Download Bone and Muscle Review

Bone and Muscle
Review
CHAPTERS 6 AND 9
Cartilage in
external ear
Cartilage in
Intervertebral
disc
Cartilages in
nose
Articular
Cartilage
of a joint
Epiglottis
Thyroid
cartilage
Cricoid
cartilage
Larynx
Trachea
Lung
Costal
cartilage
Respiratory tube cartilages
in neck and thorax
Pubic
symphysis
Meniscus
(padlike
cartilage in
knee
joint)
Articular
cartilage
of a joint
Bones of skeleton
Axial skeleton
Appendicular skeleton
Cartilages
Hyaline cartilage CT
Elastic cartilage CT
Fibrocartilage CT
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Figure 6.1
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Figure 6.2
Last Lecture We Covered…
• Six Functions of Bone:
• 1. Protection
• 2. Support
• 3. Movement
• 4. Storage of minerals
• 5. Blood cell formation (hematopoiesis)
• 6. Fat storage
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Spongy bone inside a flat bone
Spongy bone
(diploë)
Compact
bone
Trabeculae
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Figure 6.5
Articular
cartilage
Proximal
epiphysis
Compact bone
Spongy bone
Epiphyseal
line
Periosteum
Compact bone
Medullary
cavity (lined
by endosteum)
(b)
Diaphysis
Distal
epiphysis
(a)
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Figure 6.3a-b
Structures
in the
central
canal
Artery with
capillaries
Vein
Nerve fiber
Osteons have
many layers
called lamella
Lamellae
Collagen
fibers
run in
different
directions
Twisting
force
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Figure 6.6
Bone cells
• Osteoprogenitor/Osteogenic cells
• make osteoblasts
• Osteoblasts
• secrete osteoid, make bone
• Osteocytes
• mature bone cells inside lacunae
• Osteoclasts
• absorb bone
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Osteocytes are connected by canaliculi (little canals)
through which their “arms” pass nutrients to cells far
from the blood in the central canal, and waste back.
blood
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Last Lecture We Covered…
• Formation of bone:
• Osteoblasts secrete collagen fibers and proteoglycan gel (like a
slug’s slime trail)
• Calcium ions (Ca2+) arrive from blood and bind to collagen
• Phosphate (PO4-) arrives from blood and binds to Calcium
• Hydroxyappatite crystals form (bone minerals) and hardens
matrix into bone.
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What we covered last time…
• Two Types of Ossification
• Intramembranous Ossification
• Spongy bone forms first from a primary
ossification center between two thick CT
membranes
• Endochondral Ossification
• Compact bone forms first around cartilage
as bone collar. Primary and secondary
ossification centers turn existing cartilage
into bone.
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Intramembranous ossification of flat bones
CT stem cell
Collagen
fiber
Ossification
center
Osteoid
Osteoblast
1. Early “stem” cells make a collagen sheet, or membrane.
2. Inside this membrane, osteoblasts form from other stem
cells
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Figure 6.8, (1 of 4)
Intramembranous ossification
Osteoblast
Osteoid
Osteocyte
Newly calcified
bone matrix
3. Osteoblasts secrete osteoid (a mix of gel and collagen fibers)
4. Calcium phosphate adds to the collagen, forming spongy bone.
5. Trapped osteoblasts become osteocytes.
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Figure 6.8, (2 of 4)
Intramembranous ossification
CT stem cells
condensing
to form the
periosteum
Spongy bone
Blood vessel
6. Blood vessels arrive, and more spongy bone forms
7. Nearby connective tissue becomes the periosteum cover.
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Figure 6.8, (3 of 4)
Intramembranous ossification
Fibrous
periosteum
Osteoblast
Plate of
compact bone
Spongy bone
cavities
contain red
marrow
8. Osteoblasts change the way they lay down collagen,
and form compact bone around the spongy bone,
and below the periosteum.
9. Red marrow appears as blood cells are produced in the
marrow cavities.
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Figure 6.8, (4 of 4)
Month 3
Week 9
After conception
Birth
Articular
cartilage
Secondary
ossification
center
Epiphyseal
blood vessel
Area of
deteriorating
cartilage matrix
Hyaline
cartilage
Spongy
bone
formation
Bone
collar
Primary
ossification
center
1 A hyaline
cartilage “model”
of a bone forms.
Compact bone collar
forms around it
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2 Central
cartilage area
has a planned
cell death
Childhood to
adolescence
Spongy
bone
Epiphyseal
plate
cartilage
Medullary
cavity
Blood
vessel of
periosteal
bud
3 Blood vessels
enter, ostepblasts
and minerals arrive
and spongy bone
forms in diaphyses.
4 The diaphysis elongates
and osteoclasts form
the marrow cavity.
In the epiphyses, cartilage
dies and spongy bone forms.
