Skeletal Muscle Tissue

Lecture Presentation by Lori Garrett

Learning Outcomes 9.1 Describe the functions of skeletal muscle tissue. 9.2 Describe the organization of skeletal muscle at the tissue level. 9.3 Describe the structures of a sarcomere. 9.4 Describe the structures of a thin filament and a thick filament. 9.5 Describe a major characteristic of excitable membranes and its importance in generating an action potential.

Learning Outcomes (continued) 9.6 Identify the components of the neuromuscular junction, and summarize the events involved in the control of skeletal muscles by motor neurons. 9.7 Describe the role of ATP in a muscle contraction, and explain the steps involved in the contraction of a skeletal muscle fiber.

Muscle tissue—mostly muscle cells specialized for contraction. . 3 types: skeletal muscle, cardiac muscle, smooth muscle Skeletal muscle cell = muscle fiber Skeletal muscle . = an organ made of mostly skeletal muscle tissue, plus connective tissue, nerves, blood vessels . Directly/indirectly attached to bones (hence skeletal muscle)

Functions of skeletal muscle tissue 1. Produce body movement Muscle tendons pull and move bones 2. Maintain posture and body Stabilize joints position 3. Support soft tissues Surround, support, and shield internal structures, such as tissues and organs 4..Guard[Insert body fig_09_01A -L.jpgSphincters here] encircle openings; provide entrances/exits voluntary control of swallowing, defecation, and urination 5. Maintain body temperature Contraction uses energy; energy use generates heat 6. Store nutrients Muscle proteins can break down; release amino acids—can be used to synthesize glucose or provide energy

Comparison of muscle tissue types Skeletal muscle tissue . Voluntary control . Produce movement by pulling on bones

Cardiac muscle tissue . Involuntary . Only in heart . Pumps blood; circulating it in vessels

Comparison of muscle tissue types (continued) Smooth muscle tissue . Involuntary . Walls of hollow organs, small arteries

A. Name the three types of muscle tissue, identify where they are found, and list their functions. B. Which muscle types are voluntary, and which are involuntary?

Learning Outcome: Describe the functions of skeletal muscle tissue.

© 2018 Pearson Education, Inc. Module 9.2: Skeletal muscle contains muscle tissue, connective tissues, blood vessels, and nerves Structure of a skeletal muscle Skeletal muscle = organ Epimysium = dense sheath of collagen fibers around muscle . Separates muscle from other tissues/organs . Connected to deep fascia (dense connective tissue layer—module 4.15)

Muscle fascicle = bundle of muscle fibers Perimysium = fibrous layer dividing muscle into compartments . Separates muscle fascicles . Has collagen and elastic fibers; blood vessels and nerves supplying muscle fibers within the fascicle

Skeletal muscle fibers = individual muscle cells . Contain myofibrils = bundles of protein filaments Endomysium = thin layer of areolar connective tissue around each muscle fiber; has collagen and elastic fibers, blood vessels/nerves supplying muscle fibers Myosatellite cells = stem cells that help repair damaged muscle tissue

Ends of skeletal muscles: connective tissue layers (epimysium, perimysium, endomysium) merge to form a tendon or aponeurosis . Tendon—attaches muscle to specific point on a bone . Aponeurosis—broad sheet with broad attachment to bone(s) . Contracting muscle pulls on tendon or aponeurosis, which pulls on and moves the bone

Skeletal muscle development

Myoblasts = embryonic cells that fuse to form multinucleate cells that differentiate into skeletal muscle fibers. Some myoblasts remain free in endomysium as myosatellite cells that help repair damaged muscle tissue

The multinucleate cells differentiate into skeletal muscle fibers (cells) and start producing proteins for contraction Mature muscle cells are quite large compared to other cells . Diameters up to 100 µm . Length up to 30 cm (12 in.)

Multiple nuclei = more copies of genes for protein/enzyme production Special terms for skeletal muscle fibers: . Sarcolemma = plasma membrane . Sarcoplasm = cytoplasm

A. Define tendon and aponeurosis. B. Describe the connective tissue layers associated with skeletal muscle tissue. C. What special terms are used to describe the plasma membrane and cytoplasm of a skeletal muscle fiber? D. How would severing a tendon attached to a muscle affect movement of that limb? Learning Outcome: Describe the organization of skeletal muscle at the tissue level.

