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S-BIOL121 BSY32 1st Sem ( 2022-2023 )

Muscular System

Lesson Proper: Muscular System

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Muscular System Physiology:

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A runner rounds the last corner of the track and sprints for the finish line. Her arms and legs are pumping as she tries to reach her maximum speed. Her heart is beating rapidly, and her breathing is rapid, deep,
and regular. Blood is shunted away from her digestive organs, and a greater volume is delivered to her skeletal muscles to maximize their oxygen supply. These actions are accomplished by muscle tissue, the
most abundant tissue of the body and one of the most adaptable.

You don’t have to be running for the muscular system to be at work. Even when you aren’t consciously moving, postural mus- cles keep you sitting or standing upright, respiratory muscles keep you
breathing, the heart continuously pumps blood to all parts of your body, and blood vessels constrict or relax to direct blood to organs where it is needed.

In fact, movement within the body is accomplished in various ways: by cilia or flagella on the surface of certain cells, by the force of gravity, or by the contraction of muscles. But most of the body’s
movement results from muscle contraction. As described in chapter 4, there are three types of muscle tissue: skeletal,

cardiac, and smooth (figure 7.1). This chapter focuses primarily on the structure and function of skeletal muscle; cardiac and smooth muscle are described only briefly. Following are the major functions of the
muscular system:

1. Movement of the body. Contraction of skeletal muscles is responsible for the overall movements of the body, such as walking, running, and manipulating objects with the hands.
2. Maintenance of posture. Skeletal muscles constantly maintain tone, which keeps us sitting or standing erect.
3. Respiration. Muscles of the thorax carry out the movements necessary for respiration.
4. Production of body heat. When skeletal muscles contract, heat is given off as a by-product. This released heat is critical to the maintenance of body temperature.
5. Communication. Skeletal muscles are involved in all aspects of communication, including speaking, writing, typing, gesturing, and facial expressions.
6. Constrictionoforgansandvessels.Thecontractionofsmooth muscle within the walls of internal organs and vessels causes those structures to constrict. This constriction can help propel and mix food and
water in the digestive tract, propel secretions from organs, and regulate blood flow through vessels.
7. Contraction of the heart. The contraction of cardiac muscle causes the heart to beat, propelling blood to all parts of
the body.

Skeletal Muscle Structure

 
Connective Tissue Coverings of Muscle
Each skeletal muscle is surrounded by a connective tissue sheath called the epimysium (ep-i-mis′̄-̆m), or muscular fascia (fash′̄-̆) (figure 7.2a). Each whole muscle is subdivided by a loose con- nective tissue
called the perimysium (per′i-mis′̄-̆m) into numerous visible bundles called muscle fasciculi (f̆-sik′̄-lı). Each fascicle is then subdivided by a loose connective tissue called the endomysium (en′d̄ -mis′̄-̆m) into
separate muscle cells, called muscle fibers (figure 7.2b).
 
Muscle Fiber Structure
Examining the structure of a muscle fiber helps us understand the mechanism of muscle contraction. A muscle fiber is a single cylindrical fiber, with several nuclei located at its periphery. The largest human
muscle fibers are up to 30 cm long and 0.15 mm in diameter. Such giant cells may contain several thousand nuclei. The cell membrane of the muscle fiber is called the sarcolemma (sar′k̄ -lem′̆; sarco, flesh)
(figure 7.2b). The multiple nuclei of the muscle fiber are located just deep to the sarcolemma. Along the surface of the sarcolemma are many tubelike invaginations, called transverse tubules, or T tubules,
which occur at regular intervals along the muscle fiber and extend inward into it. The
T tubules are associated with a highly organized smooth endoplas- mic reticulum called the sarcoplasmic reticulum (re-tik′̄-l̆ m). T tubules connect the sarcolemma to the sarcoplasmic reticulum. The
sarcoplasmic reticulum has a relatively high concentration of Ca2+, which plays a major role in muscle contraction.  Inside each muscle fiber is the cytoplasm, called the sarcoplasm (sar′ k̄ -plazm). It contains
numerous myofibrils (mı-̄-fı′brilz; myo, muscle), threadlike structures that extend from one end of the muscle fiber to the other (figure 7.2c). Myofibrils consist of two major kinds of protein fibers: actin (ak′
tin) myofilaments (mı-̄-fil′ ̆-ments) and myosin (mı′ ̄-sin) myofilaments (figure 7.2d). The actin and myosin myofilaments are arranged into highly ordered, repeating units called sarco- meres (sar′k̄ -m̄ rz),
which are joined end-to-end to form the myofibrils (figure 7.2c,d).
 
