Final Information Flashcards

(63 cards)

1
Q

What are the three influencers of contraction force?

A

1) Number of active motor units
2) Size of muscle fibers in motor unit
3) Length of sarcomere

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2
Q

Tell me about the size of muscle fibers in motor units:

A

Different motor units contain motor fibers with different widths, but all motor fibers within a motor unit are the same.

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3
Q

How does size of muscle fibers in motor units relate to contraction force?

A

Small tension: only motor unit 1 recruited
Medium tension: motor unit 1 then motor unit 2 recruited
Large tension: motor unit 1 them motor unit 2 then motor unit 3 recruited

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4
Q

What are the different types of motor units?

A

Motor unit one: small diameter muscle fibers
Motor unit two: medium diameter muscle fibers
Motor unit three: large diameter muscle fibers

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5
Q

What is tension?

A

Tension is contraction force. An increase in tension is an increase in voltage that recruits more motor units

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6
Q

How does sarcomere length relate to tension?

A

Optimal sarcomere length is at resting position: this will produce the most force
Sarcomeres that are too stretched will produce less force as thick and thin filaments are unable to interact
Sarcomeres that are too contracted will produce less force as thick and thin filaments are already overlapping

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7
Q

What are the internal structures of a muscle cell?

A

Myofibril: Contractile organelle
Mitochondria: Produces ATP (~30 each)
Sarcolemma: Cell membrane
Sarcoplasm: cytoplasm
-myoglobin: stores O2 when it is abundant and releases it during a contraction to make more ATP
-glycogen: huge carbohydrate (polysaccharide) composed of glucose monomers. Glucose is released for fast ATP
Sarcoplasmic reticulum: Specialized Smooth ER raps around myofibrils that stores Ca 2+ and release it during contraction
T (transverse) tubules: Areas where sarcolemma indents into the cell - always found with SR on either side (triad)

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8
Q

What are the aspects of the sarcomere?

A

Myofilaments: Thick and thin filaments
Thin:
-Actin: two strands twisted together with a myosin binding site on each
-Tropomyosin: regulatory protein, at rest it covers myosin binding sites
-Troponin: Attached to actin and tropomyosin (holds tropomyosin in place), binds with Ca2+ change shape take tropomyosin with it opening myosin active site.
Thick:
-Myosin “golf club”
Tail: Bundled together creating thick filament
Head: has actin binding site and ATPase to break down ATP. Is able to move on hinge creating contractile movement

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9
Q

What is the neuromuscular junction and what are the aspects of it?

A

Where the neuron and the muscle come together
Synaptic end bulb
Neurotransmitter ACh
Synaptic cleft
ACh (cholinergic)
Motor end plate: highly folded to increase surface area to increase the number of receptors

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10
Q

What are the events of the neuromuscular junction?

A

Signal: Electric-chemical-electric
1. AP comes along somatic motor neuron axon
2. Ca2+ enters the neuron causing ACh to be released
3. ACh drifts across the synaptic cleft
4. Two ACh activates a ACh receptor that opens to for Na+ and K+ (more permeable to Na than K)
5. Membrane at motor end plate to become positive–depolarization
6. Depolarization reaches threshold and causes an AP to continue down sarcolemma to T tubules (carrying positive charge into the interior of the cell)

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11
Q

What happens during the excitation contraction coupling “act” of the muscle contraction “play”?

A

When at rest a voltage sensitive protein in the T tubule prevents the leakage of Ca2+ from the SR by “plugging” the leak channel in the SR
1. AP travels down T- tubule causing depolarization
2. Voltage sensitive protein changes shape (unplugging the hole)
3. Ca2+ is released from the SR into the sarcoplasm

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12
Q

What is the Cross Bridge Cycle “act” in the muscle contraction “play”?

