Transcript Muscles - Fort Bend ISD

Muscles &
Motor Locomotion
Why Do We
Need All
That ATP?
AP Biology
2006-2007
Animal Locomotion
What are the advantages of locomotion?
sessile
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motile
Muscle
involuntary,
striated
auto-rhythmic
voluntary,
striated
heart
moves bone
multi-nucleated
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evolved first
involuntary,
non-striated
digestive system
arteries, veins
Organization of Skeletal muscle
skeletal muscle
plasma
membrane
nuclei
tendon
muscle fiber (cell)
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myofibrils
myofilaments
Human
endoskeleton
206 bones
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Muscles movement
 Volunteery striated muscle

skeletal muscles come in
antagonistic pairs
 flexor vs. extensor

contracting = shortening
 move skeletal parts

Tendon
 connect bone to muscle

Ligament
 connect bone to bone
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Structure of striated skeletal muscle
 Muscle Fiber
 Myofibril
 divided into sections = sarcomeres
 Sacromere


functional unit of muscle
contraction
alternating bands of
thin (actin) & thick (myosin)
protein filaments
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Muscle filaments & Sarcomere
 Interacting proteins

_________________
 braided strands
 ________________
 ________________
 ________________

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_________________
 ________________
Thin filaments: actin
 Complex of proteins

braid of actin molecules & tropomyosin fibers
 tropomyosin fibers secured with troponin molecules
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Thick filaments: myosin
 Single protein

myosin molecule
 long protein with globular head
bundle of myosin proteins:
globular
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Thick & thin filaments
 Myosin tails aligned together & heads pointed
away from center of sarcomere
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Interaction of thick & thin filaments
 sliding-filament model

Before contraction

During contraction
sarcomere
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sarcomere
Where is ATP needed?
binding site
thin filament
(actin)
myosin head
ADP
12
thick filament
(myosin)
ATP
11
form
cross
bridge1
3
release
cross
bridge
Cleaving ATP  ADP allows myosin 1
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head
to bind to actin filament
shorten
sarcomere
4
Closer look at muscle cell
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multi-nucleated
Ca2+ ATPase of SR
Muscle cell organelles
 Sarcoplasm


muscle cell cytoplasm
contains many mitochondria
Sarcoplasmic reticulum

organelle similar to ER

network of tubes
T tubules stimulate


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Ca2+ released from SR through channels
Ca2+ restored to SR by Ca2+ pumps
 pump Ca2+ from cytosol
 pumps use ATP
ATP
Muscle at rest
 Interacting proteins

at rest, troponin molecules hold tropomyosin
fibers so that they cover the myosin-binding
sites on actin
 troponin has Ca2+ binding sites
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The Trigger: motor neurons
 Motor neuron triggers muscle contraction

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release acetylcholine (Ach) neurotransmitter
Nerve trigger of muscle action
 Nerve signal travels
down T-tubule

stimulates
sarcoplasmic
reticulum (SR) of
muscle cell to
release stored Ca2+

flooding muscle
fibers with Ca2+
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Ca2+ triggers muscle action
 At rest, tropomyosin
blocks myosin-binding
sites on actin

secured by troponin
 Ca2+ binds to troponin

shape change
causes movement
of troponin

releasing tropomyosin

exposes myosinbinding sites on actin
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How Ca2+ controls muscle
 ____________________


exposed actin binds to
myosin
fibers slide past each
other
ATP
 ratchet system

shorten muscle cell
 muscle contraction

muscle doesn’t relax
until Ca2+ is pumped
back into SR
 requires ATP
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ATP
Put it all together…
1
2
3
ATP
7
4
6
ATP
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5
How it all works…
 Action potential causes Ca2+ release from SR

Ca2+ binds to troponin
 Troponin moves tropomyosin uncovering myosin

binding site on actin
Myosin binds actin


ATP
uses ATP to "ratchet" each time
releases, "unratchets" & binds to next actin
 Myosin pulls actin chain along
 Sarcomere shortens

Z discs move closer together
 Whole fiber shortens  contraction!
 Ca2+ pumps restore Ca2+ to SR  relaxation!

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pumps use ATP
ATP
Fast twitch & slow twitch muscles
 Slow twitch muscle fibers

contract slowly, but keep going for a long
time
 more mitochondria for aerobic respiration
 less SR  Ca2+ remains in cytosol longer
long distance runner
 “dark” meat = more blood vessels

 Fast twitch muscle fibers

contract quickly, but get tired rapidly
 store more glycogen for anaerobic respiration
sprinter
AP Biology “white” meat

Muscle limits
 Muscle fatigue

lack of sugar
 lack of ATP to restore Ca2+ gradient

low O2
 lactic acid drops pH which
interferes with protein function

synaptic fatigue
 loss of acetylcholine
 Muscle cramps



build up of lactic acid
ATP depletion
ion imbalance
 massage or stretching
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increases circulation
Diseases of Muscle tissue
 ALS
amyotrophic lateral sclerosis
 Lou Gehrig’s disease
 motor neurons degenerate

 Myasthenia gravis
auto-immune
 antibodies to
acetylcholine
receptors

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Stephen Hawking
Botox
 Bacteria Clostridium botulinum toxin


blocks release of acetylcholine
botulism can be fatal
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muscle
Rigor mortis
 After death,
 Respiration ceases to occur, depleting oxygen used in the





making of ATP.
ATP is no longer operates the SERCA pumps in the membrane
of the sarcoplasmic reticulum, which pump calcium ions into
the terminal cisternae.
This causes calcium ions to diffuse from the terminal cisternae
and extracellular fluid to the sarcomere
Ca+ binding with troponin allows for crossbridging to occur
between myosin and actin proteins.
Body is unable to complete the cycle and release the coupling
between the myosin and actin; perpetual state of muscular
contraction,
Following the breakdown of muscle tissue by digestive enzymes
during decomposition, muscles relax
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So don’t be a stiff!
Ask Questions!!
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2006-2007