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Chapter 11 Muscle Tissue Types and Characteristics of Muscular Tissue The Nerve-Muscle Relationship Behavior of Skeletal Muscle Fibers Behavior of Whole Muscles – PowerPoint PPT presentation

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Title: Chapter%2011%20Muscle%20Tissue

Chapter 11 Muscle Tissue
  • Types and Characteristics of Muscular Tissue
  • The Nerve-Muscle Relationship
  • Behavior of Skeletal Muscle Fibers
  • Behavior of Whole Muscles
  • Muscle Metabolism
  • Cardiac and Smooth Muscle

  • Relate the form to the function of the molecular
    components of muscles.
  • Identify 3 types of muscle cells from pictures
  • Explain the mechanisms of contraction
  • Describe genetic components of muscle growth
  • Describe aspects of Muscular Dystrophy
  • Pump you up

Monster Cows Belgian Blue Cattle
Dissections comparing normal, heterozygous and
homozygous mice
  • A growth factor (hormone) that surpresses muscle
  • Slows down development of muscle stem cells
  • In 2002, researchers at the University of
    Pennsylvania showed that monoclonal antibody
    specific to myostatin improves the condition of
    mice with muscular dystrophy, presumably by
    blocking myostatin's action.

Muscular Dystrophy
  • Group of hereditary diseases in which skeletal
    muscles degenerate are replaced with adipose
  • Etiology Mainly a disease of males
  • What types of genetic diseases are primarily
    found in males?
  • Sex linked, This is a gene on the X Chromosome.
  • appears as child begins to walk
  • Normal allele makes dystrophin, a protein that
    links actin filaments to cell membrane
  • absence of dystrophin leads to torn cell membranes

Muscular Dystrophy Pedigree
  • XM normal
  • Xm MD
  • Y- no allele
  • What is the genotype of
  • Individauals
  • A
  • B
  • C
  • D
  • Who is a carrier?

Duchenne's Muscular Dystrophy
  • Prevalence estimated pop. of people who are
    managing it at any given time.
  • USA 43,000
  • Incedence the annual diagnosis rate/ number of
    new cases diagnosed each year.
  • About 1 in 3,000
  • Prognosis No know cures, only treatments to
    alleviate suffering and control the rate.

Group of kids with Muscular Dystrophy
Introduction to Muscle
  • Movement is a fundamental characteristics of all
    living things
  • Cells capable of shortening transducing the
    chemical energy of ATP into mechanical energy
  • Types of muscle
  • skeletal
  • cardiac
  • smooth
  • Physiology of skeletal muscle
  • basis of warm-up, strength, endurance fatigue

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Smooth Muscle
  • Cells spindle shaped
  • Uninucleated

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Cardiac Cells
  • Shorter and thicker than skeletal
  • Can keep their own beat, because of nearby
    pacemaker cells

Universal Characteristics of Muscle
  • Responsiveness (excitability)
  • capable of response to chemical signals, stretch
    or other signals responding with electrical
    changes across the plasma membrane
  • Conductivity
  • local electrical change triggers a wave of
    excitation that travels along the muscle fiber
  • Contractility -- shortens when stimulated
  • Extensibility -- capable of being stretched
  • Elasticity -- returns to its original resting
    length after being stretched

Skeletal Muscle
  • Voluntary striated muscle attached to bones
  • Muscle fibers (myofibers) as long as 30 cm
  • Exhibits alternating light and dark transverse
    bands or striations
  • reflects overlapping arrangement of internal
    contractile proteins
  • Under conscious control

Connective Tissue Elements of Muscle
  • Found between muscle fiber and bone or other
  • endomysium, perimysium, epimysium, fascia, tendon
  • Not excitable or contractile, but are somewhat
    extensible elastic
  • stretches slightly under tension and recoils when
  • Called series-elastic components
  • are connected to each other in linear series
  • help return muscles to their resting lengths
  • adds significantly to power output and efficiency
    of muscles

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The Muscle Fiber
Why Multinucleation?
  • Physically You need a long tube
  • Problems of regulation Takes fewer neurons to
    synchronize fewer, larger cells
  • Multinucleation overcomes problems of diffusion
    because incoming chemicals can always find a
    control center.

