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Muscles
Unit 4 option C
by CSE
November 2006
Types of muscle
• Skeletal / striped / striated /voluntary
• Smooth / unstriated / involuntary
• Cardiac
Striated
• Attached to bones
• Movement of parts of the body or
locomotion
• Long fibres with cross striations
• Control by voluntary nervous system
• Contracts readily but fatigues easily
Smooth
• Present in walls of tubular organs eg gut, uterus,
bladder, blood vessels, diaphragm
• Movement of materials in the body
• Short spindle shaped cells with no cross striations
• Control by involuntary (autonomic) nervous
system
• Contracts slowly but can be maintained for long
periods
Cardiac
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Only found in heart walls
Pumping of heart maintains blood circulation
Branched cells forming a linked network
Allows waves of electrical excitation to pass easily
between them
• Toughened cell membranes between cells
• Contraction is myogenic (self initiated) but rate
changed by autonomic system
• Contraction manitained without fatigue
Skeletal muscle
• Each muscle made of large numbers of specialised
cells called myofibrils
• Myofibrils are grouped into bundles with
connective tissue and each bundle is called a
muscle fibre
• Myofibrils are very long cells with lots of nuclei
which lie close to the surface
• Fibre bounded by sarcolemma, infolded to form T
tubules which penetrate into the cell.
• Sarcoplasm – lots of mitochondria, sarcoplasmic
reticulum which stores calcium ions
Myofibril structure
• Made of 2 types of filament – thin and thick
• Thicker filaments made of a protein called
myosin
• Thinner filaments made of actin protein
• Myofibril split into repeating units called
sarcomeres.
Arrangement of proteins
• Actin filaments are attached to bands of connective
tissue called Z lines
• Sarcomere -= distance between 2 Z lines
• Myosin filaments found in central part of each
sarcomere
• In middle of myosin is a band of connective tissue
called M line
• For part of their length, actin and myosin lie between
each other (overlap) – looks dark
• Near Z line, only have thin actin filaments so looks
light.
• In centre of sarcomere, only myosin so intermediate
colour
Contraction
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Actin pulled between myosin filaments
Greater overlap area
I bands and H zones narrower
Sarcomere shorter
Z lines closer
A bands stay same length
Sliding of filaments not shortening of filaments
Contraction detail 1
• Myosin molecule has a long rod shaped tail made of
fibrous protein and 2 roundish heads of globular protein
• Heads face outwards and link to actin during contraction
• Actin made of 2 long helical chains of small globular
protein molecules twisted round each other
• Actin associated with 2 other proteins – tropomyosin
and troponin
• Tropomyosin forms long thin strands wound over actin
so blocks sites where myosin attach
• Troponin binds to calcium ions during contraction
initiation
Contraction detail 2
• Nerve impulse causes contraction (NMJ)
• Action potential spreads along sarcolemma and
down T tubules
• Sarcoplasmic reticulum becomes more permeable
to calcium ions which diffuse out into myofibrils
• Calcium ions cause a change in position of
tropomyosin and unblock actin binding sites
• Myosin heads attach to binding sites forming
actomyosin cross bridges
• Myosin head changes angle, pulling actin over
myosin towards sarcomere centre
Contraction detail 3
• A molecule of ATP attaches to each myosin head
• Hydrolysis of ATP releases energy which is used
to detach myosin head from actin and to reposition
head further along chain
• Myosin head changes position and pulls actin
again
• Cycle repeated many times – myosin head walks
along actin until the fibre end.
Relaxation
• Nerve stimualtion stops
• Calcium ions pumped out of myofibrils and back
into sarcoplasmic reticulum – needs energy
• With no calcium ions, tropomyosin changes
position and blocks binding sites on actin
• Myosin heads can’t bind with actin
• Muscle relaxed and can be extended by
contraction of antagonistic muscle
Interesting facts
• Muscle contraction 25% efficient – rest lost as
heat
• Rigor mortis – stiffening of muscles due to ATP
not available to break cross bridges between actin
and myosin so muscle can’t relax. Appears 4 hours
after death but after 24 hours muscles loosen as
enzymes destroy muscle proteins
• Cycle of myosin heads binding, detachng and
repositioning repeated 50 –100 times per second
and moves actin 10nm
Fast twitch muscle fibres
Slow twitch muscle fibres
White muscle
Red muscle
Little myoglobin present
Large amount of myoglobin
Rapid short term contraction sprinters have 62%
Energy from anaerobic resp
Slower sustained contraction –
marathon runners have 82%
Aerobic respiration
Few mitochondria
Many mitochondria
Large amounts creatine
phosphate
Less extensive blood supply
Little creatine phosphate
Fatigues quickly
Fatigues more slowly
Extensive blood supply
Creatine phosphate – reserve store of phosphate and
energy. Provides phosphate to add to ADP.When
broken down, releases energy which used to
regenerate ATP. When muscle relaxes, P from ATP
used to regenerate CP.
• Myoglobin – protein
fond in muscle.
Similar structure to
haemoglobin. Can
attach to oxygen and
store it in muscles.
Release when oxygen
supply gets low.
• Glycogen –
carbohydrate store in
muscle.
Helpful hints
• Actin has less letters than
myosin so actin is thin
fibre
• Actin begins with A (1st
letter of alphabet) has a Z
line (last letter)
• Myosin is thick fibres
• Myosin middle of
sarcomere
• Myosin mid line = M line
• Light part = only actin
(near Z line) called I
band (lIght)
• Intermediate colour =
only myosin = H zone
• Dark part = Actin +
myosin = A band
(dArk)
Neuromuscular junction
• Specialised synapse between motor neurone and skeletal
muscle
• Allows motor neurones to stimulare muscle contraction
• End of axon membrane and sarcolemma membrane of
muscle are highly folded
• Functions like normal excitatory synapse
• Axon end contains vesicles with acetylcholine + many
mitochondria
• Sodium ions diffuse into sarcolemma causes a change in
potential difference and if above threshold causes an
action potential which spreadsto muscle and causes
contraction.
Synapse working
• Nerve impulse travels down axon causing Ca channels
to open in membrane so Ca ions diffuse rapidly into
bulb from surrounding tissue
• Causes Ach vesicles to move to and fuse with
membrane, so Ach goes into cleft by exocytosis
• Ach binds with receptors on muscle fibre, causing Na
channels to open so Na+ into muscle sarcolemma.
• Inside less negative, causing an action potential if
larger than threshold value
• Ach broken down by cholinesterase and shape change
means the acetyl and choline are released from
receptors and diffuse back into presynaptic membrane
where reform Ach using energy
Training
• Proportions of fast and slow twitch fibres can not be
changed much by training
• Regular training programs where muscle made to do work
against a load eg weight training
- stimulates muscle growth, larger cross sectional area
due to an increase in number of myofibrils.
- Number of mitochondria increase
- Amount creatine phosphate increases
- Amount ATP increases
- cells more tolerant to lactic acid build up
• Useful in power events eg throwers and sprinters
Endurance events training
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Involves steadier work over longer time
Muscle bulk not increase
Increase glycogen store
Heart increases in size allowing blood to be
delivered to muscles more quickly and
efficiently
• Allow more potential for aerobic respiration