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1. The Motor Muscle Systemmr. Standring's Webware 2.0
2. The Motor Muscle Systemmr. Standring's Webware 200
3. The Motor Muscle Systemmr. Standring's Webware 2.2
4. The Motor Muscle Systemmr. Standring's Webware 2000

Learning Objectives

• Describe the layers of connective tissues packaging skeletal muscle
• Explain how muscles work with tendons to move the body
• Identify areas of the skeletal muscle fibers
• Describe excitation-contraction coupling

Figure 1.2 Schematic representation of the different levels and interconnections of the motor system hierarchy. The brain figure on the left is a schematic version of an idealized brain section that contains the major structures of the motor system hierarchy for illustrative purposes; no actual brain section would contain all of these structures. Standring's Webware 2: Home Know Your Class. The Motor/Muscle System Powered by Create your own unique website with customizable templates. Skeletal Muscles Attach to Bones. In the muscular system, skeletal muscles are connected to the skeleton, either to bone or to connective tissues such as ligaments. Muscles are always attached at two or more places. When the muscle contracts, the attachment points are pulled closer together; when it relaxes, the attachment points move apart.

The best-known feature of skeletal muscle is its ability to contract and cause movement. Skeletal muscles act not only to produce movement but also to stop movement, such as resisting gravity to maintain posture. Small, constant adjustments of the skeletal muscles are needed to hold a body upright or balanced in any position. Muscles also prevent excess movement of the bones and joints, maintaining skeletal stability and preventing skeletal structure damage or deformation. Joints can become misaligned or dislocated entirely by pulling on the associated bones; muscles work to keep joints stable. Skeletal muscles are located throughout the body at the openings of internal tracts to control the movement of various substances. These muscles allow functions, such as swallowing, urination, and defecation, to be under voluntary control. Skeletal muscles also protect internal organs (particularly abdominal and pelvic organs) by acting as an external barrier or shield to external trauma and by supporting the weight of the organs.

Skeletal muscles contribute to the maintenance of homeostasis in the body by generating heat. Muscle contraction requires energy, and when ATP is broken down, heat is produced. This heat is very noticeable during exercise, when sustained muscle movement causes body temperature to rise, and in cases of extreme cold, when shivering produces random skeletal muscle contractions to generate heat.

Each skeletal muscle is an organ that consists of various integrated tissues. These tissues include the skeletal muscle fibers, blood vessels, nerve fibers, and connective tissue. Each skeletal muscle has three layers of connective tissue (called “mysia”) that enclose it and provide structure to the muscle as a whole, and also compartmentalize the muscle fibers within the muscle (Figure 15.3). Each muscle is wrapped in a sheath of dense, irregular connective tissue called the epimysium, which allows a muscle to contract and move powerfully while maintaining its structural integrity. The epimysium also separates muscle from other tissues and organs in the area, allowing the muscle to move independently.

Inside each skeletal muscle, muscle fibers are organized into individual bundles, each called a fascicle, by a middle layer of connective tissue called the perimysium. This fascicular organization is common in muscles of the limbs; it allows the nervous system to trigger a specific movement of a muscle by activating a subset of muscle fibers within a bundle, or fascicle of the muscle. Inside each fascicle, each muscle fiber is encased in a thin connective tissue layer of collagen and reticular fibers called the endomysium. The endomysium contains the extracellular fluid and nutrients to support the muscle fiber. These nutrients are supplied via blood to the muscle tissue.

In skeletal muscles that work with tendons to pull on bones, the collagen in the three tissue layers (the mysia) intertwines with the collagen of a tendon. At the other end of the tendon, it fuses with the periosteum coating the bone. The tension created by contraction of the muscle fibers is then transferred though the mysia, to the tendon, and then to the periosteum to pull on the bone for movement of the skeleton. In other places, the mysia may fuse with a broad, tendon-like sheet called an aponeurosis, or to fascia, the connective tissue between skin and bones. The broad sheet of connective tissue in the lower back that the latissimus dorsi muscles (the “lats”) fuse into is an example of an aponeurosis.

