Puʻuwai hao kila.

Heart of steel.

Fearless.

‘Ōlelo No‘eau, compiled by Mary Kawena Pukui, #2766

Introduction

Chapter 10 investigates the structure and function of muscle tissue, expanding upon the basic introduction to muscle tissue seen in Chapter 4. The muscular system allows both voluntary and involuntary movement, responsible for both overall voluntary body movement and also involuntary movements within organ systems, such as contractions of the heart in the cardiovascular system and peristaltic waves in the visceral organs of the digestive system. Because muscle tissue is intimately related to the skeletal system, we will expand upon the structure and function of muscle tissue that we previously discussed in the skeletal system chapter. This chapter will begin with a general overview of all muscle tissue types, comparing and contrasting basic location, structure, and function. This chapter ends with a discussion of muscle tissue physiology, the effect of exercise on muscle tissue, and aging.

10.1 Muscle Tissue Overview

Chapter 4, Tissues, introduced the three major types of muscle cells: smooth, cardiac, and skeletal. Muscle tissue comprises over six hundred skeletal muscles, in addition to cardiac and smooth muscles. The primary focus of this chapter will be on skeletal muscles as smooth and cardiac muscles will be discussed in later chapters.

Development of Muscle Tissue

Most muscle tissue develops from a common cell called a myoblast, a muscle-forming stem cell, that arises from embryonic mesoderm. Myoblasts migrate to various regions of the body, eventually differentiating into one of the three types of muscle tissue: smooth, cardiac, or skeletal muscle tissue. Uninucleate (one nucleus) cardiac and smooth muscle cells originate from myoblasts that do not fuse, while multinucleated (many nuclei) muscle fiber forms from hundreds of myoblasts that fuse during development, eventually becoming a mature muscle fiber.

Figure 10.1: Types of muscle tissue in the body and their locations Left to right: Smooth (non-striated) muscles, cardiac or heart muscles, and skeletal muscles.

Table 10.1: Muscle Type – Structure, Function, Location

Figure 10.2 The Three Types of Muscle Tissue The body contains three types of muscle tissue: (a) skeletal muscle, (b) smooth muscle, and (c) cardiac muscle. (Micrographs provided by the Regents of University of Michigan Medical School © 2012)

Skeletal Muscle

Skeletal muscle is composed of muscle fibers (muscle cells), which can also be referred to as myocytes or myofibers. The word fiber (thread; string) refers to their elongated shape. Muscle organs can be composed of a small or large number of muscle fibers depending on their size and function in the body; most muscles are composed of thousands of muscle fibers. Due to the organization of the myofilaments (thread-like muscle proteins), skeletal muscles have obvious striations (stripes). These striations are visible with a light microscope under high magnification. Skeletal muscle tissue is considered voluntary (intentional), meaning when skeletal muscles contract, you want them to contract.

Cardiac Muscle

Cardiac muscle tissue exists only in one place: the heart. Myocytes of cardiac muscle tissue make up the bulk of the heart wall and are responsible for the contractions referred to as the heartbeat. Cardiac muscle is considered involuntary, meaning you do not have to remember to make your heart beat. Thank goodness! These cells are striated as skeletal muscle fiber is, however, they are branched, typically binucleate (two nuclei), and have intercalated disks. The intercalated disk is perhaps the cardiac myocytes’ most distinctive feature; it is composed of cell adhesion molecules holding the cardiac muscle cells together.

Smooth Muscle

Mature smooth muscle fibers are flat, uninucleated spindle-shaped cells that are predominantly found in the walls of hollow organs, airways, glands, blood vessels, skin, and eyes. Smooth muscle is involuntary, meaning it is not under voluntary control as skeletal muscles are. These cells are also nonstriated due to lacking the myofilament organization that causes striations in the other types of muscle tissue. Because these tissues are associated with the contraction of organs, smooth muscles are part of the visceral (organ) motor system.

Muscle Tissue Function

Muscle tissue performs at least four primary functions within the human body:

1. Producing body movements
2. Stabilizing body positions
3. Storing and moving substances within the body
4. Generating heat

Characteristics of Muscle Tissue

Muscle cells are excitable which means the plasma membranes can depolarize in response to stimuli. When one area of the membrane depolarizes, an electrical wave called an action potential moves along the entire length of the muscle cell, resulting in muscle contraction. Muscle tissues are also extensible (stretchable) and can recoil (return to their original shape). The word describing both the extensibility and recoiling properties is elasticity. The next several pages will describe in detail skeletal muscle anatomy and how a nervous signal results in muscle cell depolarization, leading to an action potential and finally contraction and recoiling.

10.2 Skeletal Muscle Structure

Gross Anatomy

Each skeletal muscle is an organ that consists of various integrated tissues. These tissues include skeletal muscle fibers, blood vessels, nerve fibers, and connective tissue. Blood vessels supply nutrients and remove wastes. Skeletal muscle is innervated (contains nervous tissue) which signals the muscle fibers to contract. Fascia is the most superficial connective tissue of skeletal muscles and anchors muscles and other organs of the body. Beneath this, each skeletal muscle has three layers of connective tissues that bind the muscle cells together. The outermost layer wrapping the entire muscle organ is the epimysium (epi = on top, mys = muscle). The epimysium allows the muscle to contract and move powerfully while maintaining its structural integrity. It also separates adjacent muscles and other tissues and organs in the area, which allows the muscle to move independently. Inside skeletal muscles, muscle fibers are divided into bundles called fascicles. The connective tissue that separates fascicles is called perimysium (peri = around, mys = muscle). This fascicular organization allows the nervous system to trigger specific movements by activating a subset of muscle fibers or fascicles. Inside each fascicle are numerous muscle fibers encased in a thin connective tissue layer of collagen and reticular fibers called the endomysium (endo = within, mys = muscle). The endomysium contains the extracellular fluid and nutrients supplied by the blood to support the muscle fiber.

Figure 10.3 The Three Connective Tissue Layers Bundles of muscle fibers, called fascicles, are covered by the perimysium. Muscle fibers are covered by the endomysium. [OpenStax]

In skeletal muscles, the three connective tissue layers fuse at the ends of the muscle organ turning into a tendon or an aponeurosis. Tendons are rope-shaped connective tissues that tie (anchor) muscles to bone. An aponeurosis is a sheet-like (flat) connective tissue that attaches muscle to bone or another muscle. The broadsheet of connective tissue of the lower back anchoring the latissimus dorsi muscle is an example of an aponeurosis.

Microanatomy

Skeletal Muscle Fibers

Skeletal muscle fiber cells are distinct in several ways. These fibers can be quite large, with diameters up to 100 μm and lengths up to 30 cm (11.8 in)! The fact that they are multinucleated means they contain multiple nuclei which permits the large production of contractile, structural and enzymatic proteins needed for muscle contraction.