Actin and Myosin Myofilaments
Actin myofilaments, or thin filaments, are made up of three com- ponents: actin, troponin, and tropomyosin. The actin strands, which resemble two minute strands of pearls twisted together, have attach- ment
sites for the myosin myofilaments (figure 7.2e). Troponin (tr̄ ′p̄ -nin) molecules are attached at specific intervals along the actin myofilaments. These molecules have binding sites for Ca2+. Tropomyosin (tr̄-p̄ -
mı′̄-sin) filaments are located along the groove between the twisted strands of actin myofilament subunits. The tropomyosin filaments block the myosin myofilament binding sites on the actin myofilaments in
an unstimulated muscle. In other words, if no Ca2+ is present, the tropomyosin filaments cover the attachment sites on the actin myofilament. However, when Ca2+ is present, it binds to troponin, which causes
the tropomyosin fila- ments to expose the attachment sites on the actin myofilaments.  Myosin myofilaments, or thick myofilaments, resemble bundles of minute golf clubs (figure 7.2f ). The parts of the
myosin molecule that resemble golf club heads are referred to as myosin heads. The myosin heads have three important properties: (1) The heads can bind to attachment sites on the actin myofilaments; (2)
they can bend and straighten during contraction; and (3) they can break down ATP, releasing energy.
 
Sarcomeres
The sarcomere is the basic structural and functional unit of skel- etal muscle because it is the smallest portion of skeletal muscle capable of contracting. The separate components of the sarcomere can slide
past each other, causing the sarcomeres to shorten. When the sarcomeres shorten, the myofibrils shorten, which is the ulti- mate cause of contraction of the muscle fiber during a contraction. Each sarcomere
extends from one Z disk to an adjacent Z disk. Each Z disk is a network of protein fibers forming an attachment site for actin myofilaments. The arrangement of the actin and myosin myofilaments in
sarcomeres gives the myofibril a banded appearance (figure 7.3). A light I band, which consists only of actin myofilaments, spans each Z disk and ends at the myosin myofilaments. A darker, central region in
each sarcomere, called an A band, extends the length of the myosin myofilaments. The actin and myosin myofilaments overlap for some distance at both ends of the A band. In the center of each sarcomere is
a second light zone, called the H zone, which consists only of myosin myofilaments. The myosin myofilaments are anchored in the center of the sarcomere at a dark-staining band, called the M line. The
alternating I bands and A bands of the sarcomeres are respon- sible for the striations in skeletal muscle fibers observed through the microscope (see table 4.10a). It is the close association of the sarcomeres,
the T tubules, and the sarcoplasmic reticulum that enables a nerve stimulus to initiate contraction of the muscle fiber.
 
