Transcript Muscle Tissue

Muscle Tissue
3 Types of Muscle Tissue
• Skeletal muscle
– attaches to bone, skin or fascia
– striated with light & dark bands visible with scope
– voluntary control of contraction & relaxation
3 Types of Muscle Tissue
• Cardiac muscle
– striated in appearance
– involuntary control
– autorhythmic because of built in pacemaker
3 Types of Muscle Tissue
• Smooth muscle
– attached to hair follicles in skin
– in walls of hollow organs -- blood vessels & GI
– nonstriated in appearance
– involuntary
Skeletal Muscles
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Attach to bones
Produce skeletal movement (voluntary)
Maintain posture
Support soft tissues
Regulate entrances to the body
Maintain body temperature
•muscle fibers increase in size during childhood = human GH
•testosterone also increases muscle size
•mature muscle fibers range from 10 to 100 microns in diameter
•typical length is 4 inches - some are 12 inches long
Properties of Skeletal Muscles
Electrical excitability
-ability to respond to stimuli by producing electrical signals
such as action potentials
-two types of stimuli: 1. autorhythmic electrical signals
2. chemical stimuli
Contractility
-ability to contract when stimulated by an AP
-isometric contraction: tension develops, length doesn’t change
-isotonic contraction: tension develops, muscle shortens
Extensibility
-ability to stretch without being damaged
-allows contraction even when stretched
Elasticity
-ability to return to its original length and shape
Gross Anatomy
•muscles are really groups of
fascicles
•the fascicles are groups of muscle
fibers = considered to be an
individual muscle cell
•the muscle fiber is made up
of protein filaments = myofibrils
•each myofibril is comprised of
repeating units = sarcomeres
Gross Anatomy
•muscle is wrapped in a protective fascia
-fascia = sheet of fibrous connective tissue that supports
and surrounds muscle or organs
•a superficial fascia separates muscle from the overlying skin
-also known as the subcutaneous layer
-made up of areolar tissue and adipose tissue
-provides support for blood vessel and nerves
-the adipose tissue stores most of the body’s triglycerides
and provides insulation
•muscles with similar functions are grouped and held together by layers
of deep fascia
-dense irregular connective tissue
-allow free movement of muscles, carries nerves, BVs
• three layers of connective tissue surround a muscle
– Epimysium
– Perimysium
– Endomysium
• these layers further strengthen and protect muscle
• outermost layer = epimysium
– encircles the entire muscle
– separates them into bundles = fascicles
• next layer = perimysium
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– divides and surrounds groups of 10 to 100 individual
muscle fibers
– give meat its “grain” because the fascicles are visible
– both epimysium and perimysium are dense irregular connective tissue
– extend off the muscle to become organized as dense regular connective tissue =
tendon
when the tendon is a broad flat sheet = aponeurosis
• penetrating the muscle fibers and separating them into myofibrils =
endomysium (areolar connective tissue)
• myofibrils are made of filaments of proteins = myofilaments
•generally muscles are supplied with one artery and two veins
•they accompany the nerve
•nerves that induce muscle contraction = somatic motor neurons (part
of the somatic division of the PNS)
•communication between muscle and these neurons
Neuromuscular junction (NMJ)
Microanatomy of Skeletal Muscle
Fibers
• New terminology
– Cell membrane = sarcolemma
– Cytoplasm = sarcoplasm
– Internal membrane system = sarcoplasmic reticulum
• Large, multinucleated cells
– embryonic development – stem cells (satellite cells) differentiate into
immature myoblasts which begin to make the proteins of the myofibrils and
myofilaments
– These myoblasts mature into myocytes
– Multiple myocytes fuse to form the muscle cell (muscle fiber)
– once fused, these muscle cells lose the ability of undergo mitosis
– number of muscle cells predetermined before birth – they get larger as we
grow
– but satellite cells can repair damaged/dying muscle cells throughout
adulthood
• Exclusive to skeletal muscle only!!!
Muscle Cell Anatomy
• Transverse tubules
– ingrowths of sarcolemma
– Carry electrical impulses deep
into the fiber
• Myofibrils within sarcoplasm
of the fiber
– Contain a“skeleton” of protein
filaments (myofilaments)
organized as Sarcomeres
• Myofilaments form the
myofibrils
– Thin filaments (actin, troponin,
tropomyosin)
– Thick filaments (myosin)
Microanatomy of Skeletal Muscle
Fibers
•muscle fibers are bound by a plasma membrane = sarcolemma
•thousands of tiny invaginations in this sarcolemma called T or transverse
tubules - tunnel in toward the center of the cell
-T tubules are open to the outside of the fiber
- filled with interstitial fluid
- action potentials generated in the neuron travel along the sarcolemma
and the T tubules
- allows for the even and quick spread of an action potential deep into the cell
•the cytoplasm is called a sarcoplasm
-substantial amounts of glycogen - can be broken into glucose
-contains myoglobin - binds oxygen needed for muscle ATP
production
-support multiple myofibrils – structures for contraction
Microanatomy of Skeletal Muscle
Fibers
•contractile elements of the myofibrils = myofilaments
-2 microns in diameter
-comprised of primarily actin or myosin
-give the muscle its striated appearance
•fibers also have a system of fluid-filled membranes = sarcoplasmic
reticulum
-encircles each myofibril
-similar to the endoplasmic reticulum of other cells
-have dilated end sacs = terminal cisterns
-stores calcium when at rest - releases it during contraction
-release is triggered by an AP
The Proteins of Muscle
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Myofibrils contain two kinds of myofilaments
• Thin
• Thick
these Myofilaments are built of 3 kinds of protein
– contractile proteins
• myosin and actin
– regulatory proteins which turn contraction on & off
• troponin and tropomyosin
– structural proteins which provide proper alignment, elasticity and
extensibility
• titin, myomesin, nebulin, actinin and dystrophin
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Dystrophin – connects myofibrils to sarcolemma
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Actinin – part of Z-line
Titin – connects myosin to Z-line and M-line
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-transmits tension along muscle
Role in recovery after being stretched
Nebulin – forms core of the actin chain/thin filament
M line
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Sarcomere
Structure
sarcomere = regions of myosin (thick myofilament) and actin (part of thin myofilament)
bounded by the Z line
thin filaments project out from Z line – actin attaches via actinin (structural protein)
thick filaments lie in center of sarcomere - overlap with thin filaments and connect to them
via cross-bridges
• myosin/thick filament only region = H zone
• myosin/thick filaments are held in place by the M line proteins at the center and titin at
the Z-line
• thin filament only region = I band
• length of myosin/thick filaments = A band
• contraction = “sliding filament theory”
-thick and thin myofilaments slide over each other and sarcomere shortens
Contraction: The Sliding Filament Theory
• Contraction:
– Active process
– Elongation is passive
– Amount of tension produced is proportional to degree of overlap of thick
and thin filaments
• SF Theory: 1954
– Explains how a muscle fiber exerts tension
– Four step process
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Active sites on actin
Crossbridge formation
Cycle of attach, pivot, detach, return
Troponin and tropomyosin control contraction
Contraction: The Sliding Filament Theory
•Actin proteins in the thin
filament have myosin
binding sites
•these sites are “covered
up” by troponin and
tropomyosin in relaxed
muscle
•removal of
troponin/tropomyosin
from these sites is
required for contraction
•removal of
troponin/tropomyosin is
done through binding of
calcium to troponin
•calcium is release from
the sarcoplasmic reticulum
upon the action potential
• myosin/thick myofilament
is a bundle of myosin
molecules
• myosin looks like a “golf
club” with a head, a hinge
region and a shaft
• each myosin protein has a
globular “head” with a site
to bind and breakdown ATP
(ATPase site) and to bind
actin (actin binding site)
• binding of actin and myosin
binding sites = crossbridging
RESETTING of
system
Increase in Cai
Removal of troponin-tropomyosin
CONTRACTION
Sliding of actin along myosin
-for cross bridging- you will need two things:
1. calcium – uncovers the myosin binding sites on actin – “pushes aside” the troponintropomyosin complex
2. myosin head bound to ADP
-for contraction – i.e. pivoting of the myosin head into the M line – the myosin head must be empty
-to “reset” for a new cycle of cross-bridging – the myosin head must detach and pivot back
-the myosin head must bind ATP
-once the myosin head pivots back – the ATP is broken down to ADP – head is ready to crossbridge again – if actin is “ready”
Contracted Sarcomere
CHECK OUT THESE ANIMATIONs!!!
http://highered.mcgrawhill.com/sites/0072495855/student_view0/chapter10/animation__myofilament_
contraction.html
http://www.youtube.com/watch?v=EdHzKYDxrKc
http://www.youtube.com/watch?v=Vlchs4omFDM
The Events in Muscle Contraction
Relaxation
• Acetylcholinesterase (AChE) breaks down ACh
within the synaptic cleft
• Muscle action potential ceases
• Ca+2 release channels close
• Active transport pumps Ca2+ back into storage in
the sarcoplasmic reticulum
• Calcium-binding protein (calsequestrin) helps
hold Ca+2 in SR
• Tropomyosin-troponin complex recovers binding
site on the actin
Rigor Mortis
• Rigor mortis is a state of muscular rigidity
that begins 3-4 hours after death and lasts
about 24 hours
• After death, Ca+2 ions leak out of the SR
and allow myosin heads to bind to actin
• Since ATP synthesis has ceased,
crossbridges cannot detach from actin until
proteolytic enzymes begin to digest the
decomposing cells.