5 The epiphyses ossify.
Hyaline Cartilage remains
only in the epiphyseal
plates and articular
cartilages.
Figure 6.9
Growth in the length of long bones occurs at epiphyseal plate
Resting zone
Proliferation zone
Cartilage cells undergo
mitosis.
1
Hypertrophic zone
Older cartilage cells
enlarge.
2
Calcified cartilage
spicule
Osteoblast depositing
bone matrix
Osseous tissue
(bone) covering
cartilage spicules
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Calcification zone
Matrix becomes calcified;
cartilage cells die; matrix
begins deteriorating.
3
4 Ossification zone
New bone formation is
occurring.
Figure 6.10
Last Time We Covered…
• Appositional Bone growth
– Bone thickening/widening
– Occurs when osteoblasts under the periosteum.
produce bone faster than osteoclasts can absorb
bone from the endosteal surface.
• Bone grows/remodels in response to the
forces placed on it. (Wolff’s Law)
– Bones thickest at midpoint of diaphysis, bones
thicker in dominant hand, thick prominences
where muscles attach, weak bones in bed ridden
people or astronauts.
Load here (body weight)
BONE SHAPE
depends on the
forces placed upon it
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Figure 6.13
What processes correct low blood calcium?
1. Falling blood
Ca2+ levels
4. Calcium is
released from bone
into blood
Thyroid
gland
3. PTH stimulates
osteoclasts to
digest bone.
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Parathyroid
glands
2. Parathyroid
glands release
parathyroid
hormone into
blood.
PTH
Figure 6.12
Last Time We Covered…
• Fracture types:
–
–
–
–
–
–
–
–
–
–
Nondisplaced/Displaced
Complete/Incomplete
Linear/Transverse
Simple/Compound
Comminuted
Compression
Spiral
Epiphyseal
Depressed
Greenstick
Hematoma
Internal
callus
(fibrous
tissue and
cartilage)
External
callus
New
blood
vessels
Bony
callus of
spongy
bone
Healed
fracture
Spongy
bone
trabecula
1 A hematoma forms. 2 Fibrocartilaginous
3 Bony callus forms.
callus forms.
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4 Bone
remodeling
occurs.
Figure 6.15
• Rickets:
Last Time We Covered…
– Vit. D or Calcium deficiency
– Causes bone deformities because bone matrix is
poorly mineralized: Soft bones called
Osteomalacia
– Rare in USA because of fortified milk
• Osteoporosis:
– Bone absorption outpaces bone formation
– Porous weak bones.
– Spine and femoral head most susceptible to
fracture.
Last Time…
• The four characteristics of skeletal muscle:
• 1. Excitable (turned on by nerves)
• 2. Contractile (shorten when stimulated)
• 3. Extensible (can elongate without damage)
• 4. Elastic (can spring back to resting length)
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Skeletal Muscles are vascular
• Each muscle is served by 1 artery, at least
1 vein, and 1 nerve
M
u
S
C
L
e
Spinal
cord
EPImysium
wraps whole muscle
Tendon
Each part of the muscle
is wrapped in a
connective tissue
wrapping which protects
the cells, and gives some
stretch to the muscle
(b)
ENDOomysium
(wraps individual
muscle cells)
PERImysium
Wraps a bundle of
muscle cells
Fascicle:
A bundle of muscle cells
Muscle CELL
(somethimes
called a fiber)
Figure 9.1
This is ONE muscle cell. What are the clues?
MYOFIBRILS are broken into smaller units called SARCOMERES
SARCOMERES are made of smaller units called FILAMENTS (myofilaments)
Z disc
Z disc
(c) Small part of one myofibril enlarged to show the myofilaments
responsible for the banding pattern. Each sarcomere extends from
one Z disc to the next.
Sarcomere
Z disc
Z disc
Thin (actin)
filament
Elastic (titin)
filaments
Thick
(myosin)
filament
(d) Enlargement of one sarcomere (sectioned lengthwise). Notice the
myosin heads on the thick filaments.
Figure 9.2c, d
A single myosin molecule
A place to bind to the actin in the thin filament
A place for ATP to bind
• Twisted double strand of G actin beads
• G actin has active sites for myosin head attachment, but
they are covered by tropomyosin
• Tropomyosin and troponin: are proteins bound to actin
that regulate whether or not the actin and myosin
attach to each other and pull
Last Time…
• Sliding filament model
• Step 1: Calcium is released from the SR and binds
Troponin.
• Step 2: Troponin changes shape and moves
tropomyosin exposing binding site for myosin
• Step 3: Myosin binds actin and ADP + Pi is released
and power stroke occurs
• Step 4: ATP binds to myosin and releases it from actin
• Step 5: ATP hydrolyzed into ADP + Pi releasing
energy and re-cocking myosin head
• Step 6: Muscle contraction ends when calcium actively
pumped back into SR
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WHY do the ions move the way they do?