Stress Fibers	Motor Neuron Fibers	Ganglion Fibers

Figure 10.4: Non-Muscle Human Cell Fibers

Because muscle fibers are so unique in appearance and function, they have a unique terminology naming the cell parts. The plasma membrane of muscle fibers is called the sarcolemma (sarco = flesh, lemma = shell; peel), the cytoplasm is referred to as sarcoplasm (sarco = flesh, plasm = fluid), and the specialized smooth endoplasmic reticulum is called the sarcoplasmic reticulum (SR) (sarco = flesh, plasm = fluid, reticulum = network) (Figure 10.6). T tubules are extensions of the sarcolemma that invaginate deep into the muscle fiber and function to allow action potentials to reach the cell interior. Myofibrils (myo = muscle, fibril = small thread) are specialized contractile organelles found within muscle fibers. They are composed of three different types of proteins; contractile, regulatory, and structural. The contractile proteins generate force during muscle contraction and include myosin and actin. The regulatory proteins determine when a muscle contracts and relaxes and include troponin and tropomyosin. Structural proteins keep the thick and thin filaments in alignment and link the myofibrils to the sarcolemma.

Myosin, a contractile protein involved in motor function, is the major component of the thick filaments and is responsible for generating the force that will pull on cellular structures within the myofibril, resulting in shortening or muscle contraction. About 300 molecules of myosin are found on a single thick filament. Myosin can be compared to two golf clubs twisted together. The tails represent the shaft of the club and the myosin heads project off the tails (similar to golf club heads). The heads project outward toward the thin filaments. There are two binding sites on each myosin head, one for ATP, which will supply the energy needed for contraction, and one for actin.

Actin is the major component of the thin filaments and resembles a double-stranded lei or pearl necklace. Each “pearl” would represent a single actin molecule. On each actin molecule, there is a corresponding myosin-binding site where the myosin head will attach during contraction. Regulatory proteins, troponin, and tropomyosin are also part of the thin filament. When the muscle is in a relaxed position, tropomyosin strands cover the myosin-binding sites, preventing contraction. The troponin locks this tropomyosin strand in place. In the next section, you will learn how calcium ions play an important role in muscle contraction by binding to troponin, changing its shape, which moves the tropomyosin strand away from the myosin-binding site, allowing for attachment between actin and myosin.

Cultural Connection

Actin filament is like a double-stranded lei or pearl necklace.

Double stranded lei	Double stranded pearl necklaces

Figure 10.6 Muscle Fiber: A skeletal muscle fiber is surrounded by a plasma membrane called the sarcolemma, which houses sarcoplasm, the cytoplasm of muscle cells. A muscle fiber is composed of many fibrils, which give the cell its striated appearance. [OpenStax]

Sarcomere

The contractile unit of muscles is the sarcomere, a highly organized arrangement of the contractile proteins actin (thin filament), myosin (thick filament), and other support proteins. These units are linked end-to-end, creating a long thread-like structure called a myofibril. Myofibrils are attached to the sarcolemma at the ends of the muscle fiber. The striated appearance of skeletal muscle fibers is due to the alignment of the thick and thin filaments within adjacent myofibrils. As each sarcomere contracts, the entire myofibril contracts, and all myofibrils in a cell contracting simultaneously contracts the entire muscle fiber. Because myofibrils are very tiny in diameter, hundreds to thousands (each with thousands of sarcomeres) are inside each muscle fiber. Sarcomeres are flanked by Z-discs, to which actin myofilaments are anchored (Figure 10.7). Because actin forms strands that are thinner than the myosin, they are called thin filaments of the sarcomere. Likewise, because the myosin strands have more mass and are thicker, they are called thick filaments.

Sarcomeres are divided into various bands and zones depending on the area and contain thick filaments, thin filaments, or both. The darker middle part includes the entire length of the thick filaments referred to as the A band. The A band creates the darker striations seen in microscope pictures because the thick fibers bind more stain than the other fibers. The I band is lighter because it contains only thin filaments. Z discs pass through the center of each I band. Recall that the Z discs are the end of the sarcomere (Z is the letter at the end of the alphabet just as the Z discs represent the end of the sarcomere). The H zone is a narrow area in the center of each A band that contains thick, but no thin, filaments. The M line is the region in the center of the H zone that contains proteins that hold thick filaments together at the center of the sarcomere (M for the middle of the sarcomere).

The dense organization of thick and thin filaments, each built with protein building blocks, is the reason why meat is a great source of protein. Consuming adequate amounts of dietary protein is essential for building a healthy body, especially for youth who are growing and aging in order to preserve their muscle mass. Luckily, in Hawai’i, there is no shortage of delicious meat dishes. So, go ahead and enjoy a plate of kalua pork and laulau, but don’t forget to put some fruits and vegetables on that plate also!

Figure 10.7 The Sarcomere The sarcomere, the region from one Z-line to the next Z-line, is the functional unit of a skeletal muscle fiber. [OpenStax]

10.3 Muscle Fiber Contraction and Relaxation

Proteins embedded in the sarcolemma include channels, gates, and pumps. These proteins regulate the concentration of ions (namely Ca2+, Na+, K+, and Cl–) in and out of the cell (review Chapter 3). Ion channel proteins selectively allow particular ions to pass into or out of the cell by diffusion. There are specific channels for each ion (Na+ channels, K+ channels, etc). Gates are similar to channels with gates that open and close. Just like channels, ion gates only allow diffusion of specific ions (Na+ gates, K+ gates) but some will allow diffusion of more than one type of ion (Na+/K+ gates). Some gates open when they must bind a ligand (ligand-activated gate) or they might open in response to a change in electric charge (voltage-activated gate). Remember the process of diffusion describes the movement of materials from high to low concentration. Therefore, if more Na+ is outside the cell than inside, Na+ will diffuse through a channel or a gate (if it’s open) into the cell. Pumps, on the other hand, do the opposite. These membrane proteins concentrate ions in or out of the cell. The most common pump is the Na+/K+ pump which kicks out 3 Na+ while bringing in 2 K+ with each pumping cycle.

Because Na+/K+ pumps kick out three + charges while only pumping in two, the electrical charge difference (voltage) between the inside and outside of the membrane is usually around -60 to -90 mV. This is referred to as a cell’s resting membrane potential and results from Na+/K+ pumps and Na+ and K+ channels reaching an equilibrium. The resting membrane potential changes to an excited state when gates open and allow a massive influx or outflux of ions. Neurons and muscle cells use this change in membrane potentials to generate and relay electrical signals. In the case of muscle fibers, this results in muscle contraction.

Figure 10:8: Resting membrane Potential with ++ and — on either side of a membrane

Every skeletal muscle fiber is supplied by a motor neuron. A motor unit consists of one motor neuron and all the muscle fibers it innervates. One motor neuron branches into many endings, each of these endings connect to a skeletal muscle fiber. In this way, a single motor neuron may stimulate many skeletal muscle fibers to contract. In the body, the number of skeletal muscle fibers that are innervated by a single motor neuron can range from just a few to several hundred. A motor unit that innervates only four skeletal muscle fibers usually exists in muscles that require fine motor control, such as in muscles that control the eye. A single motor unit that innervates hundreds of skeletal muscle fibers typically exists in large, weight-bearing muscles that are responsible for exerting a lot of force without a lot of precision, like the muscles in the leg.

At the neuromuscular junction, the nerve fiber is able to transmit a signal to the muscle fiber by releasing ACh (and other substances), causing muscle contraction.