Excitability of Muscle Fibers
Muscle fibers, like other cells of the body, have electrical properties. This section describes the electrical properties of skeletal muscle fibers, and later sections illustrate their role in contraction.
Most cells in the body have an electrical charge difference across their cell membranes. The inside of the membrane is negatively charged while the outside of the cell membrane is positively charged. In other
words, the cell membrane is polar- ized (figure 7.4, step 1). The charge difference, called the resting membrane potential, occurs because there is an uneven distri- bution of ions across the cell membrane.
The resting membrane potential develops for three reasons: (1) The concentration of K+ inside the cell membrane is higher than that outside the cell membrane; (2) the concentration of Na+ outside the cell
mem- brane is higher than that inside the cell membrane; and (3) the cell membrane is more permeable to K+ than it is to Na+. Recall from chapter 3 the different types of ion channels: nongated, or leak,
channels, which are always open, and chemically gated channels, which are closed until a chemical, such as a neurotrans- mitter, binds to them and stimulates them to open (see figure 3.5). Because excitable
cells have many K+ leak channels, K+ leaks out of the cell faster than Na+ leaks into the cell. In other words, some K+ channels are open, whereas other ion channels, such as those for Na+, are closed. In
addition, negatively charged molecules, such as proteins, are in essence “trapped” inside the cell because the cell membrane is impermeable to them. For these reasons, the inside of the cell membrane is more
negatively charged than the outside of the cell membrane.
In addition to an outward concentration gradient for K+, there exists an inward electrical gradient for K+. The resting membrane potential results from the equilibrium of K+ movement across the cell
membrane. Because K+ is positively charged, its movement from inside the cell to the outside causes the inside of the cell membrane to become even more negatively charged compared to the outside of the
cell membrane. However, potassium diffuses down its concentration gradient only until the charge difference across the cell membrane is great enough to prevent any additional diffusion of K+ out of the cell.
The resting membrane potential is an equilibrium in which the tendency for K+ to diffuse out of the cell is opposed by the negative charges inside the cell, which tend to attract the positively charged K+ into
the cell. At rest, the sodium-potassium pump transports K+ from outside the cell to the inside and transports Na+ from inside the cell to the outside. The active transport of Na+ and K+ by the sodium-potassium
pump maintains the uneven distribution of Na+ and K+ across the cell membrane (see chapter 3).
A change in resting membrane potential is achieved by changes in membrane permeability to Na+ or K+ ions. A stimula- tion in a muscle fiber or nerve cell causes Na+ channels to open
quickly and the membrane to become very permeable to Na+ for a brief time (figure 7.4, step 2). Because the Na+ concentration is much greater outside the cell than inside and the charge inside the cell
membrane is negative, some positively charged Na+ quickly diffuses down its concentration gradient and toward the negative charges inside the cell, causing the inside of the cell membrane to become more
positive than the outside of the cell. This change in the membrane potential is called depolarization. Near the end of depolarization, Na+ channels close, and additional K+ channels open (figure 7.4, step 3).
Consequently, the tendency for Na+ to enter the cell decreases, and the tendency for K+ to leave the cell increases. These changes cause the inside of the cell membrane to become more negative than the
outside once again. Additional K+ channels then close as the charge across the cell membrane returns to its resting condition (figure 7.4, step 1). The change back to the resting membrane potential is called
repolarization. The rapid depolarization and repolarization of the cell membrane is called an action potential. In a muscle fiber, an action potential results in muscle contraction. The resting membrane
potential and action potential are described in more detail in chapter 8.
 
Nerve Supply and Muscle Fiber Stimulation
Skeletal muscle fibers do not contract unless they are stimulated by motor neurons. Motor neurons are specialized nerve cells that stimulate muscles to contract. Motor neurons generate action potentials that
travel to skeletal muscle fibers. Axons of these neu- rons enter muscles and send out branches to several muscle fibers. Each branch forms a junction with a muscle fiber, called a neuro- muscular junction
(figure 7.5). A more general term, synapse (sin′aps), refers to the cell-to-cell junction between a nerve cell and either another nerve cell or an effector cell, such as in a muscle or a gland. Neuromuscular
junctions are located near the center of a muscle fiber. A single motor neuron and all the skeletal muscle fibers it innervates constitute a motor unit. A motor unit in a small, precisely controlled muscle, such
as in the hand, may have only one or a few muscle fibers per unit, whereas the motor units of
large thigh muscles may have as many as 1000 muscle fibers per motor unit. Therefore, the fewer fibers there are in the motor units of a muscle, the greater control you have over that muscle. Many motor
units constitute a single muscle.
A neuromuscular junction is formed by a cluster of enlarged axon terminals resting in indentations of the muscle fiber’s cell membrane. An enlarged axon terminal is the presynaptic terminal; the space
between the presynaptic terminal and the muscle fiber membrane is the synaptic cleft; and the muscle fiber membrane is the postsynaptic membrane. Each presynaptic terminal contains many small
vesicles, called synaptic vesicles. These vesicles con- tain acetylcholine (as-e-til-k̄ ′l̄ n), or ACh, which functions as a neurotransmitter, a molecule released by a presynaptic nerve cell that stimulates or
inhibits a postsynaptic cell.
When an action potential reaches the presynaptic terminal, it causes Ca2+ channels to open. Calcium ions enter the presynaptic terminal and cause several synaptic vesicles to release acetyl- choline into the
synaptic cleft by exocytosis (figure 7.6, steps 1 and 2). The acetylcholine diffuses across the synaptic cleft and binds to acetylcholine receptor sites on the Na+ channels in the muscle fiber cell membrane. The
combination of acetylcholine with its receptor opens Na+ channels and therefore makes the cell membrane more permeable to Na+. The resulting movement of Na+ into the muscle fiber will initiate an action
potential once threshold is reached. The action potential travels along the length of the muscle fiber and causes it to contract (figure 7.6, steps 3 and 4). The acetylcholine released into the synaptic cleft
between the neuron and the muscle fiber is rapidly broken down by an enzyme, acetylcholinesterase (as′e-til-k̄ -lin-es′ter-̄s). This enzymatic breakdown ensures that one action potential in the neuron yields
only one action potential in the skeletal muscle fibers of that motor unit and only one contraction of each muscle fiber.
 