© 2018 Pearson Education, Inc. Module 9.3: Skeletal muscle fibers contain T tubules and sarco-plasmic reticula that surround contractile myofibrils made up of sarcomeres Myofibrils Myofibril = small cylindrical structures arranged parallel inside muscle fiber; run length of muscle fiber . Myofibril arrangement gives skeletal muscle appearance of having stripes (striations) . Many mitochondria along myofibrils

Myofilaments Myofilaments = bundles of protein filaments inside myofibrils . Thin filaments mostly composed of actin . Thick filaments mostly composed of myosin

Sarcomeres and striations Sarcomeres = repeating functional units of skeletal muscle fiber . ~10,000 sarcomeres/myofibril, each ~2 µm resting length . Striations: • Z lines • I band • A band • M line • H band

Z lines—Junction of adjacent sarcomeres; proteins (actinins) connect thin filaments of adjacent sarcomeres here I band—Lighter band with only thin filaments A band—Dark/dense region containing thick filaments Zone of overlap—Within A band; overlapping thick/thin filaments M line—Center of A band where adjacent thick filaments connect H band—Lighter region on each side of M line with only thick filaments; visible only in resting sarcomeres

Sarcolemma Sarcolemma = plasma membrane of a skeletal muscle fiber . Selective permeability allows uneven distribution of +/– charges Reversal of charge is 1st step leading to muscle contraction . Change in charge initiated by nerve cell (neuron) impulse and spreads across entire sarcolemma

Transverse tubules (T tubules) . Continuous with sarcolemma and extend into sarcoplasm . Form passageways through muscle fiber and encircle sarcomere

Sarcoplasmic reticulum . Similar to smooth endoplasmic reticulum of other cells . Enlarged sections (terminal cisternae) on either side of T tubule . Triad = pair of terminal cisternae and one T tubule

Sarcoplasmic reticulum (continued) . Sarcoplasmic reticulum (SR) stores calcium ions that are actively pumped in from cytosol • Calsequestrin = protein that binds calcium inside SR . Muscle contraction starts when stored calcium ions are released from SR into cytosol (via gated calcium channels)

A. Describe the structures of a sarcomere. B. Define transverse tubules. C. Within a resting skeletal muscle fiber, where is the greatest concentration of Ca2+?

Learning Outcome: Describe the structures of a sarcomere.

Structure of thin filaments . Attached to Z lines with actinin . Composed of 4 main proteins: 1. F-actin 2. Nebulin 3. Tropomyosin 4. Troponin

Structure of thin filaments (continued) 1. F-actin (filamentous)—twisted double-strand of G-actin • G-actin molecules each have active site for binding myosin 2. Nebulin—holds two strands of G-actin molecules together

Structure of thin filaments (continued) 3. Tropomyosin—double-stranded protein wrapped around F-actin • Blocks myosin binding sites on G-actin molecules • Prevents actin/myosin interaction 4. Troponin—made of 3 subunits • Attached to tropomyosin; = troponin-tropomyosin complex • Also attached to G-actin and has binding sites for Ca2+

Structure of thick filaments . Contain ~ 300 myosin molecules • Core of titin—connects thick filaments to Z lines; recoils after stretching . Myosin molecule composed of two twisted myosin subunits • Tails face M line; free heads face out toward thin filaments

Structure of thick filaments (continued) . Myosin molecule composed of two twisted myosin subunits • Free head—two globular subunits; forms cross- bridge with actin during contraction • Connection between head/tail acts like hinge and pivots

Sliding filament theory of muscle contraction . When muscles contract, thin filaments slide over thick filaments • H and I bands get smaller; zones of overlap get larger • Z lines move closer together, but A bandwidth is unchanged . Sliding occurs in all sarcomeres in each myofibril . As myofibrils shorten, so does the muscle fiber (contraction)

A. Compare F-actin with G-actin. B. Name the proteins that make up a thick filament. C. Summarize the sliding filament theory. D. Why is the zone of overlap an important region of the sarcomere?

Learning Outcome: Describe the structures of a thin filament and a thick filament.