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Muscle Fibers (Form follows Function)
  • Multiple flattened nuclei against inside of
    plasma membrane
  • due to fusion of multiple myoblasts during
  • unfused satellite cells nearby can multiply to
    produce a small number of new myofibers
  • Sarcolemma has tunnel-like infoldings or
    transverse (T) tubules that penetrate the cell
  • carry electric current to cell interior
  • Sarcoplasm is filled with
  • myofibrils (bundles of parallel protein
    microfilaments called myofilaments)
  • glycogen for stored energy myoglobin binding
  • Sarcoplasmic reticulum is series of
    interconnected, dilated, calcium storage sacs
    called terminal cisternae

Thick Filaments
  • Made of 200 to 500 myosin molecules
  • 2 entwined polypeptides (golf clubs)
  • Arranged in a bundle with heads (cross bridges)
    directed outward in a spiral array around the
    bundled tails
  • central area is a bare zone with no heads

Thin Filaments
  • Two intertwined strands of fibrous (F) actin
  • each subunit is a globular (G) actin with an
    active site
  • Groove holds tropomyosin molecules, each blocking
    the active sites of 6 or 7 G actins
  • One small, calcium-binding troponin molecule
    stuck to each tropomyosin molecule

Elastic Filaments
  • Huge springy protein called titin (connectin)
  • runs through core of each thick filament
  • connects thick filament to Z disc structure
  • Functions
  • keep thick thin filaments aligned with each
  • resist overstretching
  • help the cell recoil to its resting length

Regulatory Contractile Proteins
  • Myosin actin are contractile proteins (they do
  • Tropomyosin troponin are regulatory proteins
  • act like a switch that starts stops shortening
    of muscle cell
  • the release of calcium into sarcoplasm and its
    binding to troponin, activates contraction
  • troponin moves the tropomyosin off the actin
    active sites

Overlap of Thick Thin Filaments
Striations Organization of Filaments
  • Dark A bands (regions) alternating with lighter I
    bands (regions)
  • anisotrophic (A) and isotropic (I) stand for the
    way these regions affect polarized light
  • A band is thick filament region
  • lighter, central H band area contains no thin
  • I band is thin filament region
  • bisected by Z disc protein called connectin,
    anchoring elastic thin filaments
  • from one Z disc (Z line) to the next is a

Striations and Sarcomeres
Relaxed versus Contracted Sarcomere
  • Muscle cells shorten because their individual
    sarcomeres shorten
  • pulling Z discs closer together
  • pulls on sarcolemma
  • Notice neither thick nor thick filaments change
    length during shortening
  • Their overlap changes as sarcomeres shorten

Skeletal muscles contract according to the
sliding-filament model An action potential
reaches the axon of the motor neuron. The action
potential activates voltage gated calcium ion
channels on the axon, and calcium rushes in. The
calcium causes acetylcholine vesicles in the axon
to fuse with the membrane, releasing the
acetylcholine into the cleft between the axon and
the motor end plate of the muscle fiber. The
acetylcholine diffuses across the cleft and binds
to nicotinic receptors on the motor end plate,
opening channels in the membrane for sodium and
potassium. Sodium rushes in, and potassium rushes
out. However, because sodium is more permeable,
the muscle fiber membrane becomes more positively
charged, triggering an action potential. The
action potential spreads through the muscle
fiber's network of T tubules, depolarizing the
inner portion of the muscle fiber. The
depolarization activates voltage-gated calcium
channels in the T tubule membrane, which are in
close proximity to calcium-release channels in
the adjacent sarcoplasmic reticulum. Activated
voltage-gated calcium channels physically
interact with calcium-release channels to
activate them, causing the sarcoplasmic reticulum
to release calcium. The calcium binds to the
troponin C present on the thin filaments of the
myofibrils. The troponin then allosterically
modulates the tropomyosin. Normally the
tropomyosin sterically obstructs binding sites
for myosin on the thin filament once calcium
binds to the troponin C and causes an allosteric
change in the troponin protein troponin T allows
tropomyosin to move, unblocking the binding
sites. Myosin (which is bound to ADP and is in a
ready state) binds to the newly uncovered binding
sites on the thin filament. It then releases ADP
and an inorganic phosphate and delivers a power
stroke. Myosin is now bound to actin in the
strong binding state. ATP binds myosin, allowing
it to release actin and be in the weak binding
state. (A lack of ATP makes this step impossible,
resulting in rigor mortis.) The myosin then
hydrolyzes the ATP and uses the enery to move
into the "cocked back" state while releasing ADP
and inorganic phosphate. Steps 7 and 8 repeat as
long as ATP is available and calcium is present
on thin filament. All the while, the calcium is
actively pumped back into the sarcoplasmic
reticulum. When calcium is no longer present on
the thin filament, the tropomyosin changes
conformation back to its previous state so as to
block the binding sites again. The myosin ceases
binding to the thin filament, and the
contractions cease. The calcium ions leave the
troponin molecule in order to maintain the
calcium ion concentration in the sarcoplasm. The
active pumping of calcium ions into the
sarcoplasmic reticulum creates a deficiency in
the fluid around the myofibrils. This causes the
removal of calcium ions from the troponin. Thus
the tropomyosin-troponin complex again covers the
binding sites on the actin fiaments and
contraction ceases.
Why warm up?
  • Release of Adrenalin
  • makes blood vessels dialate,
  • delivering more oxygen.
  • Increased temperature
  • benefits
  • More viscous blood
  • Faster enzyme action
  • Hemoglobin delivers oxygen faster
  • Psychological benefit
  • Example New Zealand Rugby team, The All Blacks
    perform a Maori war dance (Haka) as part of their
    warm up

What do you mean by stronger?
  • determined both genetically functionally
  • based upon how fast they can produce a
    contractile twitch
  • every muscle composed of varying composition of
    two types
  • Type I, slow twitch, Dark meat, endurance
  • Type II, fast twitch, Light meat, speed

TYPE I - SLOW TWITCH    Tonic muscles (red) - Leg muscles TYPE II - (IIa IIx) FAST TWITCH    Tetanic muscles (white) - Pectoral muscles
slower contraction times (100-110 msec) faster contraction times (50 msec)
contain myoglobin (red) no myoglobin (white)
continuous use muscles - prolonged performance     for endurance performance ( marathoners) one time use muscles - brief performances      for power speed (sprinters) 
marathoner 80 type I      20 type II sprinter 20 type I    80 type II 
                      Distribution of Slow Fast Twitch muscle in Humans                      down                       Distribution of Slow Fast Twitch muscle in Humans                      down
best in long slow sustained contractions best in rapid (short) contractions 
not easily fatigued easily fatigued
more capillary beds, greater VO2 max  less capillary beds
smaller in size larger in size
lower glycogen content higher glycogen content
poor anaerobic glycolysis   predominantly anaerobic glycolysis     easily converts glycogen to lactate  wo O2
  predominant aerobic enzymes metabolism some aerobic capacity
higher fat content lower fat content 
more mitochondria - Beta Oxidation high fewer mitochondria- Beta Oxidation low
poorly formed sarcoplasmic reticulum well formed sacroplasmic reticulum
slower release of Ca slower contractions quick release of Ca rapid contractions 
tropinin has lower affinity for Ca troponin - higher affinity for Ca
  • Mark Allen first male to win 5 consecutive Iron
    Man Triathlons
  • Held in Hawaii
  • Excellent example of high percentage of slow
    twitch Type I dark meat
  • Like birds or sea going mammals have.

Carl Lewis
  • Ran 100 m in 9.86s
  • 1991 world record
  • Jumps over cars
  • 9 Gold Medals
  • Excellent example of Type II fast twitch muscle
  • Also a vegan
  • Outspoken, even damning of those who used
    performance enhancers.
  • Like Ben Johnson

Ben Johnson
  • Between 1968 and 1983 the 100m record was shaved
    by 0.04s
  • In one year Johnson beat it by 0.16s
  • 1988 Seoul Olympics
  • Johnson 9.76 s
  • 27 mph
  • 45 strides
  • Ahead the whole time
  • Lewis sets an American record with 9.92s, but
    still second
  • Busted for doping

Back to Carl Lewis
  • Johnsons medal revoked and given to Lewis
  • 5 years later in 2003 Lewis admits he was busted
    3 times in 1988 for banned stimulants.
  • He thought they were herbal supplements
  • The U.S. Olympic committee found his ingestion to
    be, inadvertant
  • Since it was after the 3 year statute of
    limitations he could keep his medals
  • Stimulants could have masked more serious
    steroids from tests
  • Johnson beating Lewis in 88

Which leads to the question how do steroids work?
  • Androgenic increasing masculine traits
  • Anabolic building muscles as opposed to
  • Catabolic breaking down nutrients

Jason Giambi
Barry Bonds
Sammy Sosa
Mark McGwire
  • Testosterone best known natural steroid
  • Gets to cell, gets into cell, changed to DHT
    (Dihydrotestsoterone), DHT goes into Nucleus,
    binds to DNA and starts transcriptional
    activities to build more muscle mass.
  • Side effects include decreased sexual function,
    baldness, acne and Gynecomastia

Warm-up Strength Endurance Fatigue
Nerve-Muscle Relationships
  • Skeletal muscle must be stimulated by a nerve or
    it will not contract (paralyzed)
  • Cell bodies of somatic motor neurons are in
    brainstem or spinal cord
  • Axons of somatic motor neurons are called somatic
    motor fibers
  • each branches, on average, into 200 terminal
    branches that supply one muscle fiber each
  • Each motor neuron and all the muscle fibers it
    innervates are called a motor unit

Motor Units
  • A motor neuron the muscle fibers it innervates
  • dispersed throughout the muscle
  • when contract together causes weak contraction
    over wide area
  • provides ability to sustain long-term contraction
    as motor units take turns resting (postural
  • Fine control
  • small motor units contain as few as 20 muscle
    fibers per nerve fiber
  • eye muscles
  • Strength control
  • gastrocnemius muscle has 1000 fibers per nerve

Neuromuscular Junctions (Synapse)
  • region where a nerve fiber makes a functional
    connection with its target cell (NMJ)
  • Neurotransmitter (acetylcholine/ACh) released
    from nerve fiber causes stimulation of muscle
  • Components of synapse
  • synaptic knob is swollen end of nerve fiber
    (contains ACh)
  • motor end plate is specialized region of muscle
    cell surface
  • has ACh receptors on junctional folds which bind
    ACh released from nerve
  • acetylcholinesterase is enzyme that breaks down
    ACh causes relaxation
  • synaptic cleft tiny gap between nerve and
    muscle cells
  • schwann cell envelopes isolates NMJ

The Neuromuscular Junction
  • Poisoning by bacteria
  • Clostridium botulinum
  • Gets in through spoiled food
  • releases most potent neurotoxin known
  • Botulin, brand name Botox
  • It prevents neurons from releasing Ach
  • Muscles exhibit flaccid paralysis
  • lethal dose of about 200-300 pg/kg, meaning that
    somewhat over a hundred grams could kill every
    human living on the earth (for perspective, the
    rat poison Strychnine, often described as highly
    toxic, has an LD50 of 1 mg/kg, or 1 billion
  • Symptoms start with double vision as eye muscles
  • Ronald Reagan is rumored to have been among first
    to receive treatment in 1960s

  • Classified as WMD
  • Low vapor pressure means this
  • colorless odorless liquid evaporate
  • quickly
  • Doesnt let Acetylcholinesterase degrade, it
    builds up. so in effect any stimulus to muscles
    from nerves is continually transmitted.
  • 500 times as toxic as cyanide
  • Germans had it, but feared a chemical war with
    the allies
  • A Japanese religious sect used it to kill 12 and
    injure several thousand in a 1995 tokyo subway
  • Atropine one of the treatments

  • Derivitive of Deadly Nightshade (Belladona
  • Atropos was the fate who decided your death
  • Competitive inhibitor for AcH receptors, so it
    fills up the plug where AcH would go to excite
  • If nerve gases flood the system with AcH Atropine
    competes with the AcH for its receptor sites.

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Neuromuscular Toxins Paralysis
  • Pesticides contain cholinesterase inhibitors that
    bind to acetylcholinesterase prevent it from
    degrading ACh
  • spastic paralysis possible suffocation
  • minor startle response can cause death
  • Tetanus or lockjaw is spastic paralysis caused by
    toxin of Clostridium bacteria
  • blocks glycine release in the spinal cord
    causes overstimulation of the muscles
  • Flaccid paralysis with limp muscles unable to
    contract caused by curare that competes with ACh
  • respiratory arrest

Electrically Excitable Cells (muscle nerve)
  • Plasma membrane is polarized or charged
  • resting membrane potential is due to Na outside
    of cell and K other anions inside of cell
  • difference in charge across the membrane is
  • inside is slightly more negative (-90 mV)
  • Plasma membranes exhibit voltage changes in
    response to stimulation
  • ion gates open allowing Na to rush into cell and
    then K to rush out of cell (quick up-and-down
    voltage shift is called action potential)
  • spreads over cell surface as nerve signal or

Muscle Contraction Relaxation
  • Four actions involved in this process
  • excitation where action potentials in the nerve
    lead to formation of action potentials in muscle
  • excitation-contraction coupling refers to action
    potentials on the sarcolemma activate
  • contraction is shortening of muscle fiber or at
    least formation of tension
  • relaxation is return of fiber to its resting
  • Images will be used to demonstrate the steps of
    each of these actions

Excitation of a Muscle Fiber
Excitation (steps 1 2)
  • Nerve signal stimulates voltage-gated calcium
    channels that result in exocytosis of synaptic
    vesicles containing ACh ACh release

Excitation (steps 3 4)
  • Binding of ACh to the surface of muscle cells
    opens Na and K channels resulting in an
    end-plate potential (EPP)

Excitation (step 5)
  • Voltage change in end-plate region (EPP) opens
    nearby voltage-gated channels in plasma membrane
    producing an action potential

Excitation-Contraction Coupling
Excitation-Contraction Coupling(steps 67)
  • Action potential spreading over sarcolemma
    reaches and enters the T tubules -- voltage-gated
    channels open in T tubules causing calcium gates
    to open in SR

Excitation-Contraction Coupling(steps 89)
  • Calcium released by SR binds to troponin
  • Troponin-tropomyosin complex changes shape and
    exposes active sites on actin

Contraction (steps 10 11)
  • Myosin ATPase in myosin head hydrolyzes an ATP
    molecule, activating the head and cocking it
    in an extended position
  • It binds to an active site on actin

Contraction (steps 12 13)
  • Power stroke shows myosin head releasing the
    ADP phosphate as it flexes pulling the thin
    filament along
  • With the binding of more ATP, the myosin head
    releases the thin filament and extends to
    attach to a new active site further down the
    thin filament
  • at any given moment, half of the heads are bound
    to a thin filament, preventing slippage
  • thin and thick filaments do not become shorter,
    just slide past each other (sliding filament

12. Power Stroke sliding of thin filament over
Relaxation (steps 14 15)
  • Nerve stimulation ceases and acetylcholinesterase
    removes ACh from receptors so stimulation of the
    muscle cell ceases

Relaxation (step 16)
  • Active transport pumps calcium from sarcoplasm
    back into SR where it binds to calsequestrin
  • ATP is needed for muscle relaxation as well as
    muscle contraction

Relaxation (steps 17 18)
  • Loss of calcium from sarcoplasm results in
    troponin-tropomyosin complex moving over the
    active sites which stops the production or
    maintenance of tension
  • Muscle fiber returns to its resting length due to
    stretching of series-elastic components and
    contraction of antagonistic muscles

Rigor Mortis
  • Stiffening of the body beginning 3 to 4 hours
    after death -- peaks at 12 hours after death
    diminishes over next 48 to 60 hours
  • Deteriorating sarcoplasmic reticulum releases
  • Activates myosin-actin cross bridging muscle
    contracts, but does not relax.
  • Muscle relaxation requires ATP ATP production
    is no longer produced after death
  • Fibers remain contracted until myofilaments decay

Length-Tension Relationship
  • Amount of tension generated depends on length of
    muscle before it was stimulated
  • length-tension relationship (see graph next
  • Overly contracted (weak contraction results)
  • thick filaments too close to Z discs cant
  • Too stretched (weak contraction results)
  • little overlap of thin thick does not allow for
    very many cross bridges too form
  • Optimum resting length produces greatest force
    when muscle contracts
  • central nervous system maintains optimal length
    producing muscle tone or partial contraction

Length-Tension Curve
Muscle Twitch in Frog Experiment
  • Threshold is minimum voltage necessary to produce
    action potential
  • a single brief stimulus at that voltage produces
    a quick cycle of contraction relaxation called
    a twitch (lasting less than 1/10 second)
  • Phases of a twitch contraction
  • latent period (2 msec delay)
  • only internal tension is generated
  • no visible contraction occurs since only elastic
    components are being stretched
  • contraction phase
  • external tension develops as muscle shortens
  • relaxation phase
  • loss of tension return to resting length as
    calcium returns to SR
  • A single twitch contraction is not strong enough
    to do any useful work

Recruitment Stimulus Intensity
Maximal recruitment
  • Stimulating the whole nerve with higher and
    higher voltage produces stronger contractions
  • More motor units are being recruited
  • called multiple motor unit summation
  • lift a glass of milk versus a whole gallon of milk

Production of Variable Contraction Strengths
  • Stimulating the nerve with higher voltage get
    stronger contractions because recruit more motor
  • Stimulate the muscle at higher frequencies
  • up to 10, produces twitch contractions with full
    recovery between twitches
  • 10 - 20, each twitch develops more tension than
    the one before (treppe) due to failure to remove
    all Ca2
  • 20 - 40, each stimulus arrives before the
    previous twitch is over
  • temporal or wave summation produces incomplete
  • 40 - 50, no time to relax between stimuli so
    twitches fuse into smooth prolonged contraction
    called complete tetanus (normal smooth movements)

Production of Variable Contraction Strengths
(1) Twitch and Treppe Contractions
  • Stimulating a muscle at variable frequencies
  • low frequency (up to 10 stimuli/sec)
  • each stimulus produces an identical twitch
  • moderate frequency (between 10-20 stimuli/sec)
  • each twitch has time to recover but develops more
    tension than the one before (treppe or staircase
  • calcium was not completely put back into SR
  • heat of tissue increases myosin ATPase effeciency
    (warm-up exercises)

Production of Variable Contraction Strengths
(2) Incomplete and Complete Tetanus
  • Higher frequency stimulation (20-40
    stimuli/second) generates gradually more strength
    of contraction
  • each stimuli arrives before last one recovers
  • temporal summation or wave summation
  • incomplete tetanus sustained fluttering
  • Maximum frequency stimulation (40-50
  • muscle has no time to relax at all
  • twitches fuse into smooth, prolonged contraction
    called complete tetanus
  • rarely occurs in the body

Isometric Isotonic Contractions
  • Isometric muscle contraction
  • develops tension without changing length
  • Isotonic muscle contraction
  • tension development while shortening concentric
  • tension development while lengthening eccentric