Muscle Contraction
Contraction of skeletal muscle tissue occurs as actin and myosin myofilaments slide past one another, causing the sarcomeres to shorten. Many sarcomeres are joined end-to-end to form myofibrils.
Shortening of the sarcomeres causes myofibrils to shorten, thereby causing the entire muscle to shorten. The sliding of actin myofilaments past myosin myofilaments during contraction is called the sliding
filament model of muscle contraction. During contraction, neither the actin nor the myosin fibers shorten. The H zones and I bands shorten during contraction, but the A bands do not change in length (figure
7.7).  During muscle relaxation, sarcomeres lengthen. This length- ening requires an opposing force, such as that produced by other muscles or by gravity. This binding causes tropomyosin molecules to move
into a groove along the actin molecule, exposing myosin attachment sites on the actin myofilament. The exposed attachment sites on the actin myofilament bind to the heads of the myosin myofilaments to
form cross-bridges between the actin and myosin myofilaments.  Energy for muscle contraction is supplied to the muscles in the form of adenosine triphosphate (ATP), a high-energy molecule produced from
the energy that is released during the metabolism of food (see chapters 3 and 17). The energy is released as ATP breaks down to adenosine diphosphate (ADP) and phosphate (P). During muscle contraction,
the energy released from ATP is briefly stored in the myosin head. This energy is used to move the heads of the myosin myofilaments toward the center of the sarcomere, causing the actin myofilaments to
slide past the myosin myofilaments. In the process, ADP and P are released from the myosin heads.  As a new ATP molecule attaches to the head of the myosin molecule, the cross-bridge is released, the ATP
breaks down to ADP and P (which both remain bound to the myosin head), and the myosin head returns to its original position, where it can attach to the next site. As long as Ca2+ remains attached to tro-
ponin, and as long as ATP remains available, the cycle of cross- bridge formation, movement, and release repeats (figure 7.9). A new ATP must bind to myosin before the cross-bridge can be released. After a
person dies, ATP is not available, and the cross- bridges that have formed are not released, causing the muscles to become rigid. This condition is called rigor mortis (rig′er m̄ r′tis; stiffness + death).  Part of
the energy from ATP involved in muscle contraction is required for the formation and movement of the cross-bridges, and part is released as heat. The heat released during muscle contraction increases body
temperature, which explains why a person becomes warmer during exercise. Shivering, a type of generalized muscle contraction, is one of the body’s mechanisms for dealing with cold. The muscle movement
involved in shivering produces heat, which raises the body temperature.  Muscle relaxation occurs as Ca2+ is actively transported back into the sarcoplasmic reticulum (a process that requires ATP). As a
consequence, the attachment sites on the actin molecules are once again covered by tropomyosin so that cross-bridges cannot reform.
 