© 2018 Pearson Education, Inc. Module 9.5: Skeletal muscle fibers and neurons have excitable plasma membranes that produce and carry electrical impulses called action potentials Membrane potentials . All cells in the body are polarized • Positive and negative charges unequally distributed on either side of plasma membrane – Inside of cell slightly negative compared to outside • Unequal distribution represents potential difference, referred to as membrane potential – Measured in millivolts (mV) – Neurons have resting membrane potentials of about –70 mV – Skeletal muscle fibers resting potentials of about –85 mV

Plasma membranes are selectively permeable . Cytosol and extracellular fluid (ECF)—different compositions . Positive charges: • More Na+ outside (ECF) • More K+ inside (cytosol) . Negative charges: • Mostly proteins inside cell; cannot cross plasma membrane • More Cl– in ECF but not much diffuses across (small impact)

Movement of sodium and potassium . Leak channels—allow constant slow flow of Na+ and K+ down their concentration gradients: Na+ enters, K+ leaves . Sodium–potassium ion pumps—export 3 Na+ and import 2 K+ • Uneven distribution maintains resting membrane potential

5 steps in an action potential 1. Small increase in membrane permeability to Na+ • Na+ entering cell moves membrane potential in positive direction to threshold (–55 mV) 2. Voltage-gated Na+ channels open • Huge rush of positive Na+ ions into cell • = depolarization—change of membrane potential to positive 3. Membrane potential reaches +30 mV • Voltage-gated Na+ channels close • Voltage-gated K+ channels open and K+ leaves cell • = repolarization—membrane potential returns to polarized state © 2018 Pearson Education, Inc. Module 9.5: Excitable plasma membranes

5 steps in an action potential (continued) 4. Repolarization continues to resting membrane potential 5. Membrane potential stabilizes • Voltage-gated K+ channels close at resting potential • Na+/K+ pump restores original distribution of Na+ and K+ • Refractory period = time needed to original distribution – Membrane cannot respond to another stimulus until after refractory period

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Action potential propagation . Neurons and skeletal muscle fibers have electrically excitable membranes . Depolarization/repolarization sequence produces action potential (electrical impulse) • Propagated (spread) along plasma membrane • Generated in less than 2 msec • Travels in only one direction due to refractory period • Allows rapid communication

A. Explain the function of sodium–potassium ion pumps. B. Define depolarization, and describe the events that follow it. C. What is the general function of an excitable membrane? D. Explain why the propagation of action potentials along electrically excitable membranes occurs in only one direction. Learning Outcome: Describe a major characteristic of excitable membranes and its importance in generating an action potential.

Neuromuscular junction (NMJ) . = Location where motor neuron controls a skeletal muscle fiber . One NMJ per muscle fiber, but each motor neuron may branch and control multiple muscle fibers

Neuromuscular junction components 1. Axon terminal (synaptic terminal) of motor neuron • Has vesicles with acetylcholine (ACh)

Neuromuscular junction components (continued) 2. Motor end plate of muscle fiber • Has junctional folds (creases) that increase # of ACh receptors • Contains acetylcholinesterase (AChE); breaks down ACh

Neuromuscular junction components (continued) 3. Synaptic cleft = space between axon terminal and motor end plate

Activities at neuromuscular junction 1. Electrical impulse (action potential) arrives at axon terminal • Change in membrane permeability causes ACh vesicles to fuse with neuron plasma membrane • ACh released (exocytosis)

Activities at the neuromuscular junction (continued) 2. ACh diffuses across synaptic cleft • Binds ACh-receptor membrane channels at motor end plate • Changes sarcolemma Na+ permeability • Na+ enters muscle fiber sarcoplasm

Activities at the neuromuscular junction (continued) 3. Na+ influx generates action potential in sarcolemma • ACh diffuses away or breaks down (AChE) • ACh-receptor membrane channels close

Activities at the neuromuscular junction (continued) 4. Action potential (AP) generated at motor end plate immediately spreads across entire sarcolemma • Brief event—ACh was cleared from receptors; no other stimulus occurs until another AP occurs

Activities at the neuromuscular junction (continued) 5. Action potential moves down T tubules between terminal cisternae of sarcoplasmic reticulum (SR) • Changes permeability of SR

Activities at the neuromuscular junction (continued) 6. SR releases stored Ca2+ into sarcomeres; begins contraction = excitation-contraction coupling— excitation (action potential) is coupled with contraction (sliding filaments shorten sarcomeres)

A. Describe the neuromuscular junction. B. How would a drug that blocks acetylcholine release affect muscle contraction? C. What would happen if there were no AChE in the synaptic cleft?