Every skeletal muscle is also richly supplied by blood vessels for nourishment, oxygen delivery, and waste removal. In addition, every muscle fiber in a skeletal muscle is supplied by the axon branch of a somatic motor neuron, which signals the fiber to contract. Unlike cardiac and smooth muscle, the only way to functionally contract a skeletal muscle is through signaling from the nervous system.

Because skeletal muscle cells are long and cylindrical, they are commonly referred to as muscle fibers. Skeletal muscle fibers can be quite large for human cells, with diameters up to 100 μm and lengths up to 30 cm (11.8 in) in the sartorius of the upper leg. During early development, embryonic myoblasts, each with its own nucleus, fuse with up to hundreds of other myoblasts to form the multinucleated skeletal muscle fibers. Multiple nuclei mean multiple copies of genes, permitting the production of the large amounts of proteins and enzymes needed for muscle contraction.

The myofibrils are the contractile organelles in the muscle fibers. Some other terminology associated with muscle fibers is rooted in the Greek sarco, which means “flesh.” The plasma membrane of muscle fibers is called the sarcolemma, the cytoplasm is referred to as sarcoplasm, and the specialized smooth endoplasmic reticulum, which stores, releases, and retrieves calcium ions (Ca⁺⁺) is called the sarcoplasmic reticulum (SR) (Figure 15.4). And the myofibrils are composed of sarcomeres, the functional contractile unit of a skeletal muscle fiber. The sarcomere is a highly organized arrangement of the contractile myofilaments, actin (thin filament) and myosin (thick filament), along with other support proteins.

The striated appearance of skeletal muscle fibers is due to the special arrangement of the actin and myosin myofilaments in the sarcomere. The arrangement of the thick and thin filaments creates light and dark regions along the myofibril. It is the light and dark regions of the sarcomere that give the muscle fiber the striated appearance. Each packet of these microfilaments and their regulatory proteins, troponin and tropomyosin (along with other proteins) is called a sarcomere.

Interactive Link

Watch this video to learn more about macro- and microstructures of skeletal muscles. (a) What are the names of the “junction points” between sarcomeres? (b) What are the names of the “subunits” within the myofibrils that run the length of skeletal muscle fibers? (c) What is the “double strand of pearls” described in the video? (d) What gives a skeletal muscle fiber its striated appearance?

The sarcomere is the functional unit of the muscle fiber. The sarcomeres are bundled within the myofibril, which runs the entire length of the muscle fiber and attaches to the sarcolemma at its end. As myofibrils contract, the entire muscle cell contracts. Because myofibrils are only approximately 1.2 μm in diameter, hundreds to thousands (each with thousands of sarcomeres) can be found inside one muscle fiber. Each sarcomere is approximately 2 μm in length with a three-dimensional cylinder-like arrangement and is bordered by structures called Z-discs (also called Z-lines, because pictures are two-dimensional), to which the actin myofilaments are anchored (Figure 15.5). The actin myofilaments are the main protein of the thin filament, but there are 2 regulatory proteins that are also part of the thin filament, troponin and tropomyosin. Likewise, because the myosin strands and their multiple heads (projecting from the center of the sarcomere, toward but not all to way to, the Z-discs) have more mass and are thicker, they are called the thick filament of the sarcomere.

The different regions of the sarcomere are:

I band: defined by where there are only thin filaments present

A band: defined by the length of the thick filament Kody morrellamerican meadows equestrian center.

H zone: part of the A band where only the thick filament is present

M line: connective proteins in the middle of the H zone

Z discs (Z lines): proteins that form the boundary of the sarcomere

Another specialization of the skeletal muscle is the site where a motor neuron’s terminal meets the muscle fiber—called the neuromuscular junction (NMJ). This is where the muscle fiber first responds to signaling by the motor neuron. Every skeletal muscle fiber in every skeletal muscle is innervated by a motor neuron at the NMJ. Excitation signals from the neuron are the only way to functionally stimulate the fiber to contract. The motor neurons that tell the skeletal muscle fibers to contract originate in the spinal cord, with a smaller number located in the brainstem for activation of skeletal muscles of the face, head, and neck. These neurons have long processes, called axons, which are specialized to transmit action potentials long distances— in this case, all the way from the spinal cord to the muscle itself (which may be up to three feet away). The axons of multiple neurons bundle together to form nerves, like wires bundled together in a cable.

