Muscle

I. SKELETAL MUSCLE. The terms muscle fiber and muscle cell are synonymous.

A. Fiber (cell) types. Skeletal muscle fibers can be classified mainly into red (type I) and white (type II) fibers that have quite different characteristics based on their function

1. Red fibers are slow-twitch fibers and are largely present, for example, in the long muscles of the back (antigravity muscles).

2. White fibers are fast-twitch fibers and are largely present, for example, in the extraocular muscles of the eye.

B. Cross-striations (Figure 6-1)

1. The A band contains both thin and thick myofilaments and is the dark band seen when using an electron microscope.

2. The 1 band contains only thin myofilaments and is the light band seen when using an electron microscope.

3. The H band bisects the A band and contains only thick myofilaments.

Table 6-1

Characteristics of Muscle Fiber

Table 6-1

Characteristics of Muscle Fiber

Characteristic

Red Fiber

White Fiber

Speed of contraction

Slow

Fast

Myoglobin content*

High

Low

Generation of ATP

Aerobic glycolysis* Oxidative phosphorylation

Anaerobic glycolysis?

Number of mitochondria

Many

Few

Glycogen content

Low

High

Succinate dehydrogenase NADH dehydrogenase

High

Low

Glycolytic enzymes

Low

High

♦Myoglobin is an oxygen-binding protein similar to hemoglobin and accounts for the reddish appearance of red (type I) fibers.

f Aerobic glycolysis (conversion of glucose to carbon dioxide and water) is a relatively slow process so that it can meet the demands of red fibers, but it yields 36 to 38 moles of ATP per mole of glucose.

t Anaerobic glycolysis (conversion of glucose to lactate) is a relatively fast process so that it can meet the demands of white fibers, but it yields only 2 moles of ATP per mole of glucose. NADH = reduced nicotinamide adenine dinucleotide.

Z disk-

Sarcomere-

Z disk

-Actinin

Thick myofilament

Z disk-

Sarcomere-

Z disk

-Actinin

Thick myofilament

F-actin

Light meromyosin Heavy 1

meromyosin

Figure 6-1. Organization of thin and thick myofilaments in skeletal muscle.

F-actin

Light meromyosin Heavy 1

meromyosin

Figure 6-1. Organization of thin and thick myofilaments in skeletal muscle.

4. The Z disk bisects the I band. The distance between two Z disks delimits a sarcomere, which is the basic unit of contraction for the myofibril. The Z disk contains «-actinin, which anchors thin filaments to the Z disk.

C. Thin myofilaments

1. F actin has an active site that interacts with the cross-bridges of myosin.

2. Tropomyosin blocks the active site on F actin during relaxation.

3. Troponin C is a calcium-binding protein.

D. Thick myofilaments

1. Myosin can be cleaved by trypsin into light meromyosin and heavy meromyosin, which contains crossbridges. The cross-bridges have actin-binding sites and ATPase activity.

2. Titin anchors myosin to the Z disks and helps the muscle to accommodate extreme stretching.

E. Changes in contracted and stretched muscle. The cross-striational pattern of skeletal muscle changes when it is contracted or stretched. These changes are caused by the degree of interdigitation of the thin and thick myofilaments (Table 6-2).

F. Contraction of skeletal muscle (Figure 6-2)

1. A triad consists of a transverse tubule (T tubule) located at the A-I junction flanked on either side by two terminal cisternae.

a. AT tubule is an invagination of the cell membrane and transmits an action potential to the depths of a muscle cell.

b. Terminal cisternae are dilated sacs of sarcoplasmic reticulum that store, release, and reaccumulate calcium ions.

2. In response to an action potential, calcium ions are released from the terminal cisternae.

3. Calcium ions bind to troponin, which allows the myosin crossbridge-ADP-phosphate complex to bind to actin. Repetitive action potentials may produce saturating levels of calcium ions for troponin and thereby cause tetany.

4. ADP-phosphate is released, leaving the myosin crossbridge bound to actin.

5. The myosin crossbridge binds ATP, which detaches the myosin crossbridge from actin. (If ATP is not available, the muscle will not relax, and rigor mortis results.)

6. ATP is hydrolyzed by myosin ATPase, and the products (ADP and phosphate) remain bound to the myosin crossbridge, thereby reforming the myosin cross-bridge—ADP—phosphate complex.