Length of Muscle Fibers
• Optimal overlap of thick & thin filaments
– produces greatest number of crossbridges and the
greatest amount of tension
• As stretch muscle (past optimal length)
– fewer cross bridges exist & less force is produced
• If muscle is overly shortened (less than optimal)
– fewer cross bridges exist & less force is produced
– thick filaments crumpled by Z discs
• Normally
– resting muscle length remains between 70 to 130% of
the optimum
The Neuromuscular Junction
• end of neuron (synaptic terminal or
axon bulb) is in very close association
with the muscle fiber
• distance between the bulb and the folded
sarcolemma = synaptic cleft
• nerve impulse leads to release of
neurotransmitter (acetylcholine)
• N.T. binds to receptors on myofibril
surface
• binding leads to influx of sodium,
potassium ions (via channels)
• eventual release of calcium by
sarcoplasmic recticulum = contraction
• Acetylcholinesterase breaks down ACh
• Limits duration of contraction
Motor Units
• Each skeletal fiber has only ONE NMJ
• MU = Somatic neuron + all the
skeletal muscle fibers it innervates
• Number and size indicate precision
of muscle control
• Muscle twitch
– Single momentary contraction
– Response to a single stimulus
• All-or-none theory
– Either contracts completely or not at
all
• Motor units in a whole muscle fire asynchronously
some fibers are active others are relaxed
delays muscle fatigue so contraction can be sustained
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Muscle fibers of different motor units are intermingled so that net distribution of force
applied to the tendon remains constant even when individual muscle groups cycle
between contraction and relaxation.
Muscle Metabolism
• Production of ATP:
-contraction requires huge amounts of ATP
-muscle fibers produce ATP three ways:
1. Creatine phosphate
2. Aerobic metabolism
3. Anaerobic metabolism
Creatine Phosphate
• Muscle fibers at rest produce more ATP then they need for resting metabolism
• Excess ATP within resting muscle used to form creatine phosphate
– creatine – arginine, glycine and methionine
• made by kidneys and liver
• phosphorylated in muscle to make creatine phosphate
• phosphorylated by the enzyme creatine kinase
• takes a phosphate off of ATP and transfers it creatine
• takes the phosphate off of creatine phosphate and transfers it back to ADP –
to make ATP
• Creatine phosphate: 3-6 times more plentiful than ATP within muscle
• Sustains maximal contraction for 15 sec (used for 100 meter dash).
• Athletes often use creatine supplementation
– gain muscle mass but shut down bodies own synthesis (safety?)
Anaerobic Cellular Respiration
• Muscles deplete creatine – can make ATP
in anaerobically or aerobically
• Glycogen converted into glucose first
• ATP produced from the breakdown of
glucose into pyruvic acid (sugar) during
glycolysis
– if no O2 present (anaerobic) - pyruvic
converted to lactic acid which diffuses
into the blood
• Glycolysis can continue anaerobically to
provide ATP for 30 to 40 seconds of
maximal activity (200 meter race)
• If O2 is present the pyruvic acid is
converted into acetyl coA (aerobic)
Aerobic Cellular Respiration
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ATP for any activity lasting over 30 seconds
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if sufficient oxygen is available, pyruvic acid is converted into acteyl coA
Acetyl coA enters the mitochondria to enter the Kreb’s cycle
Kreb’s cycle generates NADH and FADH2 (electron carriers)
The electrons are carried to an enzymes located on the inner mitochondrial membrane
The electrons are then transported along three complexes of enzymes – ultimately transported to oxygen
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Provides 90% of ATP energy if activity lasts more than 10 minutes
Each glucose = 36 ATP
fatty acids and amino acids can also be used by the mitochondria
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This results in the synthesis of ATP, water and heat
Fatty acid = ~100 ATP
Sources of oxygen – diffusion from blood, released by myoglobin
Types of Muscle Fibers
• Fast fibers = glycolytic
• Slow fibers = oxidative
• Fibers of one motor unit all the same type
• Percentage of fast versus slow fibers is genetically
determined
• Proportions vary with the usual action of the muscle
- neck, back and leg muscles have a higher proportion of postural, slow oxidative fibers
- shoulder and arm muscles have a higher proportion of fast glycolytic fibers
Fast Fibers
• Large in diameter
• Contain densely packed myofibrils
• Large glycogen reserves
• Fast oxidative-glycolytic (fast-twitch A)
– red in color (lots of mitochondria, myoglobin & blood vessels)
– split ATP at very fast rate; used for walking and sprinting
• Fast glycolytic (fast-twitch B)
– white in color (few mitochondria & BV, low myoglobin)
– anaerobic movements for short duration; used for weight-lifting
• Slow fibers
– Half the diameter of fast fibers
– Three times longer to contract
– Continue to contract for long periods of time
• e.g. marathon runners
Exercise-Induced Muscle Damage
• Intense exercise can cause muscle damage
– electron micrographs reveal torn sarcolemmas,
damaged myofibrils an disrupted Z discs
– increased blood levels of myoglobin & creatine
phosphate found only inside muscle cells
• Delayed onset muscle soreness
– 12 to 48 Hours after strenuous exercise
– stiffness, tenderness and swelling due to
microscopic cell damage
• Atrophy
– wasting away of muscles
– caused by disuse (disuse atrophy) or severing of the
nerve supply (denervation atrophy)
– the transition to connective tissue can not be reversed
• Hypertrophy
– increase in the diameter of muscle fibers
– resulting from very forceful, repetitive muscular
activity and an increase in myofibrils, SR &
mitochondria