Muscle Twitch, Summation, Tetanus,  and Recruitment
 
A muscle twitch is the contraction of a muscle fiber in response to a stimulus. Because most muscle fibers are grouped into motor units, a muscle twitch usually involves all the muscle fibers in a motor unit.
A muscle twitch has three phases (figure 7.10). The lag phase, or latent phase, is the time between the application of a stimulus and the beginning of contraction. The contraction phase is the time during
which the muscle contracts, and the relaxation phase is the time during which the muscle relaxes.  During the lag phase, action potentials are produced in one or more motor neurons. An action potential
travels along the axon of a motor neuron to a neuromuscular junction (see figure 7.5). Once the stimulus reaches the neuromuscular junction, acetyl- choline must be released from the presynaptic terminal,
diffuse across the synaptic cleft, and bind to receptors that allow the entry of Na+, which initiates an action potential on the postsynaptic  membrane (see figure 7.6). Before the contraction phase can occur, the
action potential must result in the release of Ca2+ from the sarcoplasmic reticulum and the formation of cross-bridges (see figure 7.9, steps 1–2).  The contraction phase results from cross-bridge movement and
cycling (see figure 7.9, steps 3–6), which increases the tension produced by the muscle fibers (see figure 7.10).  During the relaxation phase, Ca2+ is actively transported back into the sarcoplasmic reticulum.
As Ca2+ diffuses away from the troponin molecules, tropomyosin molecules once again block the attachment sites. Cross-bridge formation is prevented, and the ten- sion produced by the muscle fibers
decreases (see figure 7.10).  The strength of muscle contractions varies from weak to strong. For example, the force muscles generate to lift a feather is much less than the force required to lift a 25-pound
weight. The force of contraction a muscle produces is increased in two ways: (1) Summation involves increasing the force of contraction of the muscle fibers within the muscle, and (2) recruitment involves
increasing the number of muscle fibers contracting.
In summation, the force of contraction of individual muscle fibers is increased by rapidly stimulating them. When stimulus fre- quency, which is the number of times a motor neuron is stimulated per second,
is low, there is time for complete relaxation of muscle fibers between muscle twitches (figure 7.11, stimulus frequency 1). As stimulus frequency increases (figure 7.11, stimulus frequencies 2–3), there is not
enough time between contractions for muscle fibers to relax completely. Thus, one contraction summates, or is added onto, a previous contraction. As a result, the overall force of contraction increases.
Tetanus (tet′a-nus; convulsive tension) is a sustained contraction that occurs when the frequency of stimula- tion is so rapid that no relaxation occurs (figure 7.11, stimulus frequency 4). It should be noted,
however, that complete tetanus is rarely achieved under normal circumstances and is more commonly an experimentally induced muscular response. The increased force of contraction produced in summation
and tetanus occurs because Ca2+ builds up in myofibrils, which promotes cross-bridge forma- tion and cycling. The buildup of Ca2+ occurs because the rapid
production of action potentials in muscle fibers causes Ca2+ to be released from the sarcoplasmic reticulum faster than it is actively transported back into the sarcoplasmic reticulum.
In recruitment, the number of muscle fibers contracting is increased by increasing the number of motor units stimulated, and the muscle contracts with more force. When only a few motor units are
stimulated, a small force of contraction is produced because only a small number of muscle fibers are contracting. As the number of motor units stimulated increases, more muscle fibers are stimulated to
contract, and the force of contraction increases. Maximum force of contraction is produced in a given muscle when all the motor units of that muscle are stimulated (recruited).
If all the motor units in a muscle could be stimulated simulta- neously, the resulting motion would be quick and jerky. However, because the motor units are recruited gradually, some are stimulated and held
in tetanus while additional motor units are recruited; thus, contractions are slow, smooth, and sustained. In the same way, smooth relaxation of muscle occurs because some motor units are held in tetanus
while other motor units relax.
Fiber Types
Muscle fibers are sometimes classified as either slow-twitch or fast-twitch fibers (table 7.1). This classification is based on differ- ences in the rod portion of the myosin myofilament (see figure 7.2). Slow-
twitch fibers contain type I myosin as the predominant or even exclusive type. Fast-twitch fibers contain either type IIa or type IIb myosin myofilaments. Each of these three myosin types is the product of a
different myosin gene.
The fast and slow names of these fibers indicate their contrac- tion speeds. Fast-twitch muscle fibers contract quickly, whereas slow-twitch muscle fibers contract more slowly. Among the fast- twitch fibers,
type IIb fibers are the fastest and type IIa fibers contract at an intermediate speed. The type IIb fibers can contract ten times faster than slow-twitch (type I) fibers. However, while slower, the slow-twitch
fibers can sustain the contraction for longer than the fast-twitch fibers. Likewise, type IIa fibers can sustain contractions longer than type IIb, but not as long as type I.
Muscular System 161

Energy Requirements for Muscle Contraction

Muscle fibers are very energy-demanding cells whether at rest or during any form of exercise. This energy comes from either aerobic (with O2) or anaerobic (without O2) ATP production (see chapter 17).

Generally, ATP is derived from four processes in skeletal muscle:

1. Aerobic production of ATP during most exercise and normal conditions

2. Anaerobic production of ATP during intensive short-term work
3. Conversion of a molecule called creatine (kr̄ ′a-t̄ n) phosphate to ATP
4. Conversion of two ADP to one ATP and one AMP (adenosine monophosphate) during heavy exercise

