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Introduction
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Effectors are tissues and organs that carry out responses to commands from the central nervous system.
Animal movement involves an array of adaptations to respond to signals from the nervous system.
Microtubules, Microfilaments, and Cell Movement
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Two components of the cytoskeleton—microtubules and microfilaments—generate cell movement. Both are
long protein molecules that change length or shape.
Microtubules are components of the cytoskeleton
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Microtubules are important intracellular effectors for changing cell shape, moving organelles, and enabling
cells to respond to their environment.
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They generate forces by polymerizing and depolymerizing the protein tubulin.
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The spindle that moves chromosomes to the mitotic poles at anaphase is made up of microtubules.
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In the developing nervous system, microtubules help growing neurons search for the appropriate contact
cells.
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Microtubules also generate the small-scale movements of cilia and flagella.
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Many protists and small invertebrates use cilia for locomotion; larger multicellular animals use cilia to move
fluids and particles over cell surfaces.
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In humans, cilia remove wastes from the lung and sweep eggs from the ovary into the oviducts.
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Flagellated cells maintain the flow of water through the bodies of sponges; flagella power the movement of
sperm in most species.
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(See Videos 47.1, 47.2, and 47.3.)
Microfilaments change cell shape and cause cell movements
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Microfilament proteins—actin and myosin—generate contractile forces in cell movement and in the
alteration of cell shape.
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The dominant of the two is actin, which may form structural parts of cells and change cell shape by
polymerizing and depolymerizing.
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The microvilli that increase the absorptive surface area of the cells lining the gut, and the stereocilia of the
sensory hair cells in the mammalian ear, are stiffened by actin microfilaments.
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Microfilaments reach their highest level of organization in muscle cells, which generate large-scale
movements.
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The contractile ring that divides an animal cell during cytokinesis is made of actin and myosin filaments.
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Endocytosis (engulfment of materials) relies on interactions of actin and myosin.
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Cells traveling within the body by amoeboid movement (e.g., phagocytic cells) also rely on these proteins.
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The name “amoeboid” comes from the type of movement exhibited by the freshwater protist, the amoeba.
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This motion is accomplished by the cell’s squeezing itself into a lobe-shaped projection called a pseudopod.
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By reversing its plasmasol (liquid portion of cytoplasm) with its plasmagel (thicker gel cytoplasm), it moves
the cytoplasm.
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It is the interacting network of contracting actin and myosin that squeezes the plasmasol into a pseudopod.
Muscle Contraction
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In the animal kingdom, wherever whole tissues contract, muscle cells are responsible.
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These specialized cells have high densities of actin and myosin.
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Actin filaments consist of a twisted chain of actin molecules.
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Myosin filaments are bundles of many myosin molecules.
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The actin and myosin filaments lie parallel to each other. At contraction, the actin and myosin filaments slide
past each other like a telescope.
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The three types of vertebrate muscle are smooth, cardiac (heart), and skeletal. (See Figure 47.1.)
Smooth muscle causes slow contractions of many internal organs
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Smooth muscle provides contraction for internal organs, which are under the control of the autonomic
nervous system.
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Smooth muscle moves food through the digestive tract, controls the flow of blood, and empties the urinary
bladder.
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Smooth muscle cells are the simplest muscle cells structurally; they have a single nucleus and are usually
long and spindle-shaped.
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Unlike other muscles that have a striated appearance, smooth muscles appear—smooth! (See Figure 47.1.)
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The cells are arranged in sheets and are in electrical connection with one another via gap junctions.
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This arrangement allows an action potential generated in the membrane to spread to all the cells in the sheet.
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The resting potential of the membrane is sensitive to being stretched. (See Animated Tutorial 47.2.)
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When stretched, the cells depolarize and fire action potentials, causing contraction.
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Neurotransmitters of the autonomic nervous system can also alter the membrane potential.
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In the digestive tract, acetylcholine causes smooth muscle cells to depolarize, thus making them more likely
to contract; norepinephrine causes them to hyperpolarize, thus making them less likely to contract.