Figure 15.6 shows an enlarged neuromuscular junction. This junction consists of the end of the axon, the axon terminal (also known as the synaptic bulb or synaptic terminal) and the specialized region of the sarcolemma across from the synaptic terminal, the motor end plate. In the motor end plate, the sarcolemma is highly folded and contains special proteins (see below). There is no physical contact between the neuron and muscle fiber, the small space between them is the synaptic cleft. Signaling begins when a neuronal action potential travels along the axon of a motor neuron, then along the axonal branches and then enters the axon terminal. When the action potential reaches the axon terminal, it stimulates the release of a chemical messenger, or neurotransmitter, called acetylcholine(ACh). The ACh molecules diffuse across the synaptic cleft and bind to specialized receptors called ACh receptors in the motor end-plate of the sarcolemma. Once ACh binds to the receptor, a channel in the ACh receptor opens and positively charged ions can pass through into the muscle fiber, causing it to depolarize, meaning that the membrane potential of the muscle fiber becomes less negative (closer to zero). This depolarization is known as the end-plate potential. In the motor end plate is also an enzyme called acetylcholinesterase that hydrolyzes ACh which helps to end stimulation of the muscle fiber by the motor neuron.

Interactive Link

Every skeletal muscle fiber is supplied by a motor neuron at the NMJ. Watch this video to learn more about what happens at the NMJ. (a) What is the definition of a motor unit? (b) What is the structural and functional difference between a large motor unit and a small motor unit? (c) Can you give an example of each? (d) Why is the neurotransmitter acetylcholine degraded after binding to its receptor?

The Motor Muscle Systemmr. Standring's Webware 2.0

All living cells have membrane potentials, or electrical gradients across their membranes. The inside of the membrane is usually around -60 to -90 mV, relative to the outside. This is referred to as a cell’s membrane potential. Neurons and muscle cells can use their membrane potentials to generate electrical signals. They do this by controlling the movement of charged particles, called ions, across their membranes to create electrical currents. This is achieved by opening and closing specialized proteins in the membrane called ion channels. Although the currents generated by ions moving through these channel proteins are very small, they form the basis of both neural signaling and muscle contraction.

Both neurons and skeletal muscle cells are electrically excitable, meaning that they are able to generate action potentials. An action potential is a special type of electrical signal that can travel along a cell membrane as a wave. This allows a signal to be transmitted quickly and faithfully over long distances.

Although the term excitation-contraction coupling confuses or scares some students, it comes down to this: for a skeletal muscle fiber to contract, its membrane must first be “excited”—in other words, it must be stimulated to fire an action potential. The muscle fiber action potential, which sweeps along the sarcolemma as a wave, is “coupled” to the actual contraction through the release of calcium ions (Ca⁺⁺) from the SR. Once released, the Ca⁺⁺ interacts with the shielding proteins, forcing them to move aside so that the actin-binding sites are available for attachment by myosin heads. The myosin then pulls the actin filaments toward the center, shortening the muscle fiber.

In skeletal muscle, this sequence begins with signals from the somatic motor division of the nervous system. In other words, the “excitation” step in skeletal muscles is always triggered by signaling at the neuromuscular junction (Figure 15.6).

The depolarization of the motor end plate spreads along the adjacent regions of the sarcolemma and a different class of ion channels, the voltage-gated sodium channels, are triggered to open. Sodium ions enter the muscle fiber, and an action potential rapidly spreads (or “fires”) along the entire membrane to initiate excitation-contraction coupling.