Muscle Contraction Phases
  • Isometric isotonic phases of lifting a heavy
  • Tension builds even though the box is not moving
  • Then muscle begins to shorten maintains the
    same tension from then on

ATP Sources
  • All muscle contraction depends on ATP
  • Pathways of ATP synthesis
  • anaerobic fermentation (ATP production limited)
  • occurs without oxygen, but produces toxic lactic
  • aerobic respiration (far more ATP produced)
  • requires continuous oxygen supply, produces H2O

Muscle Immediate Energy Needs
  • In a short, intense exercise (100 m dash), oxygen
    need is supplied by myoglobin
  • Most ATP demand is met by transferring Pi from
    other molecules (phosphagen system)
  • myokinase transfers Pi groups from one ADP to
    another, converting the latter to ATP
  • creatine kinase obtains Pi groups from creatine
    phosphate and donates them to ADP to make ATP
  • Result is power enough for 1 minute brisk walk or
    6 seconds of sprinting

Muscle Short-Term Energy Needs
  • Once phosphagen system is exhausted,
    glycogen-lactic acid system (anaerobic
    fermentation) takes over
  • produces ATP for 30-40 seconds of maximum
  • muscles obtain glucose from blood stored
  • while playing basketball or running around
    baseball diamonds

Muscle Long-Term Energy Needs
  • After 40 seconds of exercise, respiratory
    cardiovascular systems catch up and begin to
    deliver enough oxygen for aerobic respiration
  • oxygen consumption rate increases for first 3-4
    minutes then levels off to a steady state
  • ATP production keeps pace with demand
  • Limits are set by depletion of glycogen blood
    glucose, loss of fluid and electrolytes through
  • little lactic acid buildup occurs

  • Fatigue is progressive weakness loss of
    contractility from prolonged use
  • Causes
  • ATP synthesis declines as glycogen is consumed
  • ATP shortage causes sodium-potassium pumps to
    fail to maintain membrane potential
  • lactic acid lowers pH of sarcoplasm inhibiting
    enzyme function
  • accumulation of extracellular K lowers the
    membrane potential excitability
  • motor nerve fibers use up their acetylcholine

  • Ability to maintain high-intensity exercise is
    determined by maximum oxygen uptake and nutrient
  • VO2 max is proportional to body size, peaks at
    age 20, is larger in trained athlete males
  • depends on the supply of organic nutrients
  • fatty acids, amino acids glucose
  • carbohydrate loading is used by some athletes
  • dietary strategy used to pack glycogen into
    muscle cells
  • may add water at same time (2.7 g water with each
  • side effects include heaviness feeling

Oxygen Debt
  • Need to breathe heavily after strenuous exercise
  • known as excess postexercise oxygen consumption
  • typically about 11 liters extra is consumed
  • Purposes for extra oxygen
  • replace oxygen reserves (myoglobin, blood
    hemoglobin, in air in the lungs dissolved in
  • replenishing the phosphagen system
  • reconverting lactic acid to glucose in kidneys
    and liver
  • serving the elevated metabolic rate that occurs
    as long as the body temperature remains elevated
    by exercise

Slow- and Fast-Twitch Fibers
  • Not all muscle fibers are metabolically alike,
    but all fibers of a single motor unit are similar
  • Slow oxidative, slow-twitch fibers
  • more mitochondria, myoglobin capillaries
  • adapted for aerobic respiration resistant to
  • soleus postural muscles of the back
  • Fast glycolytic, fast-twitch fibers
  • rich in enzymes for phosphagen glycogen-lactic
    acid systems
  • sarcoplasmic reticulum releases calcium quickly
    so contractions are quicker (7.5 msec/twitch)
  • extraocular eye muscles, gastrocnemius and biceps
  • Proportions of different muscle types determined
    genetically born sprinter

Types of Muscle Fibers
Strength and Conditioning
  • Factors that increase strength of contraction
  • muscle size and fascicle arrangement
  • size of motor units and motor unit recruitment
  • frequency of stimulations, length of muscle at
    start of contraction and fatigue
  • Resistance training (weight lifting)
  • stimulates cell enlargement due to synthesis of
    more myofilaments -- some cell splitting may
  • Endurance training (aerobic exercise)
  • produces an increase in mitochondria, glycogen
    density of capillaries

