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Objective
1. Specify the functions of skeletal muscle tissue.
Skeletal muscles are the muscles attached to the skeletal system, which allow us
to move. The muscular system includes only skeletal muscles.
Objectives
1. Describe the organization of muscle at the tissue level
2. Explain the unique characteristics of skeletal muscle fibers.
3. Identify the structural components of a sarcomere.
Figure 10-1
Muscles have 3 layers of connective tissues:
1. the epimysium: an exterior collagen layer connected to the deep fascia
which separates the muscle from surrounding tissues.
2. the perimysium: surrounds bundles of muscles fibers called fascicles.
Perimysium holds the blood vessels and nerves that supply the fascicles.
3. the endomysium: surrounds individual muscle cells (the muscle fibers),
and contains the capillaries and nerve fibers that directly contact the
muscle cells. Endomysium also contains satellite cells (stem cells) that
repair damaged muscles.
At each end of the muscle, the endomysium, perimysium and epimysium come
together to form a connective tissue attachment to the bone matrix, either a tendon
(a bundle) or an aponeurosis (a sheet).
Blood Vessels and Nerves, p. 285
Skeletal muscles are voluntary muscles, controlled by nerves from the central
nervous system.
Figure 10-2
Skeletal muscle cells (fibers) are very different from typical cells. The long fibers
develop through the fusion of mesodermal cells (myoblasts) until they become
very large and contain hundreds of nuclei.
Figure 10-3
The cell membrane of a muscle cell is called the sarcolemma, which surrounds the
sarcoplasm or cytoplasm of the muscle fiber. Muscle contractions begin with a
change in the transmembrane potential.
Because the whole muscle fiber must contract at the same time, the signal (action
potential) is conducted through the cell by transverse tubules (T tubules) which
have the same properties as the sarcolemma.
Ion pumps concentrate calcium ions (Ca++) in the cisternae. The calcium ions are
released into the contractile units of the muscle (sarcomeres) at the beginning of a
muscle contraction.
Figure 10-4
Sarcomeres (the contractile units of muscle) are structural units of myofibrils
resulting from the organization or pattern of thick and thin filaments within the
myofibril.
The center of the A band is the midline or M line of the sarcomere. The centers of
the I bands are Z lines. One sarcomere is measured from one Z line to another.
Thick filaments and thin filaments overlap in the zone of overlap, which is the
densest, darkest area on a light micrograph.
The area around the M line, which has thick filaments but no thin filaments, is
called the H zone.
Strands of protein (titin) reach from the tips of the thick filaments to the Z line
and stabilize the filaments.
Figure 10-5
Two transverse tubules encircle each sarcomere near the 2 zones of overlap.
When calcium ions are released by the sarcoplasmic reticulum, thin and thick
filaments interact.
Figure 10-6
(Review the functional organization of a skeletal muscle fiber.)
Figure 10-7
The complex interactions of thick and thin filaments which cause muscle
contraction are determined by the structures of their protein molecules.
When a Ca++ ion binds to the receptor on a troponin molecule, the troponin-
tropomyosin complex changes, exposing the active site of the F actin and
initiating contraction.
Thick Filaments contain twisted myosin subunits. The tail binds to other myosin
molecules. The free head, made of 2 globular protein subunits, reaches out to the
nearest thin filament.
During a contraction, myosin heads interact with actin filaments to form cross-
bridges. The myosin head pivots, producing motion.
Figure 10-8
In skeletal muscle contraction, the thin filaments of the sarcomere slide toward
the M line, in between the thick filaments. This is called the sliding filament
theory. The width of the A zone stays the same, but the Z lines move closer
together.
Objectives
1. Identify the components of the neuromuscular junction, and summarize
the events involved in the neural control of skeletal muscles.
2. Explain the key steps involved in the contraction of a skeletal muscle
fiber.
Figure 10-9
Muscle fiber contraction is initiated by neural stimulation of a sarcolemma,
causing excitation-contraction coupling. The cisternae of the sarcoplasmic
reticulum release calcium ions, which trigger the interaction of thick and thin
filaments, consuming ATP and producing a pulling force called tension.
Figure 10-10
Neural stimulation occurs at the neuromuscular junction (NMJ). The electrical
signal or action potential travels along the nerve axon and ends at a synaptic
terminal which releases a chemical neurotransmitter called acetylcholine (ACh).
ACh travels across a short gap called the synaptic cleft and binds to membrane
receptors on the sarcolemma called the motor end plate, causing sodium ions to
rush into the sarcoplasm. An enzyme in the sarcolemma (acetylcholinesterase or
AChE) then breaks down the ACh.
This step requires the myosin heads to have previously broken down ATP and
stored the potential energy in the “cocked” position.
Figure 10-12
The Contraction Cycle has 5 steps:
1. Exposure of active sites
2. Formation of cross-bridges
3. Pivoting of myosin heads
4. Detachment of cross-bridges
5. Reactivation of myosin
Figure 10-13
As the sarcomeres shorten, the muscle pulls together, producing tension that
moves whatever it is attached to.