Aerobic respiration, which occurs mostly in mitochondria, requires O2 and breaks down glucose to produce ATP, CO2, and H2O. Aerobic respiration can also process lipids or amino acids to make ATP.
Anaerobic respiration, which does not require O2, breaks down glucose to produce ATP and lactate. In general, slow-twitch fibers work aerobically, whereas fast-twitch fibers are more suited for working
anaerobically. Low-intensity, long-duration exercise is supported through mainly aerobic pathways. High-intensity, short-duration exercise, such as sprinting or carrying something very heavy, is supported
through partially anaerobic pathways. There are very few, if any, activities that are supported through exclusively anaerobic pathways and those can only be sustained for a few seconds. Because exercise is
not usually exclusively aerobic or anaerobic, we see both muscle fiber types contributing to most types of muscle function.  Historically, it was thought that ATP production in skeletal muscle was clearly
delineated into either purely aerobic activities or purely anaerobic activities, and that the product of anaerobic respiration was principally lactic acid. Lactic acid was consid- ered to be a harmful waste product
that must be removed from the body. However, it is now widely recognized that anaerobic respiration ultimately gives rise to lactic acid’s alternate chemical form, lactate. Moreover, it is now known that
lactate is a critical metabolic intermediate that is formed and utilized continuously even under fully aerobic conditions. Lactate is produced by skeletal muscle cells at all times, but particularly during exercise,
and is  subsequently broken down (70–75%) or used to make new glucose (30–35%). Thus, the aerobic and anaerobic mechanisms of ATP production are linked through lactate.

Aerobic respiration is much more efficient than anaerobic respiration, but takes several minutes. With aerobic respiration pathways, the breakdown of a single glucose molecule produces approximately 18
times more ATP than that through anaerobic respiration pathways. Additionally, aerobic respiration is more flexible than anaerobic respiration because of the ability to break down lipids and amino acids to
form ATP, as noted earlier.  Anaerobic respiration produces far less ATP than aerobic res- piration, but can produce ATP in a matter of a few seconds instead of a few minutes like aerobic respiration. However,
ATP production rate by anaerobic respiration is too low to maintain activities for more than a few minutes.  Because muscle cells cannot store ATP, how do they generate enough ATP at a rate to keep pace
with their high-energy demand? They store a different high-energy molecule called creatine phos- phate. Creatine phosphate provides a means of storing energy that can be rapidly used to help maintain
adequate ATP in contracting muscle fibers. During periods of rest, as excess ATP is produced, the excess ATP is used to synthesize creatine phosphate. During exercise, especially at the onset of exercise, the
small ATP reserve is quickly depleted. Creatine phosphate is then broken down to directly synthe- size ATP. Some of this ATP is immediately used, and some is used to restore ATP reserves. Figure 7.12
summarizes how aerobic and anaerobic respiration, lactic acid fermentation, and creatine phosphate production interact to produce a continuous supply of ATP.

When a muscle cell is working too strenuously for ATP stores and creatine phosphate to be able to provide enough ATP, anaerobic respiration predominates. Typically, the type II fibers are the primary
anaerobic fibers. The type II fibers break down glucose into the intermediate, lactate, which can be shuttled to adjacent type I fibers to make ATP, or secreted into the blood for uptake by other tissues such as
the liver to make new glucose. Thus, we see that in skeletal muscle, the type II fiber (anaerobic) pathways and the type I fiber (aerobic) pathways are not mutually exclusive. Rather, they work together, with
lactate being the product of the type II fiber pathways that then serves as the starting point of the type I fiber pathways.

Ultimately, if the use of ATP is greater than the production of ATP, the ATP:ADP ratio decreases, which interferes with the func- tioning of all of the major ATP-dependent enzymes in the muscle fibers. The
ATP-dependent enzymes include the myosin head, the sarcoplasmic reticulum Ca2+ re-uptake pump, and the Na+/K+ pump for the resting membrane potential maintenance, all of which are required for proper
muscle functioning. If the ATP:ADP ratio declines, an enzyme transfers one phosphate from one ADP to another ADP, generating one ATP and one AMP (adenosine mono- phosphate). The presence of AMP
triggers a switch from anaerobic respiration to aerobic respiration of blood glucose and fatty acids. If this switch were not to occur, the muscles could not maintain their activity and could ultimately fail (see
“Fatigue” in the next section). Figure 7.12 summarizes how aerobic and anaerobic respiration and creatine phosphate production interact to keep the muscles supplied with the ATP they need.

After intense exercise, the respiratory rate and volume remain elevated for a time, even though the muscles are no longer actively contracting. This increased respiratory activity provides the O2 to pay back
the oxygen deficit. The recovery oxygen consumption is the amount of O2 needed in chemical reactions that occur to (1) convert lactate to glucose, (2) replenish the depleted ATP and creatine phosphate stores
in muscle fibers, and (3) replenish O2 stores in the lungs, blood, and muscles. After the lactate produced by anaerobic respiration is converted to glucose and creatine phosphate levels are restored, respiration
rate returns to normal.

The magnitude of the oxygen deficit depends on the intensity of the exercise, the length of time it was sustained, and the physical condition of the individual. The metabolic capacity of an individual in poor
physical condition is much lower than that of a well-trained athlete. With exercise and training, a person’s ability to carry out both aerobic and anaerobic activities is enhanced.