The action potential first comes from the brain, and through motor neurons it reaches the muscle fiber at the motor end plates. At the axon terminal, the energy from the action potential opens the voltage gated channels, after it is opened, Calcium (Ca2+) enters the axon terminal. In turn, vesicles will carry out the Acetylcholine out of the motor neuron into the synaptic cleft. It will diffuse across the synaptic cleft to bind to the ligand (chemical) gated channel receptors on the sarcolemma. This will cause a high amount of sodium to enter and activate action potential to be sent down the t-tubules and open the Ca2+ channels in the sarcoplasmic reticulum. The Ca2+ released will be used in muscle contraction.

Figure 10.9: Parts of a Motor Unit: Initiation of voluntary skeletal muscle movement begins in the brain.

Where the neuron meets up with the skeletal muscle fiber is called the neuromuscular junction (NMJ). The specific site of the skeletal muscle fiber that participates in the NMJ is called a motor endplate. Embedded in the sarcolemma of the motor endplate are ligand-activated Na+/K+ gates. These gated channels open when a nervous signal reaches the NMJ, causing the release of the neurotransmitter acetylcholine (ACh). When a neuron releases ACh, it diffuses across space in between the neuron and muscle fiber known as the synaptic cleft. ACh (the ligand) binds gated Na+/K+ channels (the receptors) that are located within the motor endplate. When ACh binds these gated receptors, the gated channel opens, allowing the diffusion of Na+ into the cell and K+ out of the cell. Remember that Na+/K+ pumps are always working and kick 3Na+ out of the cell for every 2 K+ it brings in. Because of the 3-2 difference, there are a lot more Na+ out of the cell than K+ in. That also means at rest there is a big difference in positive charges across the sarcolemma (the cell membrane is polarized). When the motor endplate gated Na+/K+ channels open, more Na+ rushes into the cell than K+ out, this causes the muscle fiber sarcolemma to depolarize around the motor endplate. After ACh binds to the ACh receptors on the sodium channels, it is quickly broken down by the enzyme acetylcholinesterase. ACh can also be brought back into the neuron in a process called reuptake and some ACh will diffuse away from the synaptic cleft. These three mechanisms ensure that ACh doesn’t continually depolarize the muscle fiber.

Figure 10:10: Contraction of a Muscle Fiber: A cross-bridge forms between actin and the myosin heads triggering contraction. As long as Ca++ ions remain in the sarcoplasm to bind to troponin, and as long as ATP is available, the muscle fiber will continue to shorten.

Figure 10.11: Relaxation of a Muscle Fiber Ca++ ions are pumped back into the SR, which causes the tropomyosin to reshield the binding sites on the actin strands. A muscle may also stop contracting when it runs out of ATP and becomes fatigued.

The Big Picture: Going through the process of skeletal muscle contraction can be complex. Typically these events are broken up into four groups of steps:

1) Events at the Neuromuscular junction

2) Muscle fiber excitation

3) Excitation-Contraction Coupling

4) Contraction Cycle

Events at the Neuromuscular Junction

1. Action potentials in neurons cause the release of ACh molecules into the synaptic cleft.
2. ACh diffuses across the NMJ and binds gated-Na+/K+ channels
3. gated-Na+/K+ channels open, causing the diffusion of Na+ into the cell and K+ out.
4. The diffusion of Na+ into the cell depolarizes the membrane of the muscle fiber in and around the motor endplate.

[See Figure 10.11 above]

Excitation-Contraction Coupling

The Excitation Contraction Coupling is a sequence of steps in which an action potential moves along the sarcolemma, down the T-tubules, and into the interior of the muscle tissue, triggering muscle contraction. The sudden influx of sodium ions around the motor endplate initiates this sequence of events. Firstly, as the sarcolemma depolarizes the membrane around the motor endplate, this change in voltage stimulates voltage-gated sodium channels to open. Sodium ions then diffuse into the cell through this gated channel, depolarizing the area of the cell just outside of the motor endplate. As more Na+ diffuses in, this stimulates other voltage-activated Na+ gated channels to open further from the motor endplate. This chain reaction continues as newly entered sodium ions continue to change the sarcolemma membrane potential. Much like a moving wave, depolarization spreads along the length of the sarcolemma. This moving wave of depolarization is called an action potential. The action potential continues to propagate down the sarcolemma since voltage-activated Na+ gated channels are evenly dispersed so that if one opens nearby gates will also open. The sarcolemma invaginates (folds inwards) creating T-tubules. These T-tubules allow the action potential to move deep into the muscle fiber in addition to moving the length of the cell. As action potential enters the T-Tubules it continues to open voltage-activated Na+ gated channels. Eventually, the action potential causes the opening of voltage-activated calcium gates of the sarcoplasmic reticulum. When these gates open, calcium ions diffuse out of the SR and into the sarcoplasm. [See Figure 10.11 above]

Before we get into the details of how Ca2+ induces muscle contraction, it is important to note that eventually the voltage-gated sodium channels close and a process called repolarization occurs. When sodium ions rush into the cell, the membrane potential reaches +30 mV, and other voltage-gated channels begin to open in the membrane. These channels are specific for the potassium ion. A concentration gradient acts on K+, as well, and K+ ions start to leave the muscle fibers, taking a positive charge with it, the membrane potential begins to move back toward its resting voltage. The negatively charged membrane potential eventually returns, resulting in the end of the action potential.

Contraction and Relaxation of Skeletal Muscle Fibers

The Sliding Filament Model of Contraction

Before muscle contraction can begin, the sarcoplasmic reticulum releases Ca2+ into the sarcoplasm. The Ca2+ binds to troponin, changes its shape, and moves the tropomyosin strands out of the way, exposing the myosin-binding sites. The contraction cycle can now begin.

Muscle contraction, or shortening of the muscle, occurs at the level of the sarcomere (see Figure 10.12). Recall the zone of overlap, the region where thick and thin filaments overlap resulting in a dense appearance, as there is little space between the filaments. This zone where thin and thick filaments overlap is very important to muscle contraction, as it is the site where filament movement starts. Contraction occurs because the myosin heads attach to actin and pull the thin filaments in towards the M line, resulting in more overlap and a shortening of the sarcomere. Since a myofibril is composed of many sarcomeres, myofibrils collectively contract. A muscle fiber is composed of many myofibrils, therefore the entire muscle fiber and muscle contract as the sarcomeres contract.

For thin filaments to continue to slide past thick filaments during muscle contraction, myosin heads must pull actin at the binding sites, detach, re-cock, attach to more binding sites, pull, detach, re-cock, etc. This repeated movement is known as the contraction cycle. This motion of the myosin heads is similar to the oars when an individual paddles a canoe: The paddle of the oars (the myosin heads) pull, are lifted from the water (detach), repositioned (re-cocked), and then immersed again to pull (Figure 10.12). Each cycle requires energy, and the action of the myosin heads in the sarcomeres repetitively pulling on the thin filaments also requires energy, which is provided by ATP. The four steps of the contraction cycle are presented below.

1. ATP hydrolysis. Myosin heads include an ATP-binding site. This location functions as an ATP-ase (an enzyme that helps break apart ATP), hydrolyzing ATP into ADP (adenosine diphosphate) and a phosphate group. The energy released from this reaction is then stored within the myosin head to be used in later phases of the contraction cycle. The myosin head is now “cocked”.
2. Attachment of myosin to actin. The myosin head can now attach to the myosin-binding site on actin. Once attachment occurs, this is referred to as a cross-bridge formation.
3. Power stroke. Once the cross-bridge has been formed, the myosin head utilizes the energy derived from the hydrolysis of ATP and pulls the actin filament towards the center of the sarcomere. This is referred to as the power stroke.
4. Detachment of myosin from actin. Once the power stroke is complete, the myosin head remains attached to the binding site. Once another molecule of ATP binds to the myosin head it can detach from actin. As long as ATP is available, it readily attaches to myosin, the contraction cycle can recur, and muscle contraction can continue. In the absence of ATP, the myosin head will not detach from the binding site.