Cardiac muscle causes the heart to beat
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Under a microscope, cardiac muscle looks different from smooth or skeletal muscle. (See Figure 47.1.)
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Cardiac muscles are branched and appear striated because of the regular arrangement of their actin and
myosin filaments.
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Branching creates a meshwork that resists tearing and allows the heart to withstand the high pressures of
blood pumping without leaking.
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Intercalated discs provide mechanical adhesions between adjacent cells.
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Like smooth muscle cells, sheets of cardiac muscle are in electrical contact with one another, and
depolarization begun at one point in the heart rapidly spreads through the muscle mass.
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Pacemaker cells are special muscle cells that initiate the heart’s rhythmic contractions.
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These cells give the heart a myogenic capacity (self-generated heartbeat).
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Although heart activity is modified by the autonomic nervous system, the heart will beat without nervous
input.
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(See Video 47.4.)
Sliding filaments cause skeletal muscle to contract
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All voluntary movements are controlled by skeletal, or striated, muscle.
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Skeletal muscle is also called striated muscle because of its striped appearance. (See Figure 47.1.)
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Skeletal muscle cells (called muscle fibers) have many nuclei because they are a fusion of many individual
cells.
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Bundles of the contractile filaments are called myofibrils, each made up of thin actin units surrounding thick
myosin units. (See Figure 47.3.)
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The striated or band pattern of the myofibril is due to repeating sarcomeres, the units of contraction.
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Each sarcomere is bounded by Z lines, which anchor the thin actin filaments.
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The sarcomere center is the A band, housing all the myosin filaments.
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The H zone and I band are areas where actin and myosin do not overlap and appear light.
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The dark stripe in the H zone, the M band, contains proteins that support the myosin filaments.
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The bundles of myosin filaments are held in a centered position within the sarcomere by the protein titin.
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Titin runs the full length of the sarcomere from Z line to Z line, and each titin molecule runs through the
myosin bundle.
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Between the ends of the myosin bundles and the Z lines, titin molecules are very elastic, accounting for the
resistance to stretch in relaxed skeletal muscle.
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When a muscle contracts, the sarcomere shortens, the H zone and the I band become much narrower, and the
Z lines move toward the A band as if the actin filaments were sliding into the region occupied by the myosin filaments.
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Huxley and Huxley called this mechanism the sliding filament theory of muscle contraction.
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(See Video 47.5.)
Actin–myosin interactions cause filaments to slide
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The structures of actin and myosin account for the sliding of the filaments. (See Figure 47.4)
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Each myosin molecule consists of two long polypeptide chains coiled together, each ending in a large
globular head.
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A myosin filament is made of many such molecules arranged in parallel, their heads projecting from one or
the other side of the filament.
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An actin filament consists of a helical arrangement of two chains of actin molecules twisted together.
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The myosin end heads have sites that bind to actin, forming bridges between actin and myosin filaments.
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The heads also have ATPase activity; they bind and hydrolyze ATP, releasing energy. (See Figure 47.6.)
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The binding of actin exerts force to cause actin and myosin filaments to slide a short distance.
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The myosin head then binds ATP and releases actin.
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This “ratcheting” action is repeated and rebinding occurs, using the energy from ATP hydrolysis.
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Backsliding of actin does not occur because the many surrounding filaments create a system of interacting
cycles.
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The ATP is necessary for breaking actin–myosin bonds, not to form them.
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The energy is actually used to stop muscles from contracting.
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This accounts for the stiffening of muscles (rigor mortis) after death. The failure to renew ATP stores after
death causes dense actin–myosin bonds to form.
Actin–myosin interactions are controlled by calcium ions
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Muscle contractions are initiated by action potentials from motor neurons.
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Each neuron is branched to permit synapses with up to a hundred muscle fibers.
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These fibers constitute a motor unit and contract simultaneously when stimulated by a single neuron.