Fatigue

Fatigue is a temporary state of reduced work capacity. Without fatigue, muscle fibers would be worked to the point of structural dam- age to them and their supportive tissues. Historically it was thought that
buildup of lactic acid and the corresponding drop in pH (acidosis) was the major cause of fatigue. However, it is now established that there are multiple mechanisms underlying muscular fatigue.

These mechanisms include:

1. Acidosis and ATP depletion due to either an increased ATP consumption or a decreased ATP production
2. Oxidative stress, which is characterized by the buildup of excess reactive oxygen species (ROS; free radicals)
3. Local inflammatory reactions

Acidosis and ATP Depletion

Anaerobic respiration results in breakdown of glucose to lactate and protons, accounting for lowered pH. Lowered pH has several cellular effects, including decreased effectiveness of Ca2+ on actin
and overall less Ca2+ release from the sarcoplasmic reticulum. Lactic acidosis can also result when liver dysfunction results in reduced clearance of lactate (such as using it to produce glucose, for example).
Usually, increased lactate levels are due to increased anaerobic respiration production of ATP when aerobic respiration production of ATP is reduced. Increases in lactate are also seen in patients with
mitochondrial disorders and chronic obstructive pul- monary disease (COPD).
However, to what extent ATP reductions are responsible for muscular fatigue is still not clear. Recent studies have demonstrated that cytoplasmic ATP levels stay relatively constant even in the face of
decreasing muscle force production. But decreased ATP does cause fatigue. More specifically, it is the localized decreases in ATP levels or those associated with specific transport systems that are correlated
with muscle fatigue.
Oxidative Stress
During intense exercise, increases in ROS production cause the breakdown of proteins, lipids, or nucleic acids. In addition, ROS trigger an immune system chemical called interleukin (IL)-6. IL-6 is a
mediator of inflammation, which is the most likely cause of muscle soreness.
Inflammation
In addition to the stimulation of IL-6 by ROS, which causes inflammation, the immune system is directly activated by exercise. T lymphocytes, a type of white blood cell, migrate into heavily worked
muscles. The presence of immune system intermediates increases the perception of pain, which most likely serves as a signal to protect those tissues from further damage.
An example of muscle fatigue occurs when a runner col- lapses on the track and must be helped off. The runner’s muscle can no longer function regardless of how determined the run- ner is. Under conditions
of extreme muscular fatigue, muscle may become incapable of either contracting or relaxing. This condition, called physiological contracture, occurs when there is too little ATP to bind to myosin
myofilaments. Because bind- ing of ATP to the myosin heads is necessary for cross-bridge release between the actin and myosin, the cross-bridges between the actin and myosin myofilaments cannot be
broken, and the muscle cannot relax.
The most common type of fatigue, psychological fatigue, involves the central nervous system rather than the muscles them- selves. The muscles are still capable of contracting, but the individ- ual
“perceives” that continued muscle contraction is impossible. A determined burst of activity in a tired runner in response to pressure from a competitor is an example of how psychological fatigue can be
overcome.
Although fatigue reduces power output, the overall benefit is that it prevents complete exhaustion of ATP reserves, which could lead to severe damage of the muscle fibers.
 