Things happen very quickly in the world of excitable membranes (just think about how quickly you can snap your fingers as soon as you decide to do it). Immediately following depolarization of the membrane, it repolarizes, re-establishing the negative membrane potential. Meanwhile, the ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase (AChE) so that the ACh cannot rebind to a receptor and reopen its channel, which would cause unwanted extended muscle excitation and contraction.

Propagation of an action potential along the sarcolemma is the excitation portion of excitation-contraction coupling. Recall that this excitation actually triggers the release of calcium ions (Ca⁺⁺) from its storage in the cell’s SR. For the action potential to reach the membrane of the SR, there are periodic invaginations in the sarcolemma, called T-tubules (“T” stands for “transverse”). You will recall that the diameter of a muscle fiber can be up to 100 μm, so these T-tubules ensure that the membrane can get close to the SR in the sarcoplasm. The arrangement of a T-tubule with the membranes of SR on either side is called a triad (Figure 15.7). The triad surrounds the cylindrical structure called a myofibril, which contains actin and myosin.

The T-tubules carry the action potential into the interior of the cell, which triggers the opening of calcium channels in the membrane of the adjacent SR, causing Ca⁺⁺ to diffuse out of the SR and into the sarcoplasm. It is the arrival of Ca⁺⁺ in the sarcoplasm that initiates contraction of the muscle fiber by its contractile units, or sarcomeres.

The Motor Unit and Muscle Action
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ANY ACTION—ASCENDING A FLIGHT of stairs, typing on a keyboard, even holding a pose—requires coordinating the movement of body parts. This is accomplished by the interaction of the nervous system with muscle. The role of the nervous system is to activate just those muscles that will exert the force needed to move in a particular way. This is not a simple task: Not only must the nervous system decide which muscles to activate and how much to activate them in order to move one part of the body, but it must also control muscle forces on other body parts and maintain posture.

This chapter examines how the nervous system controls muscle force and how the force exerted by a limb depends on muscle structure. We also describe how muscle activation differs with different types of movement.

The Motor Unit Is the Elementary Unit of Motor Control

A Motor Unit Consists of a Motor Neuron and Multiple Muscle Fibers

The nervous system controls muscle force with signals sent from motor neurons in the spinal cord to the muscle fibers. A motor neuron and the muscle fibers it innervates are known as a motor unit, the basic functional unit by which the nervous system controls movement, a concept proposed by Charles Sherrington in 1925.

A typical muscle is controlled by a few hundred motor neurons whose cell bodies are clustered in a motor nucleus in the spinal cord or brain stem (Figure 34-1). The axon of each motor neuron exits the spinal cord through the ventral root or through a cranial nerve in the brain stem and runs in a peripheral nerve to the muscle. When the axon reaches the muscle, it branches and innervates from a few to several thousand muscle fibers.

Figure 34-1 A typical muscle consists of many thousands of muscle fibers working in parallel and organized into a smaller number of motor units. A motor unit consists of a motor neuron and the muscle fibers that it innervates, illustrated here by motor neuron A1. The motor neurons innervating one muscle are usually clustered into an elongated motor nucleus that may extend over one to four segments within the ventral spinal cord. The axons from a motor nucleus exit the spinal cord in several ventral roots and peripheral nerves but are collected into one nerve bundle near the target muscle. In the figure, motor nucleus A includes all those motor neurons innervating muscle A; muscle B is innervated by motor neurons lying in motor nucleus B. The extensively branched dendrites of one motor neuron tend to intermingle with those of motor neurons from other nuclei.

Once synaptic input depolarizes the membrane potential of a motor neuron above threshold, the neuron generates an action potential that is propagated along the axon to its terminal in the muscle. The action potential releases neurotransmitter at the neuromuscular synapse, and this causes an action potential in the sarcolemma of the muscle fibers. A muscle fiber has electrical properties similar to those of a large-diameter, unmyelinated axon, and thus action potentials propagate along the sarcolemma, although more slowly owing to the fiber’s higher capacitance. Because the action potentials in all the muscle fibers of a motor unit occur at approximately the same time, they contribute to extracellular currents that sum to generate a field potential near the active muscle fibers.