Muscle contraction is sustained by ATP. As long as Ca2+ remains in the sarcoplasm to bind to troponin, which keeps the actin-binding sites “unshielded, and as long as ATP is available to drive the contraction cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit.

Figure 10.12 Skeletal Muscle Contraction — (a) The active site on actin is exposed as calcium binds to troponin. (b) The myosin head is attracted to actin, and myosin binds actin at its actin-binding site, forming the cross-bridge. (c) During the power stroke, the phosphate generated in the previous contraction cycle is released. This results in the myosin head pivoting toward the center of the sarcomere, after which the attached ADP and phosphate group are released. (d) A new molecule of ATP attaches to the myosin head, causing the cross-bridge to detach. (e) The myosin head hydrolyzes ATP to ADP and phosphate, which returns the myosin to the cocked position. [OpenStax]

Note that each thick filament of roughly 300 myosin molecules has multiple myosin heads, and many cross-bridges form and break continuously during muscle contraction. Multiply this by all of the sarcomeres in one myofibril, all the myofibrils in one muscle fiber, and all of the muscle fibers in one skeletal muscle, and you can understand why so much energy (ATP) is needed to keep skeletal muscles working. In fact, it is the loss of ATP that results in the rigor mortis observed soon after someone dies. With no further ATP production possible, there is no ATP available for myosin heads to detach from the actin-binding sites, so the cross-bridges stay in place, causing rigidity in the skeletal muscles.

Relaxing skeletal muscle fibers, and ultimately, the skeletal muscle begins with the motor neuron which stops releasing its chemical signal, ACh, into the synapse at the NMJ. The muscle fiber will repolarize, which closes the gates in the SR where Ca2+ was being released. ATP-driven pumps will move Ca2+ out of the sarcoplasm back into the SR. This results in the “reshielding” of the actin-binding sites on the thin filaments. Without the ability to form cross-bridges between the thin and thick filaments, the muscle fiber loses its tension and relaxes.

10.4 Muscle Metabolism and Energy Systems

As you just learned ATP supplies the energy for muscle contraction to take place and the demand is high. Muscle contraction does not occur without sufficient amounts of ATP. The amount of ATP stored in muscle is very low, only sufficient to power a few second’s worth of contractions. As it is broken down, ATP must therefore be regenerated and replaced quickly to allow for sustained contraction. There are three mechanisms by which ATP can be regenerated: creatine phosphate metabolism, anaerobic glycolysis, and aerobic respiration.

Creatine phosphate is a molecule that can store energy in its phosphate bonds. In a resting muscle, excess ATP transfers its energy to creatine, producing ADP and creatine phosphate. This acts as an energy reserve that can be used to quickly create more ATP. When the muscle starts to contract and needs energy, creatine phosphate transfers its phosphate back to ADP to form ATP and creatine. This reaction is catalyzed by the enzyme creatine kinase and occurs very quickly; thus, creatine phosphate-derived ATP powers the first few seconds of muscle contraction. However, creatine phosphate can only provide approximately 15 seconds’ worth of energy, at which point another energy source has to be used (Figure 10.13).

Anaerobic glycolysis is a non-oxygen-dependent process that breaks down glucose (sugar) to produce ATP; however, glycolysis cannot generate ATP as quickly as creatine phosphate. As the ATP produced by creatine phosphate is depleted, muscles turn to glycolysis as an ATP source. Thus, the switch to glycolysis results in a slower rate of ATP availability to the muscle. The sugar used in glycolysis can be provided by blood glucose or by metabolizing glycogen that is stored in the muscle. The breakdown of one glucose molecule produces two ATP and two molecules of pyruvic acid, which can be used in aerobic respiration or when oxygen levels are low, converted to lactic acid (Figure 10.13b). Glycolysis itself cannot be sustained for very long (approximately 1 minute of muscle activity), but it is useful in facilitating short bursts of high-intensity output. This is because glycolysis does not utilize glucose very efficiently.

Aerobic respiration is the breakdown of glucose or other nutrients in the presence of oxygen (O2) to produce carbon dioxide, water, and ATP. Approximately 95 percent of the ATP required for resting or moderately active muscles is provided by aerobic respiration, which takes place in mitochondria. The substrates for aerobic respiration include glucose circulating in the bloodstream, pyruvic acid, and fatty acids. Aerobic respiration is much more efficient than anaerobic glycolysis, producing approximately 36 ATPs per molecule of glucose versus four from glycolysis. However, aerobic respiration cannot be sustained without a steady supply of O2 to the skeletal muscle and is much slower (Figure 10.13c). To compensate, muscles store small amounts of excess oxygen in proteins called myoglobin, allowing for more efficient muscle contractions and less fatigue. Aerobic training also increases the efficiency of the circulatory system so that O2 can be supplied to the muscles for longer periods.

Figure 10.13 Muscle Metabolism (a) Some ATP is stored in a resting muscle. As contraction starts, it is used up in seconds. More ATP is generated from creatine phosphate for about 15 seconds. (b) Each glucose molecule produces two ATP and two molecules of pyruvic acid, which can be used in aerobic respiration or converted to lactic acid. If oxygen is not available, pyruvic acid is converted to lactic acid, which may contribute to muscle fatigue. This occurs during strenuous exercise when high amounts of energy are needed but oxygen cannot be sufficiently delivered to muscle. (c) Aerobic respiration is the breakdown of glucose in the presence of oxygen (O2) to produce carbon dioxide, water, and ATP. Approximately 95 percent of the ATP required for resting or moderately active muscles is provided by aerobic respiration, which takes place in mitochondria. [OpenStax]

Muscle Fatigue

Muscle fatigue occurs when a muscle can no longer contract in response to signals from the nervous system. The exact causes of muscle fatigue are not fully known, although certain factors have been correlated with the decreased muscle contraction that occurs during fatigue. ATP is needed for normal muscle contraction, and as ATP reserves are reduced, muscle function may decline. This may be more of a factor in brief, intense muscle output rather than sustained, lower intensity efforts. Lactic acid is a strong acid and as discussed in Chapter 2, strong acids tend to generate positively charged hydrogen ions (H+). If the breakdown of glucose results in a significant amount of lactic acid, the result may be a buildup of H+, which may lower intracellular pH, affecting enzyme and protein activity. Imbalances in Na+ and K+ levels as a result of membrane depolarization may disrupt Ca2+ flow out of the SR. Long periods of sustained exercise may damage the SR and the sarcolemma, resulting in impaired Ca2+ regulation.

Intense muscle activity results in an oxygen debt, which is the amount of oxygen needed to compensate for ATP produced without oxygen during muscle contraction. Oxygen is required to restore ATP and creatine phosphate levels, convert lactic acid to pyruvic acid, and, in the liver, to convert lactic acid into glucose or glycogen. Other systems used during exercise also require oxygen, and all of these combined processes result in the increased breathing rate that occurs after exercise. Until the oxygen debt has been met, oxygen intake is elevated, even after exercise has stopped.