G. Neuromuscular junction (also called myoneural junction or motor endplate)

1. Synaptic terminals of alpha motoneurons contain synaptic vesicles, which store acetylcholine (ACh). ACh is synthesized by the condensation of acetyl Co A and

Table 6-2

Changes in Contracted and Stretched Muscle

Change Compared with Relaxed Muscle

Table 6-2

Changes in Contracted and Stretched Muscle

Change Compared with Relaxed Muscle

Band

Contracted

Stretched

A band

No change

No change

1 band

Shortens

Lenghtens

H band

Shortens

Lengthens

Z disks

Move closer together

Move farther apart

Receptors

Muscle spindle

Shortens

Lengthens

Golgi tendon organ

Moves closer together

Moves farther apart

Myosin crossbridge-ADP- PO42" binds to actin

Figure 6-2. Events in skeletal muscle contraction. Note the points where tetany and rigor mortis occur.

choline, whicli is catalyzed by choline-O-acetyltransferase. Choline is obtained by active uptake from the extracellular fluid.

2. The cell membrane of the synaptic terminal is called the presynaptic membrane and is where exocytotic release of ACh occurs. The cell membrane of the muscle fiber is callcd the postsynaptic membrane, and it contains the nicotinic acetylcholine receptor (nAChR).

3. The space between the presynaptic and postsynaptic membrane is called the synaptic cleft, and it contains the basal lamina associated with the enzyme acetylcholinesterase (AChE), which hydrolyzes ACh into acctatc and choline.

4. nAChR is a transmitter-gated ion channcl such that when nAChR binds ACh, the "gate" is opened and allows an influx of sodium ions. This influx causes depolarization of the postsynaptic membrane called the endplate potential.

5. Endplate potentials spread to areas of the muscle fiber cell membrane and T tubule by electrotonic conduction until a threshold is reached and an action potential is generated. (Note: An action potential is not generated at the neuromuscular junction itself.)

6. a-Bungarotoxin (a snake venom a-toxin) and curare (a plant toxin) bind to nAChR, thereby preventing ACh from binding.

H. Innervation. A single axon of an alpha motoneuron may innervate 1 to 5 muscle fibers (forming a small motor unit), or the axon may branch and innervate >150 muscle fibers (forming a large motor unit). A motor unit (not a muscle fiber) is the functional contractile unit of a muscle.

I. Denervation. If a nerve to a muscle is severed, muscle fasciculations (small irregular contractions) occur caused by release of ACh from the degenerating axon. Several days after denervation, muscle fibrillations (spontaneous repetitive contractions) occur caused by a supersensitivity of the muscle to ACh as ACh receptors spread out over the entire cell membrane of the muscle fiber.

J. Skeletal muscle repair (regeneration) is limited. Skeletal muscle fibers develop em-bryologically from rhabdomyoblasts. Afrer injury or extensive exercise, satellite cells present in the adult proliferate and fuse to form new skeletal muscle fibers. Adult skeletal muscle fibers do not undergo mitosis.

K. Stretch (sensory) receptors

1.. Muscle spindles activate the myotatic (stretch) reflex and consist of nuclear bag fibers or nuclear chain fibers.

a. Nuclear bag fibers contain nuclei that are bunched together centrally and that transmit sensory information to group la afferent neurons.

b. Nuclear chain fibers contain nuclei that are linearly arranged and that transmit sensory information (muscle length and rate of change in muscle length) to group la and group II afferent neurons.

C. Nuclear bag fibers and nuclear chain fibers are innervated by y-motoneu-rons that set the sensitivity of the muscle spindle. The activity of "/-motoneurons is controlled by descending pathways of higher brain centers (upper motoneurons) such that after spinal cord transection, hyperactivity of 7-motoneurons plays a role in muscle spasticity and muscle hypertonia.

2. Golgi tendon organs activate the inverse myotatic (stretch) reflex and consist of a bundle of collagen fibers within the muscle tendon that transmit sensory information (force on the muscle) to group lb afferent neurons.

L. Clinical considerations

1. Duchenne muscular dystrophy (DMD) is a generic disease that shows X-linked recessive inheritance.

a. The DMD gene is located on the short (p) arm of chromosomc X in band 21 (i.e., Xp21) and encodes for the dystrophin protein.

b. Dystrophin anchors within skeletal muscle fibers to the extracellular matrix, thereby stabilizing the cell membrane.

C. A mutation of the DMD gene alters the normal function of dystrophin, leading to progressive muscle weakness and wasting.

2. Myasthenia gravis is an autoimmune disease characterized by circulating antibodies against the ACh receptor (anti-AChR) and decreased number of ACh receptors.

a. It is characterized by muscle weakness that fluctuates daily or even within hours.

b. The extraocular muscles are generally involved, with ptosis and diplopia being the first disability.

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