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Human Physiology 2 > Metabolism Cont'd, Control & Skeletal Muscle > Flashcards

Metabolism Cont'd, Control & Skeletal Muscle Flashcards

1
Q

Glycolysis

A

10 enzymatic reactions that converts a 6-carbon molecule of glucose into 2,3-carbon molecule of pyruvate (forward reaction)

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2
Q

describe glycolysis

A
  • > requires glycolytic enzymes and carbohydrates
  • > occurs in the cytosol of most cells
  • > produces little energy by can proceed without oxygen or mitochondria
  • > catabolizes carbs (primarily glucose), can use fructose and galactose as these are converted into intermediates of glycolysis early in the pathway
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3
Q

which types of cells use the glycolysis pathway for energy production, why?

A

Red blood cells
- > does not contain any organelles (no mitochondria) but they do have cytosolic enzymes required for glycolysis
Certain types of skeletal muscles
- > some have low levels of mitochondria

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4
Q

characteristics of glycolysis

A
  • > uses monosaccharides
  • > occurs in cytosol (not organelle dependant)
  • > net 2 ATP formed/molecule glucose (4 total but we need to use 2 to continue the process)
  • > less ATP formed than other pathways, but supplies pyruvate to Kreb’s cycle and NADH + H+ to oxidative phosphorylation pathways
  • some pyruvate is converted to lactate which can be used to regenerate NAD+
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5
Q

Starting/input equation for glycolysis

A

Glucose + 2ADP + 2Pi + 2NAD

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6
Q

final equation of glycolysis

A

2 Pyruvate + 2ATP +2NADH+ 2H+ +2H2O

  • > 2NADH+ 2H+ are then used in oxidative phosphorylation
  • > pyruvate can be used in the Kreb’s cycle or converted into lactate and used in OP
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7
Q

increased metabolic demands in the body (i.e. intense muscle exercise) causes what?

A

Incr. metabolic demands leads to increased lactate production (pyruvate conversion) which is released into the blood and sent to either the liver, where it’s used as a precursor for glucose production, or it’s used by the heart, brain, and other tissues where it is converted back to pyruvate.

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8
Q

Krebs Cycle

A
  • > aka. tricarboxylic acid cycle (TCA cycle) and citric acid cycle
  • > occurs in the mitochondria of most cells (red blood cells can’t use this pathway
  • > utilizes molecular fragments formed during carb, proteins and fat breakdown
  • > requires acetyl CoA (derived from Vit B5), that is supplied by glycolysis, as an entering substrate
  • > require aerobic conditions (although oxygen is not directly used)
  • > does not produce much ATP but does produce products required by OP
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9
Q

How does the Kreb cycle work?

A
  • > it works by transferring acetyl groups from one molecule to another
  • > 2 carbon atoms enter the Krebs cycle as part of the acetyl group and 2 carbons leave in the form of CO2, where the O2 is not from molecular oxygen but rather from the carboxyl groups of Krebs cycle intermediates
  • > the intermediates in the Krebs cycle generate H+ atoms, most of which are transferred to co enzymes: NAD+ and FAD to form NADH and FADH2
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10
Q

characteristics of the Krebs Cycle

A
  1. acetyl group required
  2. Occurs in mitochondria
  3. 1 GTP formed which can be converted to 1 ATP
  4. Occurs in the presence of oxygen
  5. Produces: 3 NADH, 3 H+, 1 FADH2
  6. 2 CO2 final product
  7. intermediates can be used for AA production, but if it’s removed from the KC then it has to be replaced
  8. provides H+ for OP
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11
Q

Krebs Cycle summary

A

Acetyl CoA + 3NAD + FAD + GDP + Pi +2H2O - > 2 CO2 + CoA + 3NADH +3H + FADH2 + GTP
- > GTP can give ADP a phosphate to make ATP

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12
Q

Oxidative phosphorilation

A
  • > occurs in the mitochondria
  • > basic principle: energy transferred to ATP is derived from energy released when hydrogen ions combine with molecular oxygen to form water
  • > oxygen/aerobic conditions required
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13
Q

Which 2 groups of enzymes does OF use to transfer energy from fuel to ATP

A
  1. Enzymes that mediate a series of reactions by which H+ ions are transferred to O2 = cytochromes (most contain iron and copper cofactors)
  2. Enzymes that couple the energy released by the above reactions to the synthesis of ATP
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14
Q

Characteristics of OP

A
  1. H+ primary substrate (from Krebs cycle)
  2. Requires oxygen - in fact, most of the oxygen we breath is used here
  3. occurs in the inner mitochondrial membrane where the required enzymes are embedded
  4. 5 molecules of ATP produced from 2HADH + 2H
  5. 3 molecules of ATP produced from 2FADH2
  6. final product is H2O and ATP
  7. Forms majority of ATP
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15
Q

describe how OP forms ATP

A
  • > ATP formed through a series of reactions (electron transfer=electron transport chain) from NADH, H, and FADH2
  • > 2 electrons from H atoms are initially transferred from NADH + H or FADH2 (from the krebs cycle) to one of the elements in the electron transport chain
  • > 2 electrons are then successively transferred to other compounds in the chain (often to or from iron or copper) until transfer to molecular oxygen which then combines with 2H to form H20
  • > transferring H+ to H20 regenerates H+ free forms of the co-enzymes and allows for new reactions to occur
  • > at each step, small amounts are released and linked to ATP formation
  • > ATP is formed at 3 points in the chain through the chemiosmotic hypothesis
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16
Q

chemiosmotic hypothesis

A
  • > the energy that is released as electrons are transferred is used to move H from the mitochondrial matrix into the compartment between the inner and outer membranes resulting in a H+ gradient
  • > at 3 points along the inner membrane, H+ channels form allowing for the influx of H back into the matrix and the transfer of oxygen to ADP +Pi = ATP
  • > see page 38 for diagram
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17
Q

Reactive Oxygen Species (ROS)

A

during electron transfer, highly reactive oxygen derivatives can be formed

  • > molecules such as hydrogen peroxide (H2O2) and free radicals such as superoxide (O^2-) and the hydroxyl radical (OH)
  • > these reactive oxygen species can cause damage to cells through reactions with proteins and with membrane phospholipids (ROS can “pull” hydrogens off fatty acