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

1. Skeletal muscle is voluntary striated muscle usually attached to bone. A typical muscle cell (fiber) is 100 um to 30 cm long.

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

1. The series-elastic components of muscular tissue include the stretchy endomysium, perimysium, and epimysium that 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.

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

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

3. Sarcoplasmic reticulum (a reservoir for calcium) joins with T tubules to form terminal cisternae. A T tubule with terminal cisternae on each side is a triad.

4. The sarcoplasm contains abundant glycogen and myoglobin.

1. Myofilaments are central to muscle contraction. Two kinds exist.

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

3. The thin myofilaments are made up of fibrous actin with bead-like subunits of globular actin, each of which has an active site that can bind the head of a myosin molecule.

4. 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.

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

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

1. Skeletal muscle is innervated by somatic motor neurons.

2. Each muscle fiber is supplied by only one motor nerve fiber.

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. 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".

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 expands 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; the neurotransmitter is always acetylcholine (ACh) at a neuromuscular junction.

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

1. Muscles 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).

4. RMP is measured in mV, and is determined by: 1) diffusion of ions down their concentrations gradients; 2) selective permeability of the plasma membrane; and 3) electrostatic attraction.

5. 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.

6. 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 changes in membrane voltage called action potential.

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 in to 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 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.

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

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

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

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

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

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 hydrolyses 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.

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.

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.

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 cycle of contraction and relaxation, called a twitch. During the twitch, it has a contraction phase followed by a relaxation phase.

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

1. The muscle fiber exhibits a maximum contraction response or it exhibits none at all, a phenomenon called the all-or-none law.

2. The strength of contraction of a whole muscle is graded as more motor units join in.

1. 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.

1. After a twitch, a short refractory period of 5 msec exists when the muscle cannot respond to another stimulus.

2. 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.

3. 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.

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.

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

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.

2. Immediate Energy (p. 414; Fig. 12.20; Transp. 222)

3. Short-Term Energy (p. 414)

4. Long-Term Energy (p. 414)

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.

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.

1. Slow-twitch fibers are small and produce twitches up to 100 msec long. They have more mitochondria and capillaries, and are high-endurance fibers. These fibers impart a red, or "dark-meat" quality to 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; athletic conditioning cannot change the genetic component of ability.

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.

1. 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.

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

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

1. Delayed onset muscle soreness is unusual pain, stiffness, or tenderness that is felt several hours to a day after strenuous exercise. This is due to muscle microtrauma.

1. The central nervous system occasionally triggers painful, spasmodic contractions (cramps). These are initiated by extreme cold, heavy exercise, lack of blood flow, electrolyte depletion, dehydration, and low blood glucose.