Most muscle contractions involve the activation of many motor units, whose currents sum to produce signals detected by electromyography. In many instances the electromyogram (EMG) signal is large and can be easily recorded with electrodes placed on the skin over the muscle. The timing and amplitude of EMG activity, therefore, reflect the activation of muscle fibers by the motor neurons. EMG signals are useful for studying the neural control of movement and for diagnosing pathology (see Chapter 14).

In most mature vertebrate muscles each fiber is innervated by a single motor neuron. The number of muscle fibers innervated by one motor neuron, the innervation number, varies with the muscle type and function. In human skeletal muscles it ranges from average values of 5 for an eye muscle to 1,800 for a leg muscle (Table 34-1). Because the innervation number denotes the number of muscle fibers within a motor unit, differences in innervation number indicate differences in the average increment in force that occurs each time a motor unit in the same muscle is activated. Thus the innervation number also indicates the fineness of control of the muscle; the smaller the innervation number, the finer the control achieved by varying the number of activated motor units.

Table 34-1 Innervation Numbers in Human Skeletal Muscles

Not all motor units in a muscle have the same innervation number. Indeed, the differences can be substantial. For example, motor units of the first dorsal interosseous muscle of the hand have innervation numbers ranging from approximately 21 to 1,770. Consequently, the strongest motor unit in the hand’s first dorsal interosseous muscle can exert about the same force as the average motor unit in the leg’s medial gastrocnemius muscle.

The muscle fibers of a single motor unit are distributed throughout the muscle and intermingle with fibers innervated by other motor neurons. The muscle fibers of a single motor unit can occupy from 8% to as much as 75% of the volume in a limb muscle, with 2 to 5 muscle fibers per 100 belonging to the same motor unit. Therefore the muscle fibers in a given volume of muscle belong to 20 to 50 different motor units. This distribution changes with age and with some neuromuscular disorders. For example, muscle fibers lose their innervation after the death of a motor neuron and can be reinnervated by collateral sprouts from neighboring axons.

In some muscles the fibers of motor units are confined to discrete compartments that correspond to the regions of the muscle supplied by the primary branches of the muscle nerve. Selective activation of different compartments that exert forces in different directions provides a biomechanical advantage. Branches of the median and ulnar nerves in the forearm, for example, innervate distinct compartments in three multitendon extrinsic hand muscles that enable the fingers to be moved relatively independently. A muscle can therefore consist of several functionally distinct regions.

The Properties of Motor Units Vary

The force exerted by a muscle depends not only on the number of motor units that are activated during a contraction but also on three properties of those motor units: contraction speed, maximal force, and fatigability. These properties are assessed by examining the force exerted by individual motor units in response to variations in the number and rate of evoked action potentials.

The response to a single action potential is known as a twitch contraction. The time it takes the twitch to reach its peak force, the contraction time, is one measure of the contraction speed of the muscle fibers that comprise a motor unit. Slow-twitch motor units have long contraction times; fast-twitch units have shorter contraction times. A rapid series of action potentials elicits superimposed twitches known as a tetanic contraction or tetanus.

The force exerted during a tetanic contraction depends on the extent to which the twitches overlap and summate: The force varies with the contraction time of the motor unit and the rate at which the action potentials are evoked. At lower rates of stimulation the ripples in the tetanus denote the peaks of individual twitches (Figure 34-2A). The peak force achieved during a tetanus varies as a sigmoidal function of action potential rate, with the shape of the curve depending on the contraction time of the motor unit (Figure 34-2B). Maximal force is reached at different action potential rates for fast-twitch and slow-twitch motor units and is often greater in fast-twitch units.

Figure 34-2 The force exerted by a motor unit varies with the rate of the action potentials.

