Chapter 9 Review APHY 201

STUDY AND REVIEW

9: Muscle

STUDY AND REVIEW 9.1

■ Skeletal muscles: composed of cylindrical, multinucleated muscle fibers (cells) derived from myoblasts

  • linked to bones by tendons at each end of a muscle
  • Satellite cells: undifferentiated stem cells that proliferate and differentiate into myoblasts in response to damage of a muscle
  • Hypertrophy: an increase in size of muscle fibers that may occur in response to injury or to exercise

■ Sarcomeres: repeating, striated pattern of light and dark bands observed when viewing skeletal muscle fibers under a microscope

  • Striated pattern is due to arrangement of thick and thin filaments arranged in bundles (myofibrils); form A and I bands; Z and M lines, and H zone.
  • Thin filaments: contain actin, troponin, and tropomysin; anchored to the Z lines at each end of a sarcomere; free ends partially overlap the myosin-containing thick filaments in the A band at the center of the sarcomere
  • Thick filament: made up of myosin molecules with extensions called cross-bridges that span the gap between the thick and thin filaments
  • Each cross-bridge has two globular heads that contain a binding site for actin and an enzymatic site (myosin-ATPase) that hydrolyzes ATP

■ Electrical activation of skeletal muscle fibers: transmitted via elaborations of the plasma membrane (sarcolemma) called transverse tubules (T-tubules).

  • T-tubules interact with terminal cisternae of the sarcoplasmic reticulum, to release stored Ca2+ into the cytosol

Review Question: Describe the arrangement of thick and thin filaments in a sarcomere. Include in your answer a description of the proteins that make up each filament and how those proteins are arranged.

STUDY AND REVIEW 9.2

■ Contraction: activation of force generation in a muscle fiber; relaxation refers to turning off the force-generating mechanisms and allowing a decrease in tension.

■ Alpha motor neurons: the neurons that innervate skeletal muscle fibers; one motor neuron innervates many muscle fibers, forming a motor unit.

■ Neuromuscular junction: formed from branches of a motor neuron axon that contact a muscle fiber at a region of the fiber called a motor end plate

  • Acetylcholine is the neurotransmitter released by motor neurons; it binds to receptors on the motor end plate of the muscle membrane, causing depolarization (end plate potential).
  • A single action potential in a motor neuron is sufficient to produce an action potential in a skeletal muscle fiber.
  • Signaling at the neuromuscular junction can be disrupted by a number of toxins, drugs, and diseases; overstimulation is normally prevented by acetylcholinesterase.

■ Excitation–contraction coupling: sequence of events beginning with action potentials and leading to contraction of a skeletal muscle fiber:

  • Cytosolic Ca2+ concentration is increased following electrical excitation of a fiber.
  • Ca2+ binds to troponin, which causes tropomyosin to move away from (unblock) the myosin-binding sites on actin.
  • Cross-bridges bind to the thin filaments.
  • Relaxation occurs when Ca2+ is pumped back into the sarcoplasmic reticulum, allowing troponin and tropomysin to resume their blocking action.

■ Sliding-filament mechanism: The thin filaments are propelled toward the center of a sarcomere by movements of the myosin cross-bridges that bind to actin, thereby shortening the fiber.

■ The cross-bridges undergo repeated cycles during a contraction, each cycle producing only a small increment of movement.

■ ATP has two roles in the cross-bridge cycle:

  • an allosteric function that induces cross-bridges to detach from actin
  • provision of energy for cross-bridge movement

Review Question: Describe the four steps in one cross-bridge cycle. At what steps does ATP act, and in what ways? What event in a muscle cell must precede contraction?

STUDY AND REVIEW 9.3

■ Contraction: refers only to activation of the cross-bridge cycle

■ Tension: force exerted on an object by a contracting muscle

■ Load: force exerted on a muscle by an object (its weight)

■ Whether there is an accompanying change in muscle length depends upon the external forces acting on the muscle.

■ Types of contractions:

  • Isometric contraction: the muscle generates tension but does not change length
  • Isotonic contraction: the muscle either shortens (concentric contraction) or lengthens (eccentric contraction) while moving a load that remains constant

■ Twitch contraction: mechanical response of a muscle fiber to a single action potential

  • Latent period: short interval following an action potential before tension rises in a muscle fiber during which events of excitation–contraction coupling are beginning
  • Fiber types: Fast-twitch fibers have very short contraction times (interval from beginning of latent period to the time of peak tension development); slow-twitch fibers have longer contraction times.