 
Effect of Fiber Type on Activity Level
The white meat of a chicken’s breast is composed mainly of fast- twitch fibers. The muscles are adapted to contract rapidly for a short time but fatigue quickly. Chickens normally do not fly long distances.
They spend most of their time walking. Ducks, on the other hand, fly for much longer periods and over greater distances. The red, or dark, meat of a chicken’s leg or a duck’s breast is com- posed of slow-
twitch fibers. The darker appearance is due partly to a richer blood supply and partly to the presence of myoglobin, which stores oxygen temporarily. Myoglobin can continue to release oxygen in a muscle
even when a sustained contraction has interrupted the continuous flow of blood.
Humans exhibit no clear separation of slow-twitch and fast- twitch muscle fibers in individual muscles. Most muscles have both types of fibers, although the number of each type varies in a given muscle. The
large postural muscles contain more slow-twitch fibers, whereas muscles of the upper limb contain more fast-twitch fibers.
Average, healthy, active adults have roughly equal numbers of slow- and fast-twitch fibers in their muscles and over three times as many type IIa as type IIb fibers. In fact, athletes who are able to perform a
variety of anaerobic and aerobic exercises tend to have a balanced mixture of fast-twitch and slow-twitch muscle fibers. However, a world-class sprinter may have over 80% type II fibers, with type IIa
slightly predominating, whereas a world-class endur- ance athlete may have 95% type I fibers.
The ratio of muscle fiber types in a person’s body apparently has a large hereditary component but can also be considerably influ- enced by training. Exercise increases the blood supply to muscles, the
number of mitochondria per muscle fiber, and the number of myofibrils and myofilaments, thus causing muscle fibers to enlarge, or hypertrophy (hı-per′tr̄-f̄). With weight training, type IIb myosin
myofilaments can be replaced by type IIa myosin myofilaments as muscles enlarge. Muscle nuclei quit expressing type IIb genes and begin expressing type IIa genes, which are more resistant to fatigue. If the
exercise stops, the type IIa genes turn off, and the type IIb genes turn back on. Vigorous exercise programs can cause a limited number of type I myofilaments to be replaced by type IIa myofilaments.
The number of cells in a skeletal muscle remains somewhat con- stant following birth. Enlargement of muscles after birth is primarily the result of an increase in the size of the existing muscle fibers. As
people age, the number of muscle fibers actually decreases. However, there are undifferentiated cells just below the endomysium called satellite cells. When stimulated, satellite cells can differentiate and
develop into a limited number of new, functional muscle fibers. These cells are stimulated by the destruction of existing muscle fibers, such as by injury or disease, or during intensive strength training.
 
Types of Muscle Contractions
 
Muscle contractions are classified as either isometric or isotonic. In isometric (equal distance) contractions, the length of the muscle does not change, but the amount of tension increases during the
contraction process. Isometric contractions are responsible for the constant length of the body’s postural muscles, such as the muscles of the back. On the other hand, in isotonic (equal tension) contractions,
the amount of tension produced by the muscle is constant during contraction, but the length of the muscle decreases. Movements of the arms or fingers are predominantly isotonic
contractions. Most muscle contractions are a combination of iso- metric and isotonic contractions in which the muscles shorten and the degree of tension increases.
Smooth muscle cells are small and spindle-shaped, usually with one nucleus per cell (table 7.2). They contain less actin and myosin than do skeletal muscle cells, and the myofilaments are not organized into
sarcomeres. As a result, smooth muscle cells are not striated. Smooth muscle cells contract more slowly than skeletal muscle cells when stimulated by neurotransmitters from the nervous system and do not
develop an oxygen deficit. The rest- ing membrane potential of some smooth muscle cells fluctuates between slow depolarization and repolarization phases. As a result, smooth muscle cells can periodically
and spontaneously generate action potentials that cause the smooth muscle cells to contract. The resulting periodic spontaneous contraction of smooth muscle is called autorhythmicity. Smooth muscle is
under involuntary control, whereas skeletal muscle is under voluntary motor control. Some hormones, such as those that regulate the digestive system, can stimulate smooth muscle to contract.
Smooth muscle cells are organized to form layers. Most of those cells have gap junctions, specialized cell-to-cell contacts (see chapter 4), that allow action potentials to spread to all the smooth muscle cells in
a tissue. Thus, all the smooth muscle cells tend to function as a unit and contract at the same time.
Cardiac muscle shares some characteristics with both smooth and skeletal muscle (table 7.2). Cardiac muscle cells are long, stri- ated, and branching, with usually only one nucleus per cell. The actin and
myosin myofilaments are organized into sarcomeres, but the distribution of myofilaments is not as uniform as in skeletal muscle. As a result, cardiac muscle cells are striated, but not as distinctly striated as
skeletal muscle. When stimulated by neu- rotransmitters, the rate of cardiac muscle contraction is between
Concentric (kon-sen′ trik) contractions are isotonic contrac- tions in which muscle tension increases as the muscle shortens. Many common movements are produced by concentric muscle con- tractions.
Eccentric (ek-sen′trik) contractions are isotonic contrac- tions in which tension is maintained in a muscle, but the opposing resistance causes the muscle to lengthen. Eccentric contractions are used when a
person slowly lowers a heavy weight. Substantial force is produced in muscles during eccentric contractions, and muscles can be injured during repetitive eccentric contractions, as some- times occurs in the
hamstring muscles when a person runs downhill.
 
Muscle Tone
Muscle tone is the constant tension produced by body muscles over long periods of time. Muscle tone is responsible for keeping the back and legs straight, the head in an upright position, and the abdomen
from bulging. Muscle tone depends on a small percent- age of all the motor units in a muscle being stimulated at any point in time, causing their muscle fibers to contract tetanically and out of phase with one
another.