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Skeletal muscle fibers in vertebrates are excitable and are depolarized by a threshold action potential.
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This opens sodium channels, permitting the muscle plasma membrane to generate action potentials just like
the axon of the delivering neuron.
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Neurotransmitter from the motor neuron binds to receptors, opening these channels.
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Most of the ions flowing through the channels in the motor end plate are Na +.
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This depolarization of the motor end plate spreads to the surrounding plasma membrane, and when the
threshold is reached, the plasma membrane fires.
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All points on the muscle surface are stimulated, as well as deep areas within the cytoplasm of the muscle fiber
(also called the sarcoplasm). (See Figure 47.5.)
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Within this sarcoplasm and in contact with every myofibril are T tubules.
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The T tubules come into very close contact with the sarcoplasmic reticulum, a network of membranes
surrounding every myofibril in the muscle fiber.
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When the muscle is at rest, the interior of the sarcoplasmic reticulum has a higher concentration of Ca2+ than
the exterior.
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This gradient is maintained by calcium pumps in the membrane of the sarcoplasmic reticulum.
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When an action potential spreads through the T tubule system, it causes calcium channels in the sarcoplasmic
reticulum to open.
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Ca2+ diffuses out of the reticulum into the sarcoplasm surrounding the myofibrils.
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The Ca2+ stimulates the interaction of actin and myosin and the sliding of the filaments.
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How do the Ca2+ ions do this?
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When the muscle is at rest, two proteins, tropomyosin and troponin, block the myosin binding sites on the
actin filament, preventing actin and myosin from interacting.
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When Ca2+ binds to troponin, troponin and tropomyosin change shape, exposing the actin–myosin binding
sites.
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With the binding sites exposed, the actin–myosin bonds are made, and the filaments are pulled past each
other, resulting in muscle fiber contraction.
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ATP then binds to myosin, causing it to release actin.
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ATP is hydrolyzed, and myosin heads return to their resting conformation.
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If Ca2+ remains available, the cycle repeats and muscle contraction continues.
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When the T tubule system repolarizes, calcium pumps remove Ca2+ ions from the sarcoplasm, untwisting the
troponin and tropomyosin molecules and blocking the actin–myosin connection.
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Figure 47.6 summarizes this cycle.
Calmodulin mediates Ca2+ control of contraction in smooth muscle
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Smooth muscle lacks the troponin–tropomyosin mechanism for control of contraction.
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In smooth muscle, Ca2+ entering the sarcoplasm combines with a protein called calmodulin.
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This complex activates the enzyme myosin kinase, which phosphorylates the myosin heads.
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Thus chemically activated, myosin goes through cycles of binding and releasing actin, causing muscle
contraction.
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Another enzyme, myosin phosphatase, dephosphorylates the myosin and helps stop the actin–myosin
interactions.
Single skeletal muscle twitches are summed into graded contractions
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The minimum unit of contraction, a twitch, is measured in terms of the tension, or force, it generates. (See
Figure 47.7a.)
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The force generated by a muscle depends on how many muscle fibers are in its motor units. In muscles used
for fine movement, motor units have only one or a few fibers.
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Each twitch is an all-or-none phenomenon, and if action potentials are fired more rapidly, before the
myofibrils return to rest, the tension (accumulated twitches) sums up and becomes more sustained.
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At high stimulation levels, the calcium pumps in the sarcoplasmic reticulum can no longer remove Ca 2+ ions
between action potentials.
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At this point, when the contractile machinery generates maximum tension, tetanus is reached. (See Figure
47.7b.)
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The length of time in tetanus depends on the supply of ATP.
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The actin–myosin bonds have to keep cycling to maintain muscle tension.
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Faster twitching of individual fibers causes temporal summation.
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An increase in the number of motor units (all the muscle fibers served by a single neuron) in the contraction
causes spatial summation.
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A low level of tension in muscles is called muscle tone and is in constant readjustment by the nervous system
(for example, body posture in response to gravity).