■ Increasing the frequency of action potentials in a muscle fiber increases the mechanical response (tension or shortening) up to the level of maximal tetanic tension (maintained contraction in response to repetitive stimulation).

■ Maximum isometric tetanic tension: produced at optimal length (Lo) of a sarcomere

  • Stretching a fiber beyond Lo or decreasing it below Lo decreases the tension generated, because of reduced cross-bridge access to thin filaments at short and long sarcomere lengths.

■ The velocity of muscle fiber shortening decreases with increases in load. Maximum velocity occurs at zero load.

Review Question: Distinguish between isometric, concentric, and eccentric contractions. In what way is fiber length related to its ability to generate maximal isometric tension?

STUDY AND REVIEW 9.4

■ Muscle fibers form ATP by 3 mechanisms:

  • transfer of phosphate from creatine phosphate to ADP
  • oxidative phosphorylation of ADP in mitochondria
  • phosphorylation of ADP in the glycolytic pathway

■ The fuel consumed by skeletal muscle changes with the duration of activity during low-intensity exercise.

  • beginning of exercise: muscle glycogen is the major fuel consumed
  • continued exercise: glucose and fatty acids from the blood provide most of the fuel
  • prolonged exercise: fatty acids become progressively more important

■ When exercise intensity is sufficiently high, glycolysis begins to contribute an increasingly large fraction of the total ATP generated.

■ Muscle fatigue results from several factors:

  • a decrease in ATP concentration
  • increases in the cellular concentrations of ADP, Pi, Mg2+, H+ , and oxygen free radicals
  • These changes have effects such as decreasing Ca2+ uptake and storage by the sarcoplasmic reticulum, decreasing the sensitivity of the thin filaments to Ca2+, and inhibiting the binding and power-stroke motion of the cross-bridges.

Review Question: What fuel molecules are metabolized to provide ATP during skeletal muscle activity? How does creatine phosphate contribute to ATP homeostasis in a muscle cell?

STUDY AND REVIEW 9.5

■ Three types of skeletal muscle fibers can be distinguished by their maximal shortening velocities and the predominant pathway they use to form ATP:

  • slow-oxidative fibers (type 1)
  • fast-oxidative-glycolytic fibers (type 2A)
  • fast-glycolytic fibers (type 2X)

■ Differences in maximal shortening velocities are due to different myosin enzymes with high or low ATPase activities, giving rise to fast and slow fibers.

■ Oxidative fibers have many mitochondria and possess a high amount of the oxygen-binding protein myoglobin.

■ Glycolytic fibers have few mitochondria but have a high concentration of glycolytic enzymes and little or no myoglobin.

■ Fast-glycolytic fibers have a larger average diameter than oxidative fibers and therefore produce greater tension, but they also fatigue more rapidly.

■ All muscle fibers in a single motor unit belong to the same fiber type; most muscles contain all three types.

Review Question: What are the major characteristics of the three types of skeletal muscle fibers?

STUDY AND REVIEW 9.6

■ The tension produced by whole-muscle contraction depends on the amount of tension each fiber develops and the number of active fibers in the muscle.

■ Muscles that produce delicate movements have a small number of fibers per motor unit; large, powerful muscles have much larger motor units.

■ Fast-glycolytic motor units not only have large-diameter fibers but also tend to have large numbers of fibers per motor unit.

■ Recruitment: process by which increases in muscle tension are controlled primarily by increasing the number of active motor units in a muscle

  • order of recruitment: slow-oxidative motor units, then fastoxidative-glycolytic motor units, then fast-glycolytic motor units (only during very strong contractions)

■ Increasing motor-unit recruitment increases the velocity at which a muscle will move a given load.

■ Exercise can alter a muscle’s strength and susceptibility to fatigue.

■ Movement around a joint generally involves groups of antagonistic muscles; some flex a limb at the joint (flexion) and others extend the limb (extension).

■ The lever action of muscles and bones generally requires muscle tension far greater than the load in order to sustain a load in an isometric contraction, but the lever system produces a shortening velocity at the end of the lever arm that is greater than the muscle-shortening velocity.

Review Question: What is meant by the term recruitment in muscle physiology? How does it relate to the velocity with which a muscle can move a load? How is the velocity of shortening affected by the lever system of muscles and bones?

STUDY AND REVIEW 9.7

■ Muscle cramps: involuntary tetanic contractions related to heavy exercise; may be due to dehydration and electrolyte imbalances in the fluid surrounding muscle and nerve fibers

■ Hypocalcemic tetany: excessive muscle contractions caused when extracellular Ca2+ decreases below normal, spontaneously opening Na+ channels of nerve and muscle

■ Muscular dystrophy: genetic disorder that results from defects of muscle-membrane-stabilizing proteins such as dystrophin. Muscles of individuals with Duchenne muscular dystrophy progressively degenerate with use.