• Why does Ca+ move INTO the nerve cell?
• Why does Na+ move INTO the muscle cell?
• Why does K+ move OUT of the muscle cell?
• HINT: you learned this in General Biology
OUTSIDE
IN
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Lo Na+
Lo ClLo Ca+
Hi K+
Hi Na+
Hi ClHi Ca+
Lo K+
IN
Lo Na+
Lo ClLo Ca+
Hi K+
A nerve cell (brain or spinal cord must
signal a muscle cell!
Myelinated axon
of motor neuron
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
Action
potential (AP)
Nucleus
1 Action potential arrives at
axon terminal of motor neuron.
2 Voltage-gated
Ca2+
channels
open and Ca2+ enters the axon
terminal.
Ca2+
Ca2+
Axon terminal
of motor neuron
3 Ca2+ entry causes some
Fusing synaptic
vesicles
synaptic vesicles to release
their contents (acetylcholine)
by exocytosis.
ACh
4 Acetylcholine, a
neurotransmitter, diffuses across
the synaptic cleft and binds to
receptors in the sarcolemma.
Na+
K+
channels that allow simultaneous
passage of Na+ into the muscle
fiber and K+ out of the muscle
fiber.
by its enzymatic breakdown in
the synaptic cleft by
acetylcholinesterase.
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Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
5 ACh binding opens ion
6 ACh effects are terminated
Synaptic vesicle
containing ACh
Mitochondrion
Synaptic
cleft
Ach–
Degraded ACh
Na+
Acetylcholinesterase
K+
Postsynaptic membrane
ion channel opens;
ions pass causing a brief
depolarization and
repolarization.
Postsynaptic membrane
ion channel closed;
ions cannot pass so no
further depolarization
occurs.
Figure 9.8
The Action potential is a signal that moves along
the sarcolemma and down the T tubules, and then
Ca++ is released from the SR into the cytoplasm
Steps in
E-C Coupling:
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cisterna
of SR
Ca2+
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Figure 9.11, step 3
Steps in E-C Coupling:
Sarcolemma
Voltage-sensitive
tubule protein
T tubule
1 Action potential is propagated along
the sarcolemma and down the T tubules.
Ca2+
release
channel
2 Calcium ions are released.
Terminal
cisterna
of SR
Ca2+
Actin
Troponin
Ca2+
Tropomyosin
blocking active sites
Myosin
3 Calcium binds to troponin and
removes the blocking action of
tropomyosin.
Active sites exposed and
ready for myosin binding
4 Contraction begins
Myosin
cross
bridge
The aftermath
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Figure 9.11, step 8
Actin
Ca2+
Myosin
cross bridge
Thin filament
ADP
Pi
Thick filament
Myosin
1 Cross bridge formation.
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Figure 9.12, step 1
ADP
Pi
2 The power (working) stroke.
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Figure 9.12, step 3
ATP
3 Cross bridge detachment.
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Figure 9.12, step 4
ADP
ATP
Pi
hydrolysis
4 Cocking of myosin head.
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Figure 9.12, step 5
Spatial
summation Go to gym
Large
number of
muscle
fibers
activated
Large
muscle
cells
Temporal
summation
Best sarcomere
length
High
frequency of
stimulation
Muscle and
sarcomere
stretched to
slightly over 100%
of resting length
FOUR WAYS TO INCREASE THE FORCE OF CONTRACTION
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Figure 9.21
What does TRYING HARDER mean?!
Think harder
(stimulate
more brain
cells)
Turn on more
nerves going
to muscles
Stimulus strength
Maximal
stimulus
Threshold
stimulus
Proportion of motor units excited
Strength of muscle contraction
Turn on more
muscle cells to
create more
FORCE
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Maximal contraction
Figure 9.16
Very low frequency of stimulation leads to low force production
Single stimulus
SINGLE
MUSCLE
TWITCH
Contraction
Relaxation
Stimulus
A single stimulus is delivered. The muscle
contracts and relaxes (muscle twitch) with low force
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Figure 9.15a
Apply another stimulus before the first totally
relaxes and the forces sum!
Low stimulation frequency
INCOMPLETE
TETANUS
Partial relaxation
Stimuli
The faster you stimulate the muscle, the more forcefully it contracts
…………….UP TO A POINT….
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Figure 9.15b
Repeated fast stimulation makes the maximum force possible
High stimulation frequency
COMPLETE TETANUS
Stimuli
Probably because large amounts of calcium are entering the cell
and allowing very rapid thin and thick filament pulling.