A. Traces show the forces exerted by fast- and slow-twitch motor units in response to a single action potential (top trace) and a series of action potentials (set of four traces below). The time to the peak twitch force, or contraction time, is briefer in the fast-twitch unit. The rates of the action potentials used to evoke the tetanic contractions ranged from 17 to 100 Hz in the slow-twitch unit to 46 to 100 Hz in the fast-twitch unit. The peak force for the 100 Hz tetanus is greater in the fast-twitch unit. Note the different force scales for the two sets of traces. (Adapted with permission from Botterman et al. 1986; Fuglevand, Macefield, and Bigland-Ritchie 1999; and Macefield, Fuglevand, and Bigland-Ritchie 1996.)

The Motor Muscle Systemmr. Standring's Webware 200

B. Relation between peak force and the rate of action potentials for fast- and slow-twitch motor units. The absolute force (left plot) is greater for the fast-twitch motor unit at all frequencies. At lower stimulus rates (right plot) the force evoked in the slow-twitch motor unit summed to a greater relative force (longer contraction time) than in the fast-twitch motor unit (briefer contraction time).

The functional properties of motor units vary across the population and between muscles. At one end of the distribution motor units have long twitch contraction times and produce small forces, but are difficult to fatigue. These motor units are the first activated during a voluntary contraction. In contrast, the last motor units activated have short contraction times, produce large forces, and are easy to fatigue. As observed by Jacques Duchateau and colleagues, most human motor units produce low forces and have intermediate contraction times (Figure 34-3).

Figure 34-3 Distributions of motor unit properties. (Reproduced, with permission, from Van Cutsem et al. 1997.)

A. Distribution of twitch torques for 528 motor units in the tibialis anterior muscle.

B. Distribution of twitch contraction times for 528 motor units in the tibialis anterior muscle.

Because these contractile properties of a motor unit depend on the characteristics of its muscle fibers, we can distinguish different types of muscle fibers. This distinction stems from structural specializations and differences in the metabolic properties of muscle fibers. All muscle fibers belonging to a motor unit have similar biochemical and histochemical properties.

One commonly used scheme distinguishes muscle fibers by their reactivity to histochemical assays for the enzyme myosin adenosine triphosphatase (ATPase), which is used as an index of contractile speed. Based on histochemical stains for myosin ATPase, it is possible to identify type I and type II muscle fibers. Slow contracting motor units contain type I muscle fibers, and fast contracting units include type II fibers. The type II fibers can be further classified into the least fatigable (type IIa) and most fatigable (type IIb, IIx, or IId). Another commonly used scheme distinguishes muscle fibers on the basis of genetically defined isoforms of the myosin heavy chain. Those in slow contracting motor units express myosin heavy chain-I, those in fast contracting and least fatigable units express myosin heavy chain-IIa, and fibers in fast contracting and most fatigable units express myosin heavy chain-IIb or -IIx. There is a high degree of correspondence between the two classification schemes for muscle fibers.

Physical Activity Can Alter Motor Unit Properties

Alterations in habitual levels of physical activity can influence the three contractile properties of motor units (contraction speed, maximal force, and fatigability). A decrease in muscle activity, such as occurs with aging, bed rest, limb immobilization, or space flight, reduces the maximal capabilities of all three properties. The effects of increased physical activity depend on the intensity and duration of the activity. Brief sets of high-intensity contractions performed a few times each week can increase contraction speed and motor unit force, whereas prolonged periods of low-intensity contractions can reduce motor unit fatigability. Physical activity regimens that involve such differences are often described as strength training and endurance training, respectively.

Changes in the contractile properties of motor units involve adaptations in the structural specializations and biochemical properties of muscle fibers. The improvement in contraction speed caused by strength training, for example, is associated with an increase in the maximal shortening velocity of a muscle fiber caused by the enhanced capabilities of the myosin molecules in the fiber. Similarly, the increase in maximal force is associated with the enlarged size and increased intrinsic force capacity of the muscle fibers produced by an increase in the number and density of the contractile proteins.