Learning Outcome: Identify the components of the neuromuscular junction, and summarize the events involved in the control of skeletal muscles by motor neurons.

© 2018 Pearson Education, Inc. Module 9.7: A muscle fiber contraction uses ATP in a cycle that repeats during the contraction Steps of a muscle fiber contraction cycle 1. Resting sarcomere: • Myosin heads are all “energized” and “cocked” • Cocking head requires breakdown of ATP – Myosin head acts as ATPase; ADP and P stay attached to head

Contraction cycle (continued) 2. Contraction cycle begins • Calcium ions arrive from SR

3. Active sites exposed • Calcium binds to troponin • Troponin changes position, moves tropomyosin and exposes active sites on actin

Contraction cycle (continued) 4. Cross-bridges form • Myosin heads bind to exposed active sites on actin • Forms cross-bridges

5. Myosin heads pivot • Cross-bridge formation causes myosin heads to pivot toward M line (center of sarcomere • = power stroke • ADP and P release

Contraction cycle (continued) 6. Cross-bridges detach • A new ATP attaches to each myosin head, myosin releases from actin • Active site available to form another cross-bridge

7. Myosin reactivates • Free myosin head splits ATP into ADP and phosphate • Released energy used to “recock” myosin head

Contraction cycle (continued) . Cycle repeats while Ca2+ is high and ATP is available • Calcium levels stay high only if action potentials continue . When stimulus ends: • SR calcium channels close • Calcium ion pumps return Ca2+ into terminal cisternae (SR) • Troponin–tropomyosin complex resumes original position, covering active sites, blocking new cross- bridge formation

A. What molecule supplies the energy for a muscle fiber contraction? B. List the interrelated steps that occur once the contraction cycle begins.

Learning Outcome: Describe the role of ATP in a muscle contraction, and explain the steps involved in the contraction of a skeletal muscle fiber.

Learning Outcomes 9.8 Describe how muscle tension develops with respect to neural control and excitation-contraction coupling. 9.9 Describe the mechanism responsible for tension production in a muscle fiber, and discuss the factors that determine the peak tension developed during a contraction.

Learning Outcomes (continued) 9.10 Discuss the factors that affect peak tension production during the contraction of an entire skeletal muscle, and explain the significance of the motor unit in this process. 9.11 Compare the different types of muscle contractions. 9.12 Describe the processes by which muscle fibers obtain the energy to power contractions.

Learning Outcomes (continued) 9.13 Describe the factors that contribute to muscle fatigue, and discuss the processes involved in the muscle’s subsequent recovery. 9.14 Relate the types of muscle fibers to muscle performance. 9.15 Clinical Module: Explain the physiological factors responsible for muscle hypertrophy, atrophy, and paralysis.

© 2018 Pearson Education, Inc. Module 9.8: Muscle tension develops from the events that occur during excitation-contraction coupling Excitation-contraction coupling = link between generation of action potential in sarcolemma and start of muscle contraction Steps: 1. Neural control 2. Excitation 3. Calcium ion release 4. Contraction cycle begins 5. Sarcomeres shorten 6. Muscle tension produced

1. Neural control . Action potential in motor neuron starts process at neuromuscular junction

2. Excitation . Action potential causes ACh release from motor neuron . Leads to excitation (action potential) in sarcolemma

3. Calcium ion release . Muscle fiber action potential travels through T tubules/triads . Triggers release of stored Ca2+

4. Contraction cycle begins . Ca2+ binds troponin . Exposes active sites on actin . Cross-bridges form; continues while ATP/Ca2+ available and action potentials generated at neuromuscular junction

5. Sarcomeres shorten . Thick and thin filaments interact (sliding filaments) . Shortens sarcomeres, pulls ends of muscle fiber closer

6. Muscle tension produced . Muscle fiber shortening causes entire muscle to shorten . Muscle contraction produces a pull or tension on tendons

A. What causes calcium to be released from the sarcoplasmic reticulum?

Learning Outcome: Describe how muscle tension develops with respect to neural control and excitation-contraction coupling.