A

*At rest myosin binds w/ ATP and ATPase breaks it into ADP and Pi then the myosin is ready to bind with an actin
1. Ca2+ binds with troponin
2. Troponin changes chape pulling the tropomyosin away from the actin and its myosin binding sight
3. Myosin binds with actin cross bridge formed
4. Pi released makes the cross bridge stronger
5. ADP released makes myosin head rotate and pull actin (and z-disk) toward the center of the sarcomere: The power stroke
6. ATP molecule binds with myosin caused myosin to detach but will be ready to bind with another actin until binding sight is blocked due to a lack of Ca2+

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13
Q

What is the sliding filament mechanism?

A

thick and thin filaments slide past each other overlapping more causes muscle to shorten

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14
Q

What are the two routes of bone formation? What are the differences between them?

A

1) Intramembranous: No hyaline precursor, only a few bones- most skull bones, mandible, and clavicles
2) Endochondral: Bones first formed by hyaline cartilage, most bones

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15
Q

What are the seven steps of Endochondral bone formation?

A

1) Cartilage model formation
2) Cartilage model increases in size
3) A shift in outer covering
4) Bone forms within the cartilage model
5) Invasion of tissue from periosteum “Periosteal bud”
6) Primary ossification center increases in size
7) Remaining hyaline cartilage

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16
Q

What happens during the cartilage model formation step of endochondral bone formation?

A

Mesenchymal cells cluster and then from chondroblasts
Chondroblasts secrete cartilage ECM to build cartilage tissue
Perichondrium forms
(At this point the model is small)

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17
Q

What are mesenchymal cells?

A

They are stem cells capable of any connective tissue production

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18
Q

What is perichondrium?

A

It is dense irregular connective tissue that covers over all cartilage.

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19
Q

What happens during the cartilage model size increase step of endochondral bone formation?

A

Chondroblasts differentiate to from chondrocytes
Chondrocytes divide increasing the length of the cartilage via interstitial growth
Perichondrium deposit more chondroblasts to allow the cartilage to increase in width via appositional growth.

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20
Q

What is the difference between interstitial and appositional growth?

A

Interstitial growth is internal growth while appositional growth is external growth

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21
Q

What happens during the shift in outer covering step of endochondral bone formation?

A

Perichondrium differentiates to periosteum
Periosteum produces bone cells and deposits osteogenic cells on cartilage model
Osteogenic cells differentiate to osteoblasts forming periosteal bone collar that wraps around the diaphysis

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22
Q

What happens during the bone forms within the cartilage model step of endochondral bone formation?

A

Chondrocytes hypertrophy (swell) and matrix changes from being gelatinous to calcifying
Chondrocytes cannot access nutrients and dies

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23
Q

What happens during the invasion of tissue from periosteum step of endochondral bone formation?

A

Periosteal bud- in pocketing of the periosteum carries nutrients, blood vessels, nerves, osteogenic cells, and osteoclasts into the model
Osteoclasts erode the calcified cartilage
Osteoblasts secrete bone ECM which hardens to form spongy bone tissue
This spongy bone is the first interior bone formation and is the primary ossification center

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24
Q

What happens during the increase of the primary ossification center step of endochondral bone formation?

A

Osteoclasts breaks down spongy bone in diaphysis to form medullary cavity
Chondrocytes hypertrophy in epiphyses (matrix calcifies cells die)
Periosteal bud enters epiphyses
-osteoclasts break down calcified chondrocytes
-osteoblasts from spongy bone
This is the secondary ossification center