Relaxation, p. 298
Since AChE quickly breaks down ACh, the duration of a contraction depends on:
1. the duration of the neural stimulus
2. the number of free calcium ions in the sarcoplasm
3. the availability of ATP
As calcium ion concentrations in the sarcoplasm fall, calcium ions detach from
troponin, and the active sites are recovered by tropomyosin. The sarcomeres will
remain in the contracted state unless an outside force returns them to their
stretched position.
Upon death, ion pumps cease to function and calcium builds up in the sarcoplasm,
causing a fixed muscular contraction called rigor mortis.
Table 10-1: A review of muscle contraction from ACh release to the end of contraction.
Key
Skeletal muscle fibers shorten as thin filaments interact with thick filaments and
sliding occurs.
The trigger for contraction is the appearance of free calcium ions in the
sarcoplasm; the calcium ions are released by the sarcoplasmic reticulum when the
muscle fiber is stimulated by the associated motor neuron.
Contraction is an active process; relaxation and return to resting length is entirely
passive.
The tension produced by the contraction of an individual muscle fiber can vary,
depending on the number of pivoting cross-bridges; the fiber’s resting length at
the time of stimulation, and the frequency of stimulation.
Figure 10-14
Length-Tension Relationships: The number of pivoting cross bridges depends on
the amount of overlap between thick and thin fibers. There is an optimum amount
of overlap to produce the greatest amount of tension; too much or too little
overlap reduces efficiency. The normal range of resting sarcomere length is 75 to
Figure 10-15
The length of a twitch depends on the type of muscle. A graph of twitch tension
development is called a myogram.
Figure 10-16a
Repeated stimulations immediately after the relaxation phase (stimulus frequency
< 50 per second) causes a series of contractions with increasing tension. This
stair-step type increase in twitch tension is called treppe.
Figure 10-16b
Repeated stimulations before the end of the relaxation phase (stimulus frequency
> 50 per second) causes increasing tension called a summation of twitches (or
wave summation).
Figure 10-16c
If rapid stimulation continues and the muscle is not allowed to relax, the twitches
will reach a maximum level of tension called incomplete tetanus.
Figure 10-16d
If stimulation frequency is so high that the muscle never begins a relaxation
phase, the muscle reaches complete tetanus, or continuous contraction.
Skeletal muscle motion results from the coordinated action of many fibers in a
muscle.
Figure 10-17
The amount of tension a whole muscle can produce depends on:
1. The internal tension produced by the muscle fibers
2. The external tension the muscle fibers exert on their elastic extracellular
fibers (series elastic elements such as tendons)
3. The total number of muscle fibers stimulated
Figure 10-18
A single motor neuron can control hundreds of muscle fibers (a motor unit) that
contract at the same time.
In a whole muscle or group of muscles, smooth motion and increasing tension are
produced by slowly increasing the size or number of motor units stimulated. This
is called recruitment or multiple motor unit summation.
Maximum tension is achieved when all motor units reach tetanus, but this can
only be sustained for a very short time. Sustained tension is less than maximum
tension, allowing some motor units to rest in rotation.
Key
All voluntary muscle contractions and intentional movements involve the
sustained, tetanic contractions of skeletal muscle fibers.
The force exerted can be increased by increasing the number of stimulated motor
units (recruitment).
The normal tension and firmness of a muscle at rest is called muscle tone. Though
not producing motion, some muscle units are always actively maintaining body
position. Increasing muscle tone leads to more active muscle fibers, which
increases the metabolic energy used, even at rest.
Figure 10-19
There are 2 basic patterns of muscle tension: isotonic contraction and isometric
contraction.
Figure 10-20
Resistance and speed of contraction are inversely related. The heavier the
resistance on a muscle, the longer it will take for the muscle to begin to shorten,
and the less the muscle will shorten.
Objectives
1. Describe the mechanisms by which muscle fibers obtain the energy to
power contractions.
2. Describe the factors that contribute to muscle fatigue, and discuss the
stages and mechanisms involved in the muscle’s subsequent recovery.
ATP is the active energy molecule. If a resting muscle has more ATP than it
needs, it transfers the excess energy to a storage molecule called creatine
phosphate (CP).
The energy in creatine phosphate is used to recharge ADP to ATP (using the
enzyme creatine phosphokinase or CPK). When the CP is used up, other
mechanisms generate ATP.
Figure 10-21
At peak levels of exertion, muscles can’t get enough oxygen to support
mitochondrial activity. The muscle then relies on glycolysis for ATP.
When muscles can no longer perform a required activity, they are fatigued.
Muscle fatigue is associated with:
1. depletion of metabolic reserves
2. damage to the sarcolemma and sarcoplasmic reticulum
3. low pH (lactic acid)
4. muscle exhaustion and pain
After high levels of exertion, it can take hours or days for muscles to return to
their normal condition.