How sarcomere length affects tension . Muscle fiber either “on” (producing tension) or “off” (relaxed) • Optimal resting length of a sarcomere – Maximum number of cross-bridges can form – Produces most tension – Normal range of sarcomere length between 75 and 130 percent of optimal length – Muscle arrangement, connective tissues, and bones usually prevent too much stretching or compression

Muscle twitch = single stimulus-contraction- relaxation sequence in a muscle fiber . Duration varies by muscle type, location, environmental factors . Fasciculation = involuntary “muscle twitch” under skin • From contraction of motor unit (group of muscle fibers controlled by single motor neuron) . Myogram = shows development of muscle tension

Phases of a muscle twitch 1. Latent period • Action potential stimulates sarcolemma • Calcium released from sarcoplasmic reticulum • No tension yet 2. Contraction phase • Calcium binds to troponin • Cross-bridge cycling • Start of tension development to peak tension

Phases of a muscle twitch (continued) 3. Relaxation phase • Calcium drops; cross-bridges detach; active sites covered • Tension returns to resting levels • From peak tension to end of twitch (about 25 msec)

A. What sarcomere characteristic affects the amount of tension produced when a skeletal muscle fiber contracts? B. Explain two key concepts of the sarcomere length–tension relationship. C. Describe the events that occur during each phase of a twitch in a stimulated muscle fiber.

Learning Outcome: Describe the mechanism responsible for tension production in a muscle fiber, and discuss the factors that determine the peak tension developed during a contraction.

© 2018 Pearson Education, Inc. Module 9.10: The peak tension developed by a skeletal muscle depends on the frequency of stimulation and the number of muscle fibers stimulated Tension produced by a skeletal muscle determined by: 1. Amount of tension produced by each muscle fiber 2. Number of muscle fibers stimulated

Stimulation frequency affects tension in single muscle fiber . Four levels of muscle tension 1. Treppe 2. Wave summation 3. Incomplete tetanus 4. Complete tetanus

Treppe (German for staircase) . Stimulation of muscle fiber immediately after relaxation phase produces increasing maximum tension . Most skeletal muscles do not demonstrate treppe

Wave summation . Addition of one twitch to another . Stimulation of muscle fiber before relaxation phase ends produces increasing maximum tension . Duration of twitch determines maximum time available to produce wave summation

Incomplete tetanus (tetanos, convulsive tension) . Rapid cycle of contraction/relaxation producing near-peak tension . Still shows some period of relaxation, so incomplete tetanus

Complete tetanus . Higher stimulation frequency eliminates relaxation phase . No calcium ions return to sarcoplasmic reticulum . Results in peak tension and continuous contraction . Seldom occurs in normally functioning muscles

Motor units and recruitment Number of stimulated muscle fibers affects muscle tension Motor unit = single motor neuron and all muscle fibers it controls . Size varies; fewer fibers per neuron gives more precise control . Motor units intermingle

Motor unit recruitment = activation of more motor units to produce more tension . Smaller motor units activated first, then larger motor units with faster/more powerful fibers . Smooth, steady increase in muscle tension Asynchronous motor unit summation . Motor units activated on rotating basis to maintain sustained contraction

Muscle tone = resting tension in a skeletal muscle . Variable number of motor units always active to produce low-level tension (not movement) . Subconscious regulation . Activated muscle fibers use energy, so increased muscle tone raises energy consumption—higher “resting” metabolism

A. Compare incomplete tetanus with wave summation. B. Define motor unit. C. Describe the relationship between the number of fibers in a motor unit and the precision of body movements.

Learning Outcome: Discuss the factors that affect peak tension production during the contraction of an entire skeletal muscle, and explain the significance of the motor unit in this process.

