Download chapt11_muscle tissue lecture

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
Objectives
Monster Cows: Belgian Blue Cattle
Dissections comparing normal,
heterozygous and homozygous mice
Myostatin
• A growth factor (hormone)
that surpresses muscle
growth.
– 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
Smooth Muscle
• Cells spindle shaped
• Uninucleated
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
attachment
– endomysium, perimysium, epimysium, fascia, tendon
• Not excitable or contractile, but are somewhat
extensible & elastic
– stretches slightly under tension and recoils when
released
• 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
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.
Muscle Fibers (Form follows Function)
• Multiple flattened nuclei against inside of plasma
membrane
– due to fusion of multiple myoblasts during development
– 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 oxygen
• 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 other
– resist overstretching
– help the cell recoil to its resting length (elasticity)
Regulatory & Contractile Proteins
• Myosin & actin are contractile proteins (they do work)
• 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 filaments
• 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
sarcomere
I
A
I
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?
• 2 TYPES of MUSCLE FIBERS
– 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
TYPE II - (IIa & IIx) FAST TWITCH
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
Tonic muscles (red) - Leg muscles
Tetanic muscles (white) - Pectoral muscles
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
• Johnson’s 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
• 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 control)
• 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 fiber
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 cell
• 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
•
•
•
•
•
Botulism
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 pg/kg).
Symptoms start with double vision as eye muscles go
Ronald Reagan is rumored to have been among first to
receive treatment in 1960s
Sarin
• Classified as WMD
• Low vapor pressure
means this
colorless odorless liquid
evaporate
quickly
• Doesn’t let
Acetylcholinesterase
degrade, it builds up. so
in effect any stimulus to
muscles from nerves is
continually transmitted.
• 500 times as toxic as
Atropine
• 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 muscles
• If nerve gases flood the
system with AcH Atropine
competes with the AcH for its
receptor sites.
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 potential
• 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 impulse
Muscle Contraction & Relaxation
• Four actions involved in this process
– excitation where action potentials in the nerve lead to
formation of action potentials in muscle fiber
– excitation-contraction coupling refers to action
potentials on the sarcolemma activate myofilaments
– contraction is shortening of muscle fiber or at least
formation of tension
– relaxation is return of fiber to its resting length
• 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 endplate 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 6&7)
• 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 8&9)
• 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
12. Power Stroke;
sliding of thin filament
myosin head releasing
over thick
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 theory)
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 troponintropomyosin 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
calcium
• 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 slide)
• Overly contracted (weak contraction results)
– thick filaments too close to Z discs & can’t slide
• 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 units
• Stimulate the muscle at higher frequencies (stimuli/sec)
– 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 Ca+2
– 20 - 40, each stimulus arrives before
the previous twitch is over
• temporal or wave summation produces incomplete tetanus
– 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 response
– moderate frequency (between 10-20 stimuli/sec)
• each twitch has time to recover but develops more tension than the one
before (treppe or staircase phenomenon)
– 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 contractions
• Maximum frequency stimulation (40-50 stimuli/second)
– 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 box
• 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 acid
– aerobic respiration (far more ATP produced)
• requires continuous oxygen supply, produces H2O & CO2
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, glycogenlactic acid system (anaerobic fermentation) takes
over
– produces ATP for 30-40 seconds of maximum
activity
– muscles obtain glucose from blood & stored
glycogen
– 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
sweating
– little lactic acid buildup occurs
Fatigue
• 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 & excitability
– 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
Endurance
• Ability to maintain high-intensity exercise is
determined by maximum oxygen uptake and
nutrient availability
– 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
gram/glycogen)
– side effects include “heaviness” feeling
Oxygen Debt
• Need to breathe heavily after strenuous exercise
– known as excess postexercise oxygen consumption (EPOC)
– typically about 11 liters extra is consumed
• Purposes for extra oxygen
– replace oxygen reserves (myoglobin, blood hemoglobin, in air
in the lungs & dissolved in plasma)
– 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 fatigue
– soleus & postural muscles of the back (100msec/twitch)
• 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 brachii
• 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 occur
• 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 Ca+2 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 fluid
• 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 Ca+2
• Uses l0-300 times less ATP to maintain the same tension
– latch-bridge mechanism maintains tetanus (muscle tone)
• 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 relaxes
• Must contract forcefully when greatly stretched
– thick filaments have heads along their entire length
– 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
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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 movement