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Muscle tone comes from a small but changing number of motor units alternating contraction and relaxation.
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(See Animated Tutorial 47.1.)
Muscle Strength and Performance
Muscle fibers determine endurance and strength
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Skeletal muscle fibers may be of different types. (See Figure 47.8.)
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Slow-twitch fibers (red muscle) have many mitochondria and much myoglobin to provide steady, prolonged
ATP production.
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Long-term aerobic work such as running and swimming depend on this type of fiber.
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Fast-twitch fibers (white muscle) have fewer mitochondria and less myoglobin.
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They develop maximum tension more rapidly and with greater tension, but fatigue rapidly.
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The myosin of fast-twitch fibers has high ATPase activity, but cannot replenish ATP fast enough to sustain
long-term contraction.
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Fast-twitch fibers are ideal for situations that require sudden, maximum strength, such as weight lifting or
sprinting.
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Genetics largely determines the proportion of these two fibers in skeletal muscles.
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Aerobic training can improve oxidative capacity, but the genes inherited are the more important factor.
The strength of a muscle fiber is related to its length
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The structure of the sarcomere explains the relationship between the strength of a muscle fiber and its length.
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When a muscle is stretched and the sarcomeres are lengthened, there is less overlap between the actin and
myosin filaments; fewer cross-bridges form, and less force can be produced.
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If the sarcomeres are stretched too much, there is no overlap between the actin and myosin, and no force can
be produced.
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A muscle recovers from such a situation by means of the elastic titin molecules that pull the actin and myosin
back into an overlapping arrangement.
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When the muscle is fully contracted, the actin and myosin filaments overlap so much that the myosin bundles
are pressed up against the Z lines and additional shortening is difficult.
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Figure 47.9 shows the relationship between the length of a muscle fiber and its ability to develop tension.
Exercise increases muscle strength and endurance
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Different types of exercise produce different physical conditioning responses.
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In general, anaerobic activities (e.g., weight lifting) increase strength and aerobic activities (e.g., jogging)
increase endurance.
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Anaerobic exercise:
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Strength is a function of the cross-sectional area of muscles; more actin and myosin filaments can produce
more tension.
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Exercise such as push-ups or weight lifting induce the formation of new actin and myosin filaments, hence,
bigger muscles.
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To a more limited extent, satellite cells in the muscle, which generate new fibers following muscle damage,
can create new muscle fibers.
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Aerobic exercise:
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Aerobic exercise enhances the oxidative capacity of muscles by means of an increased number of
mitochondria, increased enzymes, and an increase in the density of capillaries that deliver oxygen to the muscle.
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There is also an increase in myoglobin, which facilitates the diffusion of oxygen throughout the muscle fibers
and provides a store of oxygen for use when the blood supply is insufficient.
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Thus aerobic training stimulates fast-twitch fibers to increase their oxidative capacity.
Muscle fuel supply limits performance
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Muscles have three systems for obtaining the ATP they need for contraction:
The immediate system: preformed ATP and creatine phosphate
The glycolytic system: metabolizing carbohydrates to lactate and pyruvate
The oxidative system: metabolizing carbohydrates or fats to H2O and CO2.
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The capacity of these three systems and the rates at which they can produce ATP determine work capacity
and endurance. (See Figure 47.10.)
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The total energy available in the body from the immediate system (ATP and creatine phosphate, which is
transferrable to ADP) is only about 10 Calories.
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It enables fast-twitch fibers to generate force immediately, but it is quickly exhausted.
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The glycolytic system is able to take over within a few seconds because the ATP generated by glycolytic
enzymes in the muscle fiber cytoplasm is rapidly available to the myosin filaments.
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However, glycolysis rapidly leads to the accumulation of lactic acid, which slows the process.
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Thus the glycolytic system and the immediate system together provide the energy for active muscles for less
than a minute. (See Figure 47.10).
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Oxidative metabolism can come on line in about a minute and produce large amounts of ATP due to its
ability to metabolize carbohydrates and fats.