© 2018 Pearson Education, Inc. Module 9.11: Muscle contractions may be isotonic or isometric; isotonic contractions may be concentric or eccentric Isotonic contractions . Isotonic contraction (iso-, equal + tonos, tension) • Tension rises and skeletal muscle length changes • Examples: lifting an object, walking, running . Two types of isotonic contractions 1. Concentric contraction 2. Eccentric contraction

Concentric contraction . Muscle tension rises until exceeds load . As muscle shortens, tension remains constant (isotonic) . Example: flexing elbow while holding a dumbbell . Speed of contraction inversely related to load

Eccentric contraction . Peak tension produced is less than the load . Muscle lengthens (elongates) . Example: returning dumbbell from flexed position to extended . Rate of elongation varies with difference between tension/load

Eccentric contraction (continued) . When contraction ends, load stretches muscle until: • Muscle tears • Tendon breaks • Elastic recoil opposes load

. Muscle length does not change . Tension never exceeds load . Contracting muscle bulges but not as much as during isotonic contraction . Example: postural muscle contractions

A. Explain the relationship between load and speed of muscle contraction. B. Compare concentric and eccentric contractions. C. Can a skeletal muscle contract without shortening? Why or why not?

Learning Outcome: Compare the different types of muscle contractions.

© 2018 Pearson Education, Inc. Module 9.12: Muscle contraction requires large amounts of ATP that may be produced anaerobically or aerobically Sources of ATP in muscles 1. Glycolysis—anaerobic breakdown of glucose to pyruvate • Occurs in cytosol • Anaerobic means oxygen is not required • Produces 2 ATP and 2 pyruvate molecules for each glucose

Sources of ATP in muscles (continued) 2. Aerobic metabolism • Provides 95 percent of ATP demands of resting cell • Occurs in mitochondria • Most ATP comes from electron transport chain activity • Produces 15 ATP for each pyruvate

Energy reserves in a typical skeletal muscle fiber 1. Most energy stored as glycogen—up to 1.5% muscle weight 2. Free ATP • Minimal; supports only ~10 muscle twitches 3. Creatine phosphate (CP) • Supplies energy for about 15 seconds • Creatine (C) assembled from amino acids 4. Glycolysis—anaerobic metabolism 5. Aerobic metabolism

Muscle metabolism at rest . Low ATP demand . Mitochondria produce surplus ATP . Fatty acids and glucose absorbed from bloodstream • Make ATP to convert creatine to creatine phosphate and glucose to glycogen

Muscle metabolism at moderate activity levels . ATP demand increases . Relies on aerobic metabolism of pyruvate (from glycolysis) to make ATP . Increased consumption of oxygen . No fatigue until glycogen, lipid, amino acid reserves exhausted

Muscle metabolism at peak activity levels . Enormous ATP demands . Mitochondria at maximum production provides ~1/3 ATP needs . Rest produced by glycolysis • Excess pyruvate converts to lactate • Lactate and H+ increase, drops pH (lactic acidosis); causes muscle fatigue

A. What basic reactants do mitochondria absorb from the cytosol to synthesize ATP? B. Identify three sources of stored energy utilized by muscle fibers. C. When do muscle fibers produce lactate?

Learning Outcome: Describe the processes by which muscle fibers obtain the energy to power contractions.

Fatigue = muscle can no longer perform at required level . Major factor is decreased pH • Decreases calcium/troponin binding • Alters enzyme activities Recovery period = time needed to return conditions in muscle fibers to preexertion levels—may take several hours, up to a week

ATP production when oxygen is insufficient: . Glycolysis alone produces ATP (anaerobic) • Faster than aerobic metabolism, but only goes until glycogen reserves are depleted (1–2 min) • Less efficient than aerobic • Lowers pH (lactic acid produced) • Elevates body temperature; increases sweating

Recovery period . Oxygen now available . Lactate converted back to pyruvate • Pyruvate makes ATP (mitochondria) or recycled to glucose/glycogen . Most ATP production through aerobic metabolism • More efficient than glycolysis – Aerobic captures ~42 percent of energy released – Glycolysis only 4–6 percent . Heat produced—70–80 percent body heat produced by resting skeletal muscles

Cori cycle = shuttling of lactate to liver, glucose back to muscles . Most lactate produced during peak activity goes to liver . Liver converts lactate to glucose; releases back to blood

Oxygen debt (excess postexercise oxygen consumption, EPOC) . = amount of oxygen required to restore normal, preexertion conditions. . In muscles to restore ATP, creatine phosphate, glycogen levels . In liver to produce ATP to convert excess lactate to glucose

The Cori cycle . During peak activity: 1. Lactate diffuses out of muscles into blood 2. Liver converts lactate to pyruvate

The Cori cycle (continued) . During recovery period: 1. Liver continues converting lactate to pyruvate 2. 30 percent of pyruvate used to make ATP in mitochondria 3. ATP then used to convert remaining pyruvate to glucose 4. Glucose returns to muscle cells to rebuild glycogen reserves

A. How is skeletal muscle recovery different after moderate activity compared to sustained activity at higher levels? B. Define oxygen debt (excess postexercise oxygen consumption). C. What happens to the lactate produced by skeletal muscle during peak activity?