Cardiac Muscle
  • Cells are shorter, thicker, branched and linked
    to each other at intercalated discs
  • electrical gap junctions allow cells to stimulate
    their neighbors mechanical junctions keep the
    cells from pulling apart
  • sarcoplasmic reticulum is less developed but T
    tubules are larger to admit Ca2 from
    extracellular fluid
  • damaged cells repaired by fibrosis, not mitosis
  • Autorhythmic due to pacemaker cells
  • Uses aerobic respiration almost exclusively
  • large mitochondria make it resistant to fatigue
  • very vulnerable to interruptions in oxygen supply

Smooth Muscle
  • Fusiform cells with one nucleus
  • 30 to 200 microns long 5 to 10 microns wide
  • no visible striations, sarcomeres or Z discs
  • thin filaments attach to dense bodies scattered
    throughout sarcoplasm on sarcolemma
  • SR is scanty has no T tubules
  • calcium for contraction comes from extracellular
  • If present, nerve supply is autonomic
  • releases either ACh or norepinephrine
  • different effects in different locations

Types of Smooth Muscle
  • Multiunit smooth muscle
  • in largest arteries, iris, pulmonary air
    passages, arrector pili muscles
  • terminal nerve branches synapse on individual
    myocytes in a motor unit
  • independent contraction
  • Single-unit smooth muscle
  • in most blood vessels viscera as circular
    longitudinal muscle layers
  • electrically coupled by gap junctions
  • large number of cells contract as a unit

Stimulation of Smooth Muscle
  • Involuntary contracts without nerve stimulation
  • hormones, CO2, low pH, stretch, O2 deficiency
  • pacemaker cells in GI tract are autorhythmic
  • Autonomic nerve fibers have beadlike swellings
    called varicosities containing synaptic vesicles
  • stimulates multiple myocytes at diffuse junctions

Features of Contraction and Relaxation
  • Calcium triggering contraction is extracellular
  • enters cell through channels triggered by
    voltage, hormones, neurotransmitters or
    stretching of the cell
  • calcium ion binds to calmodulin -- activates
    myosin light-chain kinase which activates the
    myosin head with ATP to bind actin -- power
    stroke occurs when hydrolyzes 2nd ATP
  • Thin filaments pull on intermediate filaments
    attached to dense bodies on the plasma membrane
  • shortens the entire cell in a twisting fashion
  • Contraction relaxation very slow in comparison
  • slow myosin ATPase enzyme slow pumps that
    remove Ca2
  • Uses l0-300 times less ATP to maintain the same
  • latch-bridge mechanism maintains tetanus (muscle
  • keeps arteries in state of partial contraction
    (vasomotor tone)

Contraction of Smooth Muscle Cells
Responses to Stretch
  • Stretch opens mechanically-gated calcium channels
    causing muscle response
  • food entering the esophagus brings on peristalsis
  • Stress-relaxation response necessary for hollow
    organs that gradually fill (urinary bladder)
  • when stretched, tissue briefly contracts then
  • Must contract forcefully when greatly stretched
  • thick filaments have heads along their entire
  • no orderly filament arrangement -- no Z discs
  • Plasticity is ability to adjust tension to degree
    of stretch such as empty bladder is not flabby

Myasthenia Gravis
  • Autoimmune disease where antibodies attack NMJ
    and bind ACh receptors together in clusters
  • fibers remove the receptors
  • less and less sensitive to ACh
  • drooping eyelids and double vision
  • difficulty swallowing
  • weakness of the limbs
  • respiratory failure
  • Disease of women between ages of 20 and 40
  • Treated with cholinesterase inhibitors, thymus
    removal or immunosuppressive agents

Myasthenia Gravis
Drooping eyelids and weakness of muscles of eye