During the recovery period, oxygen is once again available and mitochondrial
activity resumes. Lactic acid is carried by the blood stream to the liver, where it is
converted back into pyruvic acid, and glucose is released to recharge the muscles’
glycogen reserves. This removal and recycling of lactic acid by the liver is called
the Cori cycle.
To process excess lactic acid and normalize metabolic activities after exercise, the
body uses more oxygen than usual. This elevated need for oxygen, called the
oxygen debt, is responsible for heavy breathing after exercise.
Key
Skeletal muscles at rest metabolize fatty acids and store glycogen.
During light activity, muscles can generate ATP through the anaerobic breakdown
of carbohydrates, lipids or amino acids.
At peak levels of activity, most of the energy is provided by anaerobic reactions
that generate lactic acid as a byproduct.
Heat Production and Loss: The more active muscles are, the more heat they
produce. During strenuous exercise, up to 70 percent of the energy produced can
be lost as heat, raising body temperature.
Objectives
1. Relate the types of muscle fibers to muscle performance.
2. Distinguish between aerobic and anaerobic endurance, and explain their
implications for muscular performance.
Table 10-3 compares the properties of the 3 types of skeletal muscle fibers.
Different muscles have different percentages of fast, slow and intermediate fibers.
Muscles with mostly fast fibers are pale (white muscle) like chicken breast.
Muscles with mostly slow fibers are dark (red muscle) like chicken legs. Most
human muscles have mixed fibers and are pink.
Atrophy: Lack of muscle activity causes reduction in muscle size, tone and power.
Key
What you don’t use, you loose.
Muscle tone is an indication of the background level of activity in the motor units
in skeletal muscles.
When inactive for days or weeks, muscles become flaccid. The muscle fibers
break down their contractile proteins and become smaller and weaker.
If inactive for long periods of time, muscle fibers may be replaced by fibrous
tissue.
VII. Cardiac Muscle Tissue, p. 317
Objective
1. Identify the structural and functional differences between skeletal muscle fibers
and cardiac muscle cells.
Figure 10-23
Cardiac muscle is a striated muscle tissue found only in the heart.
Intercalated discs join the cell membranes of adjacent cardiocytes with gap
junctions and desmosomes. They maintain structure and enhance molecular and
electrical connections. Action potentials travel easily across intercalated discs.
Because heart cells are mechanically, chemically and electrically linked, the heart
functions like a single, fused mass of cells.
Objectives
1. Identify the structural and functional differences between skeletal muscle
fibers and smooth muscle cells.
2. Discuss the role that smooth muscle plays in systems throughout the body.
Smooth muscle is a nonstriated tissue which forms around other tissues in almost
every organ system.
- In all systems, smooth muscle in blood vessels regulates blood pressure and
flow.
- In digestive and urinary systems, smooth muscle forms sphincters and produces
contractions.
- Smooth muscle also produces movements in the reproductive and glandular
systems.
- In the integumentary system, goose bumps are caused by arrector pili muscles
of hair follicles.
Figure 10-24b
The internal organization of actin and myosin in smooth muscle is different from
that in the striated muscles. Smooth muscle cells:
1. are long and slender
2. are spindle shaped, with a single, central nucleus
3. have no T tubules, myofibrils or sarcomeres
4. have scattered myosin fibers, with more heads per thick filament
5. have thin filaments attached to dense bodies
6. transmit contractile force from cell to cell through dense bodies
7. have no tendons or aponeuroses
1. Excitation-Contraction Coupling:
Free calcium ions in the cytoplasm trigger smooth muscle contraction. In the
sarcoplasm, calcium ions bind with the protein calmodulin, which activates
the enzyme myosin light chain kinase, which breaks down ATP and initiates
the contraction.
2. Length-Tension Relationships:
Thick and thin filaments are scattered, so resting length is not related to
tension development. The ability of smooth muscle to function over a wide
range of lengths is called plasticity.
3. Control of Contractions:
Smooth muscle cells are subdivided into multiunit smooth muscle cells, which
are connected to motor neurons, and visceral smooth muscle cells, which are
not. Visceral smooth muscle networks generally have rhythmic cycles of
activity controlled by pacesetter cells.
SUMMARY
In Chapter 10 we learned:
the 3 types of muscle tissue (skeletal, cardiac and smooth)
the functions of skeletal muscles
the structure of skeletal muscle cells (endomysium, perimysium, epimysium)
the functional anatomy of the skeletal muscle fiber (actin and myosin)
the nervous control of skeletal muscle fibers (neuromuscular junctions and action
potentials)
tension production in skeletal muscle fibers (twitch, treppe and tetanus)
tension production by skeletal muscles (motor units and contractions)
skeletal muscle activity and energy (ATP, CP, aerobic and anaerobic energy)
skeletal muscle fatigue and recovery
the 3 types of skeletal muscle fibers (fast, slow, intermediate)
skeletal muscle performance (white and red muscles, physical conditioning)
the structure and function of cardiac muscle tissue
the structure and function of smooth muscle tissue