Learning Outcome: Describe the factors that contribute to muscle fatigue, and discuss the processes involved in the muscle’s subsequent recovery.

© 2018 Pearson Education, Inc. Module 9.14: Fast, slow, and intermediate skeletal muscle fibers differ in size, internal structure, metabolism, and resistance to fatigue Three major types of skeletal muscle fibers 1. Fast fibers 2. Slow fibers 3. Intermediate fibers

Fast fibers—Reach peak tension in <0.01 sec . Large in diameter; densely packed myofibrils, large glycogen reserves, few mitochondria . Powerful contractions . Fatigue rapidly (most ATP produced anaerobically)

Slow fibers—take 3× longer to contract than fast fibers . Half diameter of fast fibers . Longer sustained contractions . Mostly aerobic ATP production—more oxygen • Extensive capillary network • Myoglobin pigment (binds O2) . Appear dark red (myoglobin/blood)

Transmission electron micrograph (longitudinal section) showing a fast fiber (W, white) and a slow fiber (R, red) have different sizes and densities. Slow fibers have more mitochondria (M) and an extensive capillary supply.

Intermediate fibers . More closely resemble fast fibers—little myoglobin; pale . More capillaries and more fatigue-resistant than fast fibers

Most muscles have a mixture of fiber types . Mix reflects function—back/calf dominated by slow, eye/hand may only have fast . Percentages of fast vs. slow is genetically determined . Percentage of intermediate-to-fast can be modified with athletic training

A. Contrast fast fibers with slow fibers in terms of diameter, glycogen reserves, myoglobin content, and relative abundance of mitochondria. B. Why would a sprinter experience muscle fatigue before a marathon runner would? C. Which type of muscle fiber predominates in leg muscles of endurance athletes, such as long- distance runners?

Learning Outcome: Relate the types of muscle fibers to muscle performance.

Hypertrophy = muscle enlargement . From repeated exhaustive stimulation . Size increase due to: • More mitochondria • More glycogen/glycolytic enzyme • More/wider myofibrils (stronger) • More myofilaments • Steroid hormones

Atrophy = decreased muscle size, tone, and power . From decreased stimulation • Normal aging • Paralysis/nervous system damage • Reduced use (cast after fracture) . Initially reversible; if prolonged muscle fibers can die and not be replaced

Muscular dystrophy . Several different muscular dystrophies—inherited diseases that produce muscular weakness/deterioration . Most common/understood are Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) • Childhood-onset, male only • Death usually from respiratory paralysis • Sex-linked gene, carried by female

Polio—virus attacks CNS motor neurons causing atrophy and paralysis (loss of voluntary movement)

Tetanus—toxin from bacteria (Clostridium tetani) suppresses mechanism that inhibits motor neuron activity; causes sustained, powerful muscle contractions . Thrives in low-oxygen areas (puncture wounds) . If severe—40–60 percent mortality, U.S. deaths rare (immunizations)

Botulism—toxins from bacteria (Clostridium botulinum); blocks ACh release at neuromuscular junctions . Paralysis of skeletal muscle . Acquired through bacteria-contaminated food

Myasthenia gravis—autoimmune disease causing loss of Ach receptors at neuromuscular junctions . Results in progressive muscular weakness

Rigor mortis—generalized muscle contraction shortly after death . Begins with small muscles of face, neck, arms . Depletion of ATP leaves calcium in sarcoplasm triggering sustained contraction . Myosin cross-bridges cannot detach from active sites . Ends 1–6 days later as muscle tissue decomposes

A. Define muscle hypertrophy and muscle atrophy. B. Explain how the flexibility or rigidity of a dead body can provide a clue about a murder victim’s time of death. C. Six weeks after Fred broke his leg, the cast is removed. As he steps down from the exam table, his leg gives way and he falls. Propose a logical explanation.

Learning Outcome: Explain the physiological factors responsible for muscle hypertrophy, atrophy, and paralysis.