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25
What happens during the remaining hyaline cartilage step of endochondral bone formation?
Articular cartilage covers the epiphyses Epiphyseal plate
26
What are the steps of intramembranous bone formation?
1) Mesenchymal cell differentiation 2) Osteoblasts secretion 3) Trabeculae formation 4) Compact bone and bone marrow formation
27
What happens during the mesenchymal cell differentiation step of intramembranous bone formation?
Mesenchymal cells cluster and differentiate to form osteogenic cells Osteogenic cells differentiate to form osteoblasts
28
What happens during the osteoblast secretion step of intramembranous bone formation?
Osteoblasts secrete osteoid Some osteoblasts become trapped and become osteocytes
29
What happens during the trabeculae formation step of intramembranous bone formation?
Matrix secreted and osteoblasts are trapped forms trabeculae around blood vessels Mesenchyme specialize to form periosteum
30
What happens during the compact bone and bone marrow formation step of intramembranous bone formation?
Trabeculae nearest to periosteum thickens to form compact bone Interior trabeculae remains and blood vessels form bone marrow -Red bone marrow is sometimes formed (one location is in the skull)
31
What two things must be stopped to stop muscle contraction? How are they stopped?
#1: Must get rid of ACh (neuron has stopped signaling) -Acetylcholinesterase AChE breaks down ACh in synaptic cleft -ACh can no longer function and cannot depolarize cell #2: Must put Ca2+ back in storage (Stop excitation coupling) -SR has CaATPase to pump Ca2+ against gradient and back into SR -No Ca2+ troponin goes back to its origninal shape and actin & myosin detach -Filaments slide back to their resting position
32
In what order are the ATP storage/production forms used?
Stored ATP then Phosphocreatine then Anaerobic respiration, then aerobic respiration. There is some overlap
33
What are the aspects of stored ATP?
Stored ATP is the surplus ATP in the muscle fiber while it is at rest Stored ATP powers the first few seconds of contracitons
34
What are the aspects of phosphocreatine ATP?
Phosphocreatine stores some ATP when the muscle is at rest by using creatine kinase to remove one of ATP's phosphate groups and attaching it to phosphocreatine (creating ADP) To create ATP creatine kinase is used to remove the phosphate group from phosphocreatine and combine it with ADP to create ATP Phosphocreatine is like a savings account keeping the ATP for sudden muscle activity so it is not used in other cell processes This is the fastest way to create ATP, but it only creates one net ATP. This fuels an additional few seconds of contraction
35
What are the aspects of anaerobic respirations?
Glucose is removed from glycogen via glycolysis in the sarcoplasm (does not require oxygen) Creates two net ATP and two pyruvic acid molecules Continues contractions for a few minutes
36
What are the aspects of aerobic respirations?
Oxidative phosphorylation that uses O2 and all the byproducts of glycolysis in the mitochondria Creates about 30 net ATP Continues contractions for hours
37
What are the three types of muscle fiber?
Slow-twitch oxidative (type I) Fast-twitch oxidative-glycolytic (Type IIa) Fast-twitch glycolytic (Type IIb/IIX)
38
What is the size, capillary density, mitochondria, color, endurance, use, and metabolism of slow-twitch oxidative muscle fibers?
Size: Diameter-small (++skinny) Capillary density: high Mitochondria: super numerous Color: Dark red- high amount of myoglobin Endurance: Fatigues very slow Use: Posture (Posture muscles mostly contain Type I fibers) Metabolism: Aerobic (mostly)
39
What is the size, capillary density, mitochondria, color, endurance, use, and metabolism of fast-twitch oxidative-glycolytic muscle fibers?
Size: Diameter-medium Capillary density: medium Mitochondria: moderate (between numerous and scarce) Color: Red- medium myoglobin Endurance: Fatigues medium Use: Standing & walking Metabolism: Aerobic and anaerobic
40
What is the size, capillary density, mitochondria, color, endurance, use, and metabolism of fast-twitch glycolytic muscle fibers?
Size: Diameter-large Capillary density: low Mitochondria: Few (scarce) Color: Pale- low myoglobin Endurance: Fatigues fast Use: Jumping, quick, fine, movements. Fast (eye movement/blinking), high tension (weightlifting) movements Metabolism: Anaerobic (mostly)
41
What is fatigue?
Fatigue is a reversible condition in which an exercising muscle is no longer able to generate or sustain the expected power output
42
Why does fatigue happen?
We don't know. Some speculate: a. Central fatigue: psychological effects, protective reflexes b. Peripheral fatigue: overrides central fatigue -because of events in the muscle cell: membrane potential, too much K+ lost -Depletion of resources: PCr, ATP, glycogen *NOT lactic Acid build up*
43
What are the functions of the skeleton?
Support: structure of the body, location for organ residence Protection: Hardness protects organs Movement: muscles tug on bones to move through environment Blood Cell Production: ALL blood cells are produced in the red bone marrow Energy & mineral Storage: Stores adipose tissue as yellow marrow in medullary cavity. Stores (mainly) CaPO4, calcium phosphate, in hydroxyapatite-a crystalized mineral structure
44
What does red bone marrow undergo?
Hematopoiesis: The process by which blood cells are produced
45
What are the skeletal bone shapes?
Long, irregular, flat, short, sesamoid
46
What defines a long bone? What are some examples?
A bone that is longer than it is wide Examples: Humerus and phalanges
47
What defines an irregular bone? What are some examples?
Irregular shape Examples: Vertebrae
48
What defines a flat bone? What are some examples?
Thin and flat, can be slightly curved Examples: frontal bone, sternum, ribs
49
What defines a short bone? What are some examples?
As tall as wide Examples: Tarsals, carpels
50
What defines a sesamoid bone? What are some examples?
Sesame seed shaped, tapered at end within a tendon or ligament Examples: patella
51
What are the organic components of bone?
Osteoid (mostly collagen) and cells
52
What are the two groups of bone cells?
Osteogenic (w/ osteoblast, osteocytes) and osteoclasts
53
What is the function of osteogenic cells? Where are they found? What does it differentiate to?
Osteogenic cells are very immature and are able to divide to make more bone cells Found: Periosteum and endosteum Differentiates to Osteoblast
54
What is differentiation?
The specialization of a cells structure and characteristics (such as behavior)
55
What is the function of osteoblasts? What happens to it? What does it differentiate to?
Secrete organic material between bone cells "osteoid" They secrete so much that they cannot move Differentiate to form osteocytes
56
What are osteocytes? What is their function?
Trapped osteoblast that cannot secrete. They are the living cells within the lacuna Function: Communicate with other cells in tissue, monitor stresses on bone, regulate structure of bone.
57
When do mesenchymal cells cluster? What causes them to cluster?
When: Early embryonic development Cause: chemical signaling
58
What are osteoclasts?
They are about 30 fused monocytes--really big white blood cells Function: Bone cleaving, they dissolve bones (osteoid and hydroxyapatite) with lysosomal enzymes -Reason: to free up Ca2+, for bone remodeling, general cleanup of bone debris- often fragments from breaks
59
What are the three aspects of bone growth?
Growth of length, width, and medullary cavity
60
How does a bone grow lengthwise?
Proliferative zone: Closest to epiphyses, healthy, active chondrocytes make more chondrocytes by dividing and secreting ECM to increase the size of this zone Hypertrophic zone: Closer to the diaphysis: chondrocytes hypertrophy Calcification zone: Matrix calcifies and cells die Ossification zone: Osteoclasts dissolve calcified chondrocytes and osteoblasts enter to replace with bone cells *The growth plate is pushed up* "The bone is chasing the cartilage"
61
How does a bone grow widthwise?
Periosteum deposits new osteogenic cells on bone surface 1) osteogenic cells in the periosteum differentiate to osteoblasts. Osteoblasts secrete osteoid. Osteocytes are formed as well as ridges around the periosteal blood vessels 2) Ridges of bone fuse together enclosing blood vessels *Periosteum is now called endosteum* 3) Endosteum produces osteoblasts forming lamellae leading to osteon with blood vessel in middle 4) Periosteum forms more osteoblasts around the next blood vessels
62
How does the medullary cavity grow?
Osteoclasts erode bone to make cavity larger
63
What are the aspects of bone remodeling?
Bone changes shape due to stress Resorption: osteoclasts remove fragments of damaged bone, osteoblasts reform bone in areas of stress, New, stronger bone is formed- bone is more resistant to breaking *Inactivity does not promote bone remodeling causing bones to become weaker*