■ Myasthenia gravis: autoimmune disorder in which destruction of ACh receptors of the motor end plate causes progressive loss of the ability to activate skeletal muscles.

Review Question: Describe some of the major skeletal muscle disorders or diseases mentioned in this chapter (cramps, hypocalcemic tetany, muscular dystrophies, myasthenia gravis), including the mechanisms of any defect, and propose, if possible, a mechanism by which the defect can be treated or alleviated.

STUDY AND REVIEW 9.8

■ Smooth muscle cells: spindle-shaped, non-striated cells with a single nucleus and capable of cell division

■ Contain actin and myosin filaments but no sarcomeres and contract by a sliding-filament mechanism

■ Dense bodies: cytoplasmic structures functionally similar to Z lines in skeletal muscle fibers; anchor the thin filaments

■ Isometric tension developed by smooth muscle fibers varies with fiber length as in skeletal muscle, but maximum tension is generated over a wider range.

Review Question: How does the organization of thick and thin filaments in smooth muscle fibers differ from that in striated muscle fibers? How is it similar?

STUDY AND REVIEW 9.9

■ An increase in cytosolic Ca2+ leads to a chain of events that results in phosphorylation of light chains of smooth muscle myosin by myosin light-chain kinase.

  • Only phosphorylated myosin can bind to actin and undergo cross-bridge cycling.

■ Two sources of the cytosolic calcium ions that initiate smooth muscle contraction are the sarcoplasmic reticulum and extracellular Ca2+.

  • Smooth muscle tone: a low level of basal cross-bridge activity at resting, low concentrations of cytosolic Ca2+, in the absence of external stimuli

■ The strength of smooth muscle contraction varies with the increase in cytosolic Ca2+ and is influenced by multiple stimuli including:

  • Hormones
  • autonomic neurotransmitters
  • local metabolic conditions
  • stretch
  • spontaneous electrical activity in the plasma membrane

■ Most smooth muscle cells can generate action potentials in the plasma membrane upon membrane depolarization.

  • The rising phase of the smooth muscle action potential is due to the influx of calcium ions into the cell through voltage-gated Ca2+ channels.

■ Pacemaker potentials: spontaneously generated action potentials in the absence of any external input; occur in some smooth muscle cells

  • Slow waves are a pattern of spontaneous, periodic depolarizations of the membrane potential seen in some smooth muscle pacemaker cells, particularly in the gastrointestinal tract.

■ Smooth muscle cells do not have a specialized end-plate region.

■ Multiple smooth muscle cells may be influenced by neurotransmitters released from a single neuron ending, and a single smooth muscle cell may be influenced by neurotransmitters from more than one neuron.

■ Neurotransmitters may have either excitatory or inhibitory effects on smooth muscle contraction by increasing or decreasing cytosolic Ca2+.

■ Smooth muscles can be classified broadly as single-unit or multiunit smooth muscles.

  • single-unit: cells undergo pacemaker-linked synchronous activity because of gap junction connections; sensitive to stretch like that which occurs in expandable hollow organs such as the stomach
  • multiunit: each fiber responds independently due to few if any gap junctions linking them; richly innervated by autonomic nerves

Review Question: What is a pacemaker potential, and what effect does it have on a smooth muscle cell? In what ways does neural control of smooth muscle activity differ from that of skeletal muscle?

STUDY AND REVIEW 9.10

■ Cardiac muscle combines features of skeletal and smooth muscles including the following:

  • being striated
  • being composed of myofibrils with repeating sarcomeres
  • having troponin associated with its thin filaments
  • having T-tubules that conduct action potentials
  • having sarcoplasmic reticulum terminal cisternae that store Ca2+

■ Cells are arranged in layers around hollow cavities and connected by gap junctions at intercalated disks.

■ Cardiac muscle excitation–contraction coupling involves:

  • Entry of a small amount of Ca2+ through L-type Ca2+ channels triggers opening of ryanodine receptors that release a larger amount of Ca2+ from the sarcoplasmic reticulum.
  • Ca2+ activates the thin filament and cross-bridge cycling as in skeletal muscle

■ Cardiac contractions and action potentials are prolonged, tetany does not occur, and both the strength and frequency of contraction are modulated by autonomic neurotransmitters and hormones.

Review Question: Compare the mechanisms by which an increase in cytosolic Ca2+ concentration initiates contractile activity in skeletal, smooth, and cardiac muscle cells.