10.5 Control of Muscle Tension

Types of Contractions

In order for a skeletal muscle to move an object, referred to as a load, the sarcomeres in the muscle fibers must shorten and contract. The force generated by the contraction of the muscle is called muscle tension. You may be familiar with muscle tension if you have seen how skeletal muscles contract when someone lifts weights or moves a heavy object. However, muscle tension can also be generated when a muscle is contracting against a load that does not move, such as if someone is trying to hold a yoga pose. Whether the load moves and whether the muscle changes in length determines whether either of two main types of skeletal muscle contraction is occurring. These types are isotonic contractions and isometric contractions.

In isotonic contractions, the length of a muscle changes as it tries to maintain constant tension as it moves a load. There are two subtypes of isotonic contractions: concentric and eccentric. A concentric contraction occurs when the contractile filaments in the skeletal muscle fiber shorten to move a load. An example of this is if you take a dumbbell or hand weight and curl it upward by contracting your biceps brachii muscle. During this movement, your biceps brachii will shorten as its muscle fibers and sarcomeres shorten. If you were to look at your arm during this type of contraction, you would see a bulge in the muscle due to the shortening pushing the bicep’s mass outward. In contrast, an eccentric contraction occurs when the muscle generates force as the muscle lengthens. If you take the weight in the previous example and lower it in a slow and controlled manner, you are performing an eccentric contraction. When you perform complex movements such as jumping and throwing, your muscles use both concentric and eccentric contractions to generate those movements.

An isometric contraction occurs when a muscle produces tension but without changing its length. Isometric contractions still involve muscle tension, but because the load is greater than the force produced by the muscle, there is no shortening or lengthening of the sarcomere. For example, if you attempt to lift a hand weight that is too heavy, you will still be trying to contract your biceps brachii and activate sarcomere shortening. While trying to lift that extremely heavy load, you will increase your muscle tension, but no overall change in your muscle length will occur. In your everyday life, isometric contractions are active in maintaining posture and maintaining bone and joint stability. You may be familiar with an example of an isometric contraction in physical fitness called a plank position. Another example of isometric contractions are the contractions holding your head in an upright position. These isometric contractions occur not because the muscles cannot move your head, but because the goal is to stabilize your head and keep it in place without it flopping forward, backward, or to the sides. Most actions of the body are the result of a combination of isotonic and isometric contractions working together to produce a wide range of complex movements.

Figure 10:14: Types of Muscle Contractions (concentric, eccentric, isometric)

Types of muscle contractions During isotonic contractions, muscle length changes to move a load. During isometric contractions, muscle length does not change because the load exceeds the tension the muscle can generate.

The Frequency of Motor Neuron Stimulation

Muscle tension can be recorded on a machine and the resulting graph is called a myogram. A myogram is a recording of contractile activity produced by a muscle and the lines on the myogram are called tracings. A single action potential from a motor neuron will produce a single contraction in the muscle fibers of its motor unit. This isolated contraction is called a twitch. A twitch can last for a few milliseconds or 100 milliseconds, depending on the muscle type. Myograms can measure the tension produced by a single twitch. Each twitch undergoes three phases. The first phase is the latent period, during which the action potential is being propagated along the sarcolemma and Ca2+ ions are released from the SR. This is the phase during which excitation and contraction are being coupled but contraction has yet to occur. The contraction phase occurs next. The Ca2+ ions in the sarcoplasm have bound to troponin, tropomyosin has shifted away from actin-binding sites, cross-bridges formed, and sarcomeres are actively shortening to the point of peak tension. The last phase is the relaxation phase when tension decreases as contraction stops. Ca2+ ions are pumped out of the sarcoplasm into the SR, contraction stops, returning the muscle fibers to their resting state.

Figure 10.15 A Myogram of a Muscle Twitch (OpenStax)

A single muscle twitch has a latent period, a contraction phase when tension increases, and a relaxation phase when tension decreases. During the latent period, action potentials are being propagated along the sarcolemma. During the contraction phase, Ca2+ ions released into the sarcoplasm cause sarcomeres to shorten. During the relaxation phase, tension decreases as Ca2+ ions are pumped out of the sarcoplasm and contraction cycling stops.

Although you can experience a muscle “twitch,” a single twitch does not produce any significant muscle activity in your body. In order to move a load, you need a series of action potentials to produce a muscle contraction that can produce work. Normal muscle contractions can be modified by input from the nervous system to produce varying amounts of force as needed; this is called a graded muscle response. The frequency of action potentials (nerve impulses) from a motor neuron and the number of motor neurons transmitting action potentials both affect the tension produced in skeletal muscle.

The rate at which a motor neuron fires action potentials affects the tension produced in a muscle. If muscle fibers are stimulated while a previous twitch is still occurring, the second twitch will be stronger. This stronger response is called wave summation because the excitation-contraction coupling effects of successive motor neuron signaling are summed, or added together (Figure 10.16a). At the molecular level, summation occurs because the second stimulus triggers the release of more Ca2+ ions, which can activate additional sarcomeres while the muscle is still contracting from the first stimulus. Summation results in greater tension and contraction of the motor unit.

Figure 10.16 Wave Summation and Tetanus (a) The excitation-contraction coupling effects of successive motor neuron signaling are added together which is referred to as wave summation. The bottom of each wave, the end of the relaxation phase, represents the point of stimulus. (b) When the stimulus frequency is so high that the relaxation phase disappears completely, the contractions become continuous; this is called tetanus. (OpenStax)

If the frequency of motor neuron signaling increases, summation and subsequent muscle tension in the motor unit continues to rise until it reaches a peak point of maximum tension. The tension at this point is about three to four times greater than the tension of a single twitch, a state referred to as incomplete tetanus. During incomplete tetanus, the muscle alternates between quick cycles of contraction with short relaxation phases. If the stimulus frequency is so high that the relaxation phase disappears completely, contractions become sustained and continuous in a process called complete tetanus (Figure 10.16b).

During tetanus, the concentration of Ca2+ ions in the sarcoplasm allows virtually all of the sarcomeres to form cross-bridges and shorten, so that a contraction can continue uninterrupted (until the muscle fatigues and can no longer produce tension).

Motor Units and Muscle Tension

All of these skeletal muscle activities are under the control of the nervous system. Neural control regulates concentric, eccentric, and isometric contractions, muscle fiber recruitment, and muscle tone. A crucial aspect of the nervous system’s control of skeletal muscles is the role of motor units. Motor units were introduced earlier in the text, but we will now cover them in more detail.

Every skeletal muscle fiber must be innervated by the axon terminal of a motor neuron to contract. Each muscle fiber is innervated by only one motor neuron. The group of muscle fibers in a muscle innervated by a single motor neuron is called a motor unit. The size of a motor unit is variable depending on the muscle and its function in your body.

A small motor unit is an arrangement where a single motor neuron supplies a small number of muscle fibers in a muscle. Small motor units permit very fine motor control of the muscle. The best example in humans is the small motor units of the extraocular eye muscles that move the eyeballs. There are thousands of muscle fibers in each eye muscle, but each motor neuron innervating those muscles only controls about six muscle fibers. This allows for delicate and exquisite control of eye movements so that both eyes can quickly and accurately focus on the same object. Small motor units are also involved in many fine movements of the fingers and thumb of the hand, such as movements needed for grasping, texting, and playing musical instruments.