In contrast, alterations in the fatigability of a muscle fiber can be caused by many different adaptations, such as changes in capillary density, the number of mitochondria, excitation-contraction coupling, and the metabolic capabilities of the muscle fibers. Endurance exercise can promote the biogenesis of mitochondria and enhance the oxidative capacity of a muscle fiber, thereby reducing its fatigability. Although the adaptive capabilities of muscle fibers decline with age, the muscles remain responsive to exercise even at 90 years of age.

Despite the efficacy of strength and endurance training in altering the contractile properties of muscle fibers, these training regimens have little effect on the composition of a muscle’s fibers. Although several weeks of exercise can change the proportion of type IIa and IIx fibers, there is no change in the proportion of type I fibers. All fiber types adapt in response to exercise, although to varying extents depending on the type of exercise. For example, strength training of leg muscles for 2 to 3 months can increase the cross-sectional area of type I fibers by 0% to 20% and of type II fibers by 20% to 60%, increase the proportion of type IIa fibers by approximately 10%, and decrease the proportion of type IIx fibers by a similar amount. Furthermore, endurance training may increase the enzyme activities of oxidative metabolic pathways without noticeable changes in the proportions of fiber types, but the relative proportions of type IIa and IIx fibers do change as a function of the duration of each exercise session. Conversely, several weeks of bed rest or limb immobilization do not change the proportions of fiber types in a muscle, but they do decrease the size and intrinsic force capacity of muscle fibers.

Although physical activity has little influence on the proportion of type I fibers in a muscle, more substantial interventions can have an effect. Space flight, for example, exposes muscles to a sustained decrease in gravity, reducing the proportion of type I fibers in leg muscles. A few weeks of continuous electrical stimulation at a low frequency causes a marked increase in the proportion of type I fibers and a substantial decrease in fiber size. Similarly, surgically changing the nerve that innervates a muscle alters the pattern of activation; eventually the muscle exhibits properties similar to those of the muscle that was originally innervated by the transplanted nerve. Connecting a nerve that originally innervated a rapidly contracting leg muscle to a slowly contracting leg muscle, for example, will cause the slower muscle to become more like a faster muscle.

Muscle Force Is Controlled by the Recruitment and Discharge Rate of Motor Units

The force exerted by a muscle during a contraction depends on the number of motor units that are activated and the rate at which each of the active motor neurons discharges action potentials. Force is increased during a muscle contraction by the activation of additional motor units, which are recruited progressively from the weakest to the strongest (Figure 34-4). A motor unit’s recruitment threshold is the force during the contraction at which the motor unit is activated. Muscle force decreases gradually by terminating the activity of motor units in the reverse order from strongest to weakest.

Figure 34-4 Motor units that exert low forces are recruited before those that exert greater forces. (Adapted, with permission, from Desmedt and Godaux 1977 and from Milner-Brown, Stein, and Yemm 1973.)

A. Action potentials in two motor units were recorded concurrently with a single intramuscular electrode while the subject gradually increased muscle force. Motor unit 1 began discharging action potentials near the beginning of the voluntary contraction, and its discharge rate increased during the contraction. Motor unit 2 began discharging action potentials near the end of the contraction.

B. Average twitch forces for motor units 1 and 2 as extracted with an averaging procedure during the voluntary contraction.

C. The plot shows the forces at which 64 motor units in a hand muscle of one person were recruited (recruitment threshold) during a voluntary contraction versus the twitch forces of the motor units.

The order in which motor units are recruited is highly correlated with several indices of motor unit size, including the size of the motor neuron cell bodies, the diameter and conduction velocity of the axons, and the amount of force that the muscle fibers can exert. Because the recruitment threshold of a motor unit depends on the membrane resistance of the motor neuron, which is inversely related to its surface area, a given synaptic current will produce larger changes in the membrane potential of small-diameter motor neurons. Consequently, increases in the net excitatory input to a motor nucleus cause the levels of depolarization to reach threshold in an ascending order of motor neuron size: The smallest motor neuron is recruited first and the largest motor neuron last (Figure 34-5). This effect is known as the size principle of motor neuron recruitment, a principle enunciated by Elwood Henneman in 1957.