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However, it requires many reactions and takes place in the mitochondria, so the rate at which oxidative metabolism can make ATP available to the myosin filaments is slower than that of the other two systems.
Skeletal Systems
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Skeletal systems provide rigid supports against which muscles can pull and create directed movements.
A hydrostatic skeleton consists of fluid in a muscular cavity
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The simplest type of skeleton is the hydrostatic skeleton of cnidarians, annelids, and other soft-bodied
invertebrates.
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It consists of fluid enclosed in a body cavity surrounded by muscle.
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Squeezing this fluid-filled cavity by muscle action bulges the body in a particular direction.
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This mechanism causes the extension and retraction of tentacles in the sea anemone.
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The earthworm uses its hydrostatic skeleton to crawl by exerting pressure on many separate, fluid-filled
segments. (See Figure 47.11.)
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Two muscle layers running opposite one another alternately bulge and pull the segments along, aided by
bristles extending out from the body surface.
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Hydrostatic skeletons also are used to jet-propel squid and octopus by forcefully ejecting water out of a small
body orifice, propelling the animal in the opposite direction.
Exoskeletons are rigid outer structures
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Exoskeletons are hardened outer surfaces to which muscles attach internally.
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Contractions of muscles cause jointed and articulated segments of the exoskeleton to move relative to each
other.
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The simplest example of an exoskeleton is the shell of a mollusk.
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The most complex exoskeletons are found in the arthropods.
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The arthropod exoskeleton, or cuticle, covers all body surfaces, including appendages and some internal
parts.
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This covering is made up of plates that are secreted by cells just below the exoskeleton.
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Except at the flexible joints, the cuticle contains waxes and stiffening materials.
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The layers of the cuticle include an outer, thin, waxy epicuticle, which protects the body from drying out, and
a thicker, inner, chitin-containing endocuticle, which forms most of the structure and provides armor protection.
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Despite the protection it offers, a chitin exoskeleton is subject to abrasion and crushing.
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Another drawback is that, once hardened in place, the exoskeleton must be shed (molted) to allow growth of
the animal to a larger size.
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During an extended time of molt, the animal is very vulnerable to predators and the outside environment.
Vertebrate endoskeletons provide supports for muscles
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Vertebrate endoskeletons are internal scaffoldings to which muscles attach and against which they can pull.
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Endoskeletons are made of rod, plate, and tubelike bones.
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Bones are connected by joints that allow a range of movement.
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Unlike exoskeletons, endoskeletons do not provide outer protection, but they can grow and enlarge inside the
body without a molt.
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The human body has 206 bones that make up the axial and appendicular skeletons. (See Figure 47.12.)
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Cartilage and bone are two kinds of connective tissue that create the endoskeleton.
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Cartilage is a rubbery mix of protein (collagen) and polysaccharide, which gives strength and resiliency.
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It is found in joints and in stiff but flexible structures such as the nose and ear.
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The embryonic skeleton of vertebrates is primarily cartilage, which is gradually replaced by bone during
development.
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Sharks and rays keep their cartilage skeletons for life.
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Bone is mostly extracellular matrix material made up of collagen fibers and crystals of calcium phosphate.
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Bone is rigid and hard and is a reservoir for calcium for the rest of the body.
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The living cells of bone are the osteoblasts, the osteocytes, and the osteoclasts. (See Figure 47.13.)
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Osteoblasts lay down new matrix on the bone surface and gradually become enclosed within the bone in
lacunae (cavities).
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Osteocytes are really enclosed osteoblasts that maintain cell contact and communication within the bone.
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Osteoclasts erode bone, creating cavities and tunnels, and help the osteoblasts replace and remodel the bones.
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Coordination of bone activity is not well understood, but it is known that stress on bones conveys
information that living bone cells use to modify the bone.
Bones develop from connective tissue
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One bone type, known as membranous bone (e.g., skull bones), forms on a scaffolding of connective tissue
membrane.