A large motor unit is an arrangement where a single motor neuron supplies a large number of muscle fibers in a muscle. Large motor units are concerned with simple, or “gross,” movements, such as powerfully extending the knee joint during a kick. The best example is the large motor units of the thigh muscles or back muscles, where a single motor neuron will supply thousands of muscle fibers in a muscle, as its axon splits into thousands of branches. Large motor units produce powerful movements but are less accurate and refined. For example, imagine trying to write your name by using your thigh muscles instead of your fingers and hand.

There is a wide range of motor units within many skeletal muscles, which gives the nervous system a wide range of control over the muscle. The small motor units in the muscle will have smaller, lower-threshold motor neurons that are more excitable, firing first to their skeletal muscle fibers, which also tend to be the smallest. Activation of these smaller motor units results in a relatively small degree of contractile strength (tension) generated in the muscle. As more strength is needed, larger motor units, with bigger, higher-threshold motor neurons are enlisted to activate larger muscle fibers. This increasing activation of motor units produces an increase in muscle contraction known as recruitment. As more motor units are recruited, the muscle contraction grows progressively stronger. In some muscles, the largest motor units may generate a contractile force of 50 times more than the smallest motor units in the muscle. This allows you to pick up a feather by using your biceps brachii muscle with minimal force, while a heavy textbook can be lifted by the same muscle by recruiting the largest motor units.

When necessary, the maximal number of motor units in a muscle can be recruited simultaneously, producing the maximum force of contraction for that muscle, but this cannot last for very long because of the energy requirements to sustain the contraction. To prevent complete muscle fatigue, motor units are generally not all simultaneously active. Instead, some motor units rest and “take a break”, while others are active, which allows muscle contractions to be held for longer periods of time. Your nervous system uses recruitment as a mechanism to efficiently use a skeletal muscle’s strength and endurance to carry out tasks and activities in your daily life.

The Length-Tension Range of a Sarcomere

As mentioned earlier, when a skeletal muscle fiber contracts, myosin heads attach to actin to form cross-bridges. This interaction allows thin filaments to slide over the thick filaments as the heads pull the actin, and this results in sarcomere shortening, creating the tension of the muscle contraction. Cross-bridges can only form where thin and thick filaments already overlap so that the length of the sarcomere has a direct influence on the force generated when the sarcomere shortens. This is called the length-tension relationship.

The ideal length of a sarcomere to produce maximal tension occurs at 80 percent to 120 percent of its resting length, with 100 percent being the state where the medial edges of the thin filaments are just at the most-medial myosin heads of the thick filaments (Figure 10.17). This length maximizes the overlap of actin-binding sites and myosin heads. If a sarcomere is stretched past this ideal length (beyond 120 percent), thick and thin filaments do not overlap sufficiently, which results in less tension produced. If a sarcomere is shortened beyond 80 percent, the zone of overlap is reduced with the thin filaments jutting beyond the last of the myosin heads and shrinks the H zone, which is normally composed of myosin tails. Eventually, there is nowhere else for the thin filaments to go and the amount of tension is diminished. If the muscle is stretched to the point where thick and thin filaments do not overlap at all, no cross-bridges can be formed, and no tension is produced in that sarcomere. This amount of stretching does not usually occur, as accessory proteins and connective tissue oppose extreme stretching.

Figure 10.17 The Ideal Length of a Sarcomere Sarcomeres produce maximal tension when thick and thin filaments overlap between about 80 percent to 120 percent. (OpenStax)

Muscle Tone

Skeletal muscles are rarely completely relaxed, or flaccid. Even if a muscle is not producing movement, it is contracted a small amount to maintain its contractile proteins and produce muscle tone. The tension produced by muscle tone allows muscles to continually stabilize joints and maintain posture.

Muscle tone is accomplished by a complex interaction between the nervous system and skeletal muscles that results in the activation of a few motor units at a time, most likely in a cyclical manner. In this manner, muscles never fatigue completely, as some motor units can recover while others are active.

The absence of the low-level contractions that lead to muscle tone is referred to as hypotonia and can result from damage to parts of the central nervous system (CNS), such as the cerebellum, or from loss of innervations to a skeletal muscle, as in poliomyelitis. Hypotonic muscles have a flaccid appearance and display functional impairments, such as weak reflexes. Conversely, excessive muscle tone is referred to as hypertonia, accompanied by hyperreflexia (excessive reflex responses), often the result of damage to upper motor neurons in the CNS. Hypertonia can present with muscle rigidity (as seen in Parkinson’s disease = add a link to Parkinson’s Disease in the nervous system chapter) or spasticity, a phasic change in muscle tone, where a limb will “snap” back from passive stretching (as seen in some strokes).

10.6 Types of Muscle Fibers

When classifying types of muscle fibers, two criteria are used: how fast fibers contract compared to others, and how fibers produce ATP. Using these criteria, there are three main types of skeletal muscle fibers. Slow oxidative (SO) fibers contract relatively slowly and use aerobic respiration (needing oxygen and glucose) to produce ATP. Fast oxidative (FO) fibers have fast contractions and primarily use aerobic respiration, but may switch to anaerobic respiration (glycolysis). When FO fibers switch to anaerobic respiration, they fatigue more quickly than SO fibers. Lastly, fast glycolytic (FG) fibers have fast contractions and primarily use anaerobic glycolysis. The FG fibers fatigue more quickly than the others because anaerobic glycolysis produces less ATP per glucose molecule than aerobic respiration. Most of your skeletal muscles contain all three types of fiber, although in varying proportions between muscles. The predominant fiber type in a muscle is determined by the primary function of the muscle.

The speed of a muscle fiber’s contraction depends on how quickly myosin metabolizes ATP. Fast fibers hydrolyze ATP approximately twice as quickly as slow fibers, resulting in much quicker contraction cycling (which pulls sarcomeres together at a faster rate). The primary metabolic pathway used by a muscle fiber determines whether the fiber is classified as oxidative or glycolytic. If a fiber primarily produces ATP through aerobic respiration, it is oxidative. More ATP can be produced by metabolizing nutrients through aerobic respiration versus anaerobic respiration. This increased amount of ATP produced by oxidative fibers makes them more resistant to fatigue. Glycolytic fibers primarily create ATP through anaerobic glycolysis, which produces less ATP per glucose molecule than aerobic respiration. As a result, glycolytic fibers fatigue at a quicker rate.

Slow Oxidative (SO) Fibers

Oxidative fibers contain much more mitochondria than glycolytic fibers because the mitochondria are the cellular machinery that performs aerobic respiration. Mitochondria need oxygen (O2) to metabolize nutrients and convert them into molecules needed to make ATP. Slow oxidative (SO) fibers possess a large number of mitochondria and are capable of contracting for longer periods because of the large amount of ATP they can produce. However, SO fibers have a relatively small diameter with fewer myofibrils, and thus do not produce a large amount of tension. SO fibers are extensively supplied with blood capillaries to supply O2 from the bloodstream. The SO fibers also possess myoglobin, an O2-carrying molecule similar to O2-carrying hemoglobin found in red blood cells. Similar to how hemoglobin allows red blood cells to store O2, myoglobin allows muscle fibers to store their own supply of O2. Both myoglobin and hemoglobin are reddish in color, thus myoglobin gives SO fibers their red color. All of these features allow SO fibers to store and use O2 to produce large quantities of ATP, which can sustain muscle activity without fatiguing for long periods.