Figure 34-5 The response of a motor neuron to synaptic input depends on its size. Two motor neurons of different sizes have the same resting membrane potential (V_r) and receive the same excitatory synaptic current (I_syn) from a spinal interneuron. Because the small motor neuron has a smaller surface area, it has fewer parallel ion channels and therefore a higher resistance (R_high). According to Ohm’s law (V = IR), I_syn in the small neuron produces a large excitatory postsynaptic potential (EPSP) that reaches threshold, resulting in the discharge of an action potential. The small motor neuron has a small-diameter axon that conducts the action potential at a low velocity (v_slow) to fewer muscle fibers. In contrast, the large motor neuron has a larger surface area, which results in a lower transmembrane resistance (R_low) and a smaller EPSP that does not reach threshold in response to I_syn.

The Motor Muscle Systemmr. Standring's Webware 2.2

The Motor Muscle Systemmr. Standring's Webware 2000

The size principle has two important consequences for the control of movement by the nervous system. First, the sequence of motor-neuron recruitment is determined by spinal mechanisms and not by higher regions of the nervous system. This means that the brain cannot selectively activate specific motor units. Second, motor units are activated in order of increasing fatigability, so the least fatigable motor units available produce the initial force required for a specific task.

As suggested by Edgar Adrian in the 1920s, the muscle force at which the last motor unit in a motor nucleus is recruited varies between muscles. In some hand muscles all the motor units have been recruited when the force reaches approximately 60% of maximum during a slow muscle contraction. In the biceps brachii, deltoid, and tibialis anterior muscles, recruitment continues up to approximately 85% of the maximal force. However, because the recruitment threshold of motor units decreases with contraction speed, during a rapid contraction most motor units in a muscle are recruited with a load of approximately 33% of maximum. Beyond the upper limit of motor unit recruitment, muscle force can still be increased by varying the rate of action potentials in the motor neurons. Below the upper limit of recruitment, the rate of firing can also be varied in addition to increasing the number of active motor units (Figure 34-6). In fact, beneath the upper recruitment limit variation in discharge rate can have the greater influence on muscle force.

Figure 34-6 Muscle force can be adjusted by varying the number of active motor units and their discharge rate. A gradual increase and then a decrease in the force (blue line) exerted by the knee extensor muscles involved the concurrent activation of four (out of many) motor units. The muscle force was changed by varying both the number of motor units that were active and the rate at which the motor neurons discharged action potentials. Motor unit 1 was activated when muscle force reached 20% of maximum. Initially the motor neuron discharged action potentials at a rate of 9 Hz. As force increased, the discharge rate increased up to 15 Hz, when both the force and discharge rate declined, and the motor unit was inactivated at 14% of maximal force. Motor units 2, 3, and 4 were activated at greater forces but discharge rate was modulated similarly. (Reproduced, with permission, from Person and Kudina 1972.)

The Input–Output Properties of Motor Neurons Are Modified by Input from the Brain Stem

The discharge rate of motor neurons depends on the magnitude of the depolarization generated by excitatory inputs and the intrinsic membrane properties of the motor neurons in the spinal cord. These properties can be profoundly modified by input from monoaminergic neurons in the brain stem. In the absence of this input, the dendrites of motor neurons passively transmit synaptic current to the cell body, resulting in a modest depolarization that immediately ceases when the input stops. Under these conditions the relation between input current and discharge rate is linear over a wide range.

The input–output relation becomes nonlinear, however, when the monoamines serotonin and norepinephrine activate L-type Ca²⁺ channels on the dendrites of the motor neurons. Along came a spiderebooks free download. The resulting inward Ca²⁺ currents can enhance synaptic currents by five- to tenfold (Figure 34-7). In an active motor neuron this enhanced current can sustain an elevated discharge rate after a brief depolarizing input, a behavior known as self-sustained firing. A subsequent brief inhibitory input at a low velocity returns the discharge rate to its original value.