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The other type, called cartilage bone (e.g., limb bones), forms first as cartilage, then gradually hardens to
become bone.
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Cartilage bones grow as they harden and harden first at the center, then at the ends. (See Figure 47.14.)
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Bone may be cancellous (spongy and rigid, but with cavities) or compact (solid and hard).
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Most bones have both cancellous and compact regions.
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Long limb bones have compact bone surrounding a central cavity of soft marrow, but have cancellous ends.
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Mammal compact bone is called Haversian bone; it is composed of structural units called Haversian systems,
which are sets of osteocytes and blood vessels in concentric bony cylinders. (See Figure 47.15.)
Bones that have a common joint can work as a lever
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A joint is where two bones meet.
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Muscle can only contract (pull) and then relax, never push.
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Therefore, muscle movement around joints is by antagonistic muscle pairs—one contracting, the other
relaxing.
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A bend of a joint such as the knee requires a flexor. To straighten the knee, an extensor is needed. (See
Figure 47.19.)
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Separate bones at a joint are held together by ligaments, flexible bands of connective tissue.
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Other straps of connective tissue, called tendons, attach the muscles to bones. (See Figure 47.16.)
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There are a variety of joints structured for different movements. (See Figure 47.17.)
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Bones and joints work like systems of levers.
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A power arm and a load arm work around a fulcrum, or pivot.
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The length ratio of the two arms determines whether a particular lever can exert a lot of force over a short
distance or is better at translating force into large or fast movements.
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Some parts of the human body rely on the design that produces power (e.g., the jaw); others rely on the one
that produces speed (e.g., lower leg). (See Figure 47.18.)
Other Effectors
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Defense, communication, prey capture, and predator avoidance structures are specialty effectors.
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Nematocysts
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Nematocysts are miniature harpoonlike missiles fired by certain cnidarians. (See Figure 31.7.)
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Each nematocyst consists of a tightly coiled thread inside a capsule, armed with a spinelike trigger.
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When potential prey brush the trigger, the nematocyst fires.
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The prey are poisoned or entangled by batteries of these barbed threads, and some large fish may be subdued
in this way.
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The Portuguese man-of-war has enough poison to kill a human.
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Chromatophores
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Some animals change color for camouflage or to communicate.
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Chromatophores are pigmented cells in the skin of animals such as chameleons and flounder.
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The most common type of chromatophore has fixed cell boundaries, within which pigment granules are
moved by microfilaments.
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When pigment is concentrated in the cell center, the animal looks pale. When pigment is dispersed
throughout the cell the animal is darker.
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Another type of chromatophore is capable of amoeboid movement.
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The cells can mold themselves into shapes with a minimal area, making the tissue look pale. When they are
flattened, the tissue looks darker.
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The third type of chromatophore changes shape by the action of muscle fibers that radiate outward.
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When the fibers are relaxed, the chromatophore is small, and the animal is pale. When the fibers contract, the
chromatophore expands, and the animal is dark.
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These chromatophores can change very rapidly and are used in some species in courtship and aggressive
behavior. (See Figure 47.19.)
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Glands
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Glands are effector organs that produce and release chemicals.
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Airborne chemical cues used for communication with other individuals are called pheromones and are used
by insects (particularly moths) in mating.
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Snakes, spiders, some frogs, and other organisms have poison glands for prey capture and defense.
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Some of these poisons can be highly toxic, blocking nerve–muscle junctions and calcium channels in prey or
predators.
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Skunks have an effective odoriferous spray (mercaptan) for defense.
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Electric organs
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Electric eels, catfish, and rays generate electricity to sense the environment, to communicate, and to stun prey
or predators.
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These organs evolved from muscles and produce electric potentials in the fashion of nerves and muscles, only
with far more voltage.
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An electric eel can produce 600 volts or about 100 watts, enough to light a row of light bulbs or to stun a
person.
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(See Videos 47.6 and 47.7.)