The fact that SO fibers can function for long periods without fatiguing makes them useful in maintaining posture, producing isometric contractions, stabilizing bones and joints, and making small movements that happen often, but do not require large amounts of energy. SO fibers do not produce high tension and thus are not used for powerful, fast movements that require high amounts of energy and rapid contraction cycling.

Fast Oxidative (FO) Fibers

Fast oxidative (FO) fibers are sometimes called intermediate fibers because they possess characteristics that are somewhat between fast fibers and slow fibers. FO fibers produce ATP faster than SO fibers and thus can produce relatively high amounts of tension. They are oxidative because they produce ATP aerobically, possess high amounts of mitochondria, and do not fatigue quickly. However, FO fibers do not possess significant amounts of myoglobin, giving them a lighter color than the red SO fibers. FO fibers are used primarily for movements, such as walking, that require more energy than postural control, but less energy than explosive movements such as sprinting. FO fibers are useful for walking and endurance exercises because they produce more tension than SO fibers, but are more fatigue-resistant than fast glycolytic fibers.

Fast Glycolytic (FG) Fibers

Fast glycolytic (FG) fibers primarily use anaerobic glycolysis as their ATP source. They have a large diameter and possess high amounts of glycogen, which can be broken down by glycolysis to quickly generate glucose and ATP. Anaerobic glycolysis produces fewer ATP per glucose molecule than aerobic respiration, which makes FG metabolism of glucose comparatively less efficient by generating less ATP overall. This rapid metabolism and conversion of glycogen to ATP allows FG fibers to produce high levels of tension. Because FG fibers do not primarily use aerobic metabolism, they do not possess substantial numbers of mitochondria or myoglobin, and therefore have a white color. FG fibers are used to produce rapid, forceful contractions to make quick, powerful movements. FG fibers fatigue rapidly due to the lack of O2 and burning through their glycogen and ATP stores relatively quickly, permitting them to only be used for short periods.

Table comparing slow oxidative, fast oxidative glycolytic, and fast glycolytic muscle fibers

10.7 Changes to Muscle Tissues

Exercise

Physical training alters the appearance of skeletal muscles and can produce increases in muscle size and performance. Conversely, a lack of use can result in decreased performance and muscle appearance. Although muscle cells can change in size, it is important to know that new cells are not formed when muscles grow. Instead, new thick and thin filaments are produced and added to existing muscle fibers in a process called hypertrophy. This additional amount of fibers adds mass and bulk to a muscle fiber, so the cell diameter of the fiber increases. Atrophy is the reverse situation when structural proteins are lost and muscle mass decreases.

Endurance Exercise

Slow oxidative (SO) fibers are predominantly used in endurance exercises that require little force but involve numerous repetitions over a longer period. Slow-oxidative fibers use aerobic metabolism to generate mass amounts of ATP, which gives the SO fibers energy to maintain contractions over long periods. Endurance training modifies these slow fibers to make them even more efficient by producing more mitochondria, which enables more aerobic metabolism and ATP production. Endurance exercise can also increase the amount of myoglobin in a cell, as the increased aerobic respiration in SO fibers increases the need for oxygen. Myoglobin is found in the sarcoplasm and acts as an oxygen storage supply for the mitochondria in muscle fibers.

Endurance exercises can trigger the formation of more extensive capillary networks around the fiber, a process called angiogenesis. Increasing the number of capillaries increases the muscle’s supply of oxygen and increases the rate of removing metabolic waste from the muscles. To allow these capillary networks to supply the deep portions of the muscle, muscle mass does not greatly increase to maintain a smaller area for the diffusion and distribution of nutrients and gases. All of these cellular changes result in the ability to sustain low levels of muscle contractions for longer periods without fatiguing.

The proportion of SO muscle fibers in muscle determines the endurance of that muscle over long periods of exercise and may benefit those participating in endurance activities such as marathon running. Your postural muscles that keep you upright as you stand and walk have a large number of SO fibers and relatively few FO and FG fibers, thus helping you to keep your back straight throughout the day (Figure 10.18).

Figure 10.18 Marathoners Long-distance runners have a large number of SO fibers and relatively few FO and FG fibers. (credit: “Tseo2”/Wikimedia Commons)

Resistance Exercise

Resistance exercises, as opposed to endurance exercises, require large amounts of FG fibers to produce short, powerful movements that are not sustained over long periods. The high rates of ATP hydrolysis and cross-bridge formation in FG fibers result in powerful muscle contractions. Muscles used for power have a higher ratio of FG to SO/FO fibers, and trained athletes possess even higher levels of FG fibers in their muscles. Resistance exercise affects muscles by increasing the formation of myofibrils, thereby increasing the thickness of muscle fibers. This added structure through resistance training causes hypertrophy, or the enlargement of muscles, exemplified by the large skeletal muscles seen in bodybuilders and other athletes (Figure 10.19). Because this muscular enlargement is achieved by the addition of structural proteins, athletes trying to build muscle mass often ingest large amounts of protein.

Figure 10.19 Hypertrophy Bodybuilders have a large number of FG fibers and relatively few FO and SO fibers. (credit: Lin Mei/flickr)

The cellular changes observed during endurance training do not usually occur with resistance training. There is usually no significant increase in mitochondria or capillary density. The SO and FO fibers that are more active over long periods of endurance training also do not experience as much hypertrophy as FG fibers.

The connective tissue surrounding muscles also experience changes in response to exercise. Resistance training increases the development of connective tissue, which adds to the overall mass of the muscle and helps to contain muscles as they produce increasingly powerful contractions. Tendons also become stronger to prevent tendon damage, as the force produced by muscles is transferred to tendons that attach the muscle to bone.

For effective strength training, the intensity of the exercise must continually be increased. For instance, continued resistance training without increasing the weight of the load will not increase muscle size. To produce greater hypertrophy and results, the weights lifted must become increasingly heavier, making it more difficult for muscles to move the load. The muscle then adapts to this heavier load by repairing itself in response to the stress from the load, and an even heavier load must be used if even greater muscle mass is desired.

Exercise-Induced Muscle Damage

Exercise-induced muscle damage can occur after intense exercise and causes damage to the sarcolemma and myofibrils. This muscle damage contributes to the feeling of soreness typically felt 12 to 48 hours after strenuous exercise, and is often referred to as delayed onset muscle soreness (DOMS). In response to the damage, muscle fibers try to repair themselves, which causes muscles to gain mass through the synthesis of additional muscle proteins to replace the damaged ones and repair cellular structures damaged by exercise.

Performance-Enhancing Substances

Some athletes attempt to boost their performance by using various agents that may enhance muscle performance (ergogenic aids). One of the most widely utilized ergogenic aids is creatine. Creatine phosphate provides quick bursts of ATP to muscles in the initial stages of contraction, thus giving them an additional source of energy. Increasing the amount of creatine available to cells is thought to produce more ATP and therefore increases a muscle’s explosive power output.

Aging

Although atrophy due to disuse can often be reversed with exercise, muscle atrophy with age, referred to as sarcopenia, is irreversible. This atrophy is a primary reason why even highly trained athletes succumb to declining performance with age. This decline is noticeable in athletes whose sports require strength and powerful movements, such as sprinting, whereas the effects of age are less noticeable in endurance athletes such as marathon runners or long-distance cyclists. As muscles age, muscle fibers die, and they are replaced by connective tissue and adipose tissue (Figure 10.20). Because those tissues cannot contract and generate as much force as muscle fibers, muscles lose the ability to produce powerful contractions. The decline in muscle mass with age causes a loss of strength, including the strength required for posture and mobility. The loss of strength with age may be caused by a reduction in FG fibers that produce short, powerful contractions. Muscles in older people sometimes possess greater proportions of SO fibers, which are responsible for longer contractions and do not produce powerful movements. There may also be a reduction in the size of motor units, resulting in fewer fibers being stimulated and less muscle tension being produced.

Figure 10.20: A local person with sarcopenia

Sarcopenia can be delayed to some extent by exercise, as training adds structural proteins and causes cellular changes that can offset the effects of atrophy. Increased exercise can produce greater numbers of cellular mitochondria, increase capillary density, and increase the mass and strength of connective tissue. The effects of age-related atrophy are especially pronounced in people who are sedentary, as the loss of muscle cells can result in functional impairments such as trouble with locomotion, balance, and posture. This can lead to a decrease in quality of life, medical problems, and joint weakness due to weakness in muscles that stabilize bones and joints. Muscle atrophy in the elderly can also make them more prone to injury by causing problems with locomotion and balance, thus increasing the chance of falls and injuries.

Chapter Summary

Sources

• OpenStax Anatomy and Physiology (http://openstax.org/details/books/anatomy-and-physiology)
• Principles of Anatomy and Physiology, 15th edition, Gerard J. Tortora; Brayn H. Derrickson
• Human Anatomy & Physiology, 11th edition, Elaine N Marieb; Katja Hoehn
• Ge, HY., Fernández-de-las-Peñas, C. & Yue, SW. Myofascial trigger points: spontaneous electrical activity and its consequences for pain induction and propagation. Chin Med 6, 13 (2011). https://doi.org/10.1186/1749-8546-6-13
• http://www.hawaiihistory.org/

Key Terms

acetylcholine (ACh)

neurotransmitter that binds at a motor end-plate to trigger depolarization

actin

protein that makes up most of the thin myofilaments in a sarcomere muscle fiber

aerobic respiration

production of ATP in the presence of oxygen

anaerobic glycolysis 

a non-oxygen-dependent process that breaks down glucose (sugar) to produce ATP

angiogenesis

formation of blood capillary networks

aponeurosis

broad, tendon-like sheet of connective tissue that attaches a skeletal muscle to another skeletal muscle or to a bone

atrophy

loss of structural proteins from muscle fibers

cardiac muscle

striated muscle found in the heart; joined to one another at intercalated discs and under the regulation of pacemaker cells, which contract as one unit to pump blood through the circulatory system. Cardiac muscle is under involuntary control.

concentric contraction

muscle contraction that shortens the muscle to move a load

contraction phase

twitch contraction phase when tension increases

creatine phosphate

phosphagen used to store energy from ATP and transfer it to muscle

eccentric contraction

muscle contraction that lengthens the muscle as the tension is diminished

elasticity

ability to stretch and rebound

endomysium

loose, and well-hydrated connective tissue covering each muscle fiber in a skeletal muscle

epimysium

outer layer of connective tissue around a skeletal muscle

excitation-contraction coupling

sequence of events from motor neuron signaling to a skeletal muscle fiber to contraction of the fiber’s sarcomeres

fascicle

bundle of muscle fibers within a skeletal muscle

fast glycolytic (FG)

muscle fiber that primarily uses anaerobic glycolysis

fast oxidative (FO)

intermediate muscle fiber that is between slow oxidative and fast glycolytic fibers

hypertonia

abnormally high muscle tone

hypertrophy

addition of structural proteins to muscle fibers

hypotonia

abnormally low muscle tone caused by the absence of low-level contractions

intercalated disc

part of the sarcolemma that connects cardiac tissue, and contains gap junctions and desmosomes

isometric contraction

muscle contraction that occurs with no change in muscle length

isotonic contraction

muscle contraction that involves changes in muscle length

lactic acid

product of anaerobic glycolysis

latent period

the time when a twitch does not produce contraction

motor unit

motor neuron and the group of muscle fibers it innervates

muscle fiber

a single muscle cell

muscle tension

force generated by the contraction of the muscle; tension generated during isotonic contractions and isometric contractions

muscle tone

low levels of muscle contraction that occur when a muscle is not producing movement

myoblast

muscle-forming stem cell

myofibril

long, cylindrical organelle that runs parallel within the muscle fiber and contains the sarcomeres

myofilament

thread-like muscle proteins

myogram

instrument used to measure twitch tension

myosin

protein that makes up most of the thick cylindrical myofilament within a sarcomere muscle fiber

neuromuscular junction (NMJ)

synapse between the axon terminal of a motor neuron and the section of the membrane of a muscle fiber with receptors for the acetylcholine released by the terminal

oxygen debt

amount of oxygen needed to compensate for ATP produced without oxygen during muscle contraction

perimysium

connective tissue that bundles skeletal muscle fibers into fascicles within a skeletal muscle

power stroke

action of myosin pulling actin inward (toward the M line)

pyruvic acid

product of glycolysis that can be used in aerobic respiration or converted to lactic acid

relaxation phase

period after twitch contraction when tension decreases

sarcolemma

plasma membrane of a skeletal muscle fiber

sarcomere

longitudinally, repeating functional unit of skeletal muscle, with all of the contractile and associated proteins involved in contraction

sarcopenia

age-related muscle atrophy

sarcoplasm

cytoplasm of a muscle cell

sarcoplasmic reticulum (SR)

specialized smooth endoplasmic reticulum, which stores, releases, and retrieves Ca++

skeletal muscle

striated, multinucleated muscle that requires signaling from the nervous system to trigger contraction; most skeletal muscles are referred to as voluntary muscles that move bones and produce movement

slow oxidative (SO)

muscle fiber that primarily uses aerobic respiration

smooth muscle

nonstriated, mononucleated muscle in the skin that is associated with hair follicles; assists in moving materials in the walls of internal organs, blood vessels, and internal passageways

synaptic cleft

space between a nerve (axon) terminal and a motor end-plate

T-tubule

projection of the sarcolemma into the interior of the cell

tendon

rope-shaped connective tissues that tie (anchor) muscles to bone

tetanus

a continuous fused contraction

thick filament

the thick myosin strands and their multiple heads projecting from the center of the sarcomere toward, but not all to way to, the Z-discs

thin filament

thin strands of actin and its troponin-tropomyosin complex projecting from the Z-discs toward the center of the sarcomere

tropomyosin

regulatory protein that covers myosin-binding sites to prevent actin from binding to myosin

troponin

regulatory protein that binds to actin, tropomyosin, and calcium

twitch

single contraction produced by one action potential

wave summation

addition of successive neural stimuli to produce greater contraction