to 100 msec long. They are dark in color because they have more mitochondria, capillaries and myoglobin, and thus they are called red muscles.

2. Fast-twitch fibers are larger and produce twitches as short as 7.5 msec. They produce quick energy (phosphagen system) for stop-and-go activities. These fibers impart a white appearance to muscles.

3. Individuals are born with different ratios of slow- to fast-twitch fibers; whether or not fibers can change through athletic conditioning remains an unsettled issue, but the genetic component appears to be the most influential factor.

E. Muscular Strength and Conditioning (p. 416)

1. Muscle strength depends on muscle size, fascicle arrangement, size of active motor units, multiple motor unit summation (recruitment), temporal summation, the length-tension relationship, and fatigue.

2. Resistance exercise (weight lifting) is the contraction of muscles against a load that resists movement, and is enough to stimulate muscle growth. Growth results mostly from cellular enlargement, not cell division.

3. Endurance (aerobic) exercise improves the fatigue-resistance of the muscles. Slow-twitch fibers acquire a greater density of blood capillaries.

4. Optimal performance and skeletomuscular health require cross-training, which incorporates elements of both types.

VII. Cardiac and Smooth Muscle (p. 444; table 12.5)

A. Cardiac Muscle (p. 444)

1. Like smooth muscle, cardiac muscle is involuntary, and its muscle cells are called myoctes.

2. Cardiac muscle is composed of striations, branched fibers, and intercalated discs that consist of mechanical and electrical linkages from cell to cell.

3. Cardiac muscle constitutes most of the heart, and is autorhythmic, meaning that it beats at regular time intervals without needing stimulation by the nervous system. This rhythm is set by a group of cells that form a pacemaker in the heart.

4. The high energy demand of cardiac muscle is reflected in its very large and numerous mitochondria, which compose about 25% of each cardiac muscle cell.

B. Smooth Muscle (p. 444)

1. Smooth muscle is composed of myocytes with a fusiform shape, only one nucleus, and no visible striations or sarcomeres.

2. There are no Z discs in smooth muscle, but its thin filaments attach to dense bodies on the sarcolemma.

3. There is scanty sarcoplasmic reticulum and no T tubules. Calcium enters through channels in the sarcolemma.

4. Most calcium for smooth muscle contraction comes from the extracellular fluid, not the sarcoplasmic reticulum, and it binds to calmodulin, not to troponin.

5. The two functional categories of smooth muscle are multiunit and single-unit. (fig. 12.20; TR 439)

a. Multiunit smooth muscle occurs in some arteries and pulmonary air passages, in the arrector pili, and iris. The terminal branches of an axon synapse with individual myocytes and form a motor unit.

b. Single-unit smooth muscle is the most widespread and is also called visceral muscle because it occurs in most blood vessels and in the digestive, respiratory, urinary, and reproductive tracts. (fig. 12.21; TR 440)

c. In single-unit smooth muscle, a nerve fiber does not synapse with a particular cell but releases neurotransmitter at several points within the tissue. (fig. 12.22; TR 441)

d. Single-unit smooth muscle cells also communicate electrically with each other through gap junctions.

6. Partly because of its latch-bridge mechanism, smooth muscle can remain partially contracted for a prolonged period without nervous stimulation. This ability, plus its fatigue-resistance, enables smooth muscle to maintain smooth muscle tone. (fig. 12.23; TR 442)

7. The ability of an organ such as the stomach or urinary bladder to expand results partly from the stress-relaxation response of smooth muscle.

VIII. Disorders of the Muscular System (p. 447; table 12.6)