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Figure 9.15c
4. INCREASE FORCE by changing the sarcomere length
Sarcomeres
greatly
shortened
Sarcomeres at
resting length
Sarcomeres excessively
stretched
75%
100%
170%
Optimal sarcomere
operating length
(80%–120% of
resting length)
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Figure 9.22
Does muscle contraction always produce movement?
single cells
and
whole muscles
always produces
FORCE
but
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shortens a muscle
(isotonics)
Or does NOT
shorten a
muscle(isometrics)
(you TRY to move,
and do)
(you TRY to move,
and don’t)
Short-duration exercise
STORED ATP
ATP stored in
muscles is
used first.
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ENZYMES
ATP is formed
from creatine
Phosphate
and ADP using
Enzymes in the
cytoplasm
GLYCOLYSIS
Glycogen stored in muscles is broken
down to glucose, which is oxidized to
generate ATP using enzymes in the
cytoplasm
Prolonged-duration
exercise
AEROBIC METABOLISM
ATP is generated by
breakdown of several
Nutrients in the mitochondria
And requiring oxygen.
Figure 9.20
(a)
Direct phosphorylation
Coupled reaction of creatine
phosphate (CP) and ADP
Energy source: CP
CP
ADP
Creatine
kinase
Creatine
ATP
Fuels: CP, ADP
Produces: 1 ATP
per CP
Provides ATP for
15 seconds of
Activity.
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration of energy provision:
15 seconds
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Figure 9.19a
(b)
Anaerobic pathway
Glycolysis and lactic acid formation
Energy source: glucose
Produces:
a. 2ATP per glucose and
b. Lactic acid-diffuses into
Glucose (from
glycogen breakdown or
delivered from blood)
the bloodstream and is used as
fuel by the liver, kidneys, and
heart, OR converted back into
pyruvic acid by the liver.
Glycolysis
in cytosol
2
O2
ATP
Fuel: glucose
Pyruvic acid
Provides ATP for 60 seconds
of activity.
net gain
O2
Released
to blood
Lactic acid
Oxygen use: None
Products: 2 ATP per glucose, lactic acid
Duration of energy provision:
60 seconds, or slightly more
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Figure 9.19b
(c)
Aerobic pathway
Aerobic cellular respiration
Energy source: glucose; pyruvic acid;
free fatty acids from adipose tissue;
amino acids from protein catabolism
Fuels: glycogen, glucose,
Fatty acids, amino acids
Needs: Oxygen & Mitochondria!!!
Produces: 32 ATP per glucose
Glucose (from
glycogen breakdown or
delivered from blood)
O2
Pyruvic acid
Fatty
acids
O2
Aerobic
respiration
Aerobic respiration
in mitochondria
mitochondria
Amino
acids
32
CO2
H2O
ATP
Produces 95% of ATP during rest
and light to moderate exercise.
BUT, if you go too fast, ATP
production cannot keep up, and you
FATIGUE.
net gain per
glucose
Oxygen use: Required
Products: 32 ATP per glucose, CO2, H2O
Duration of energy provision: Hours
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Figure 9.19c
So, if you want to run for a long time you need the right
resources……
You get them by aerobic (endurance) training:
-Makes chest muscles stronger to pull in more oxygen
-encourages capillary growth to bring oxygen to muscles
-increases myoglobin synthesis so cells hold more oxygen
-increases the number of mitochondria in cells, to make more ATP
Capillaries grow at
about the same
rate as grass.
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Light colored cells are called
FAST TWITCH MUSCLE CELLS
They have:
• Few myoglobin ((oxygen
holding molecule)
• Few mitochondria
• Higher glycogen stores
• Fast speed of contraction
Based on their characteristics
are these aerobic or anaerobic
cells?
Hint: think of how much ATP the
above ingredients could
produce…
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Dark colored muscle cells are called
SLOW TWITCH MUSCLE CELLS
They have:
• Lots of myoglobin (oxygen holding
molecule)
• Many mitochondria
• Lower glycogen stores
• SLOW speed of contraction
Based on their characteristics
are they aerobic or anaerobic cells?
Hint: think of how much ATP the
above ingredients could produce…
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Strategies for doing well on the test:
• Read the test first, make sure you understand what is expected of you.
• Manage your time! If you get stuck on a MC question, skip it and come back
later.
• Multiple Choice/Matching questions:
• Your first instinct is usually correct.
• If you get stuck, try and eliminate at least two responses you know are incorrect.
That way you now have a 50/50 chance, and remember your first instinct.
• You can also read the question before each response, this can help you to weed
out answers if they don’t sound right.
• Read the question CAREFULLY, make sure you know what it is asking before
selecting an answer.
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Strategies for doing well on the test:
• Written questions:
• Decide which questions you are going to answer at the beginning.
• Make an outline of the points you want to cover.
• Pay attention to information in MC questions that may help you answer
written questions.
• Use your outline to construct your response into sentences that tell a story.
• Re-read your answers as you go and make sure you are answering the
questions asked.
• If you are not sure of something, raise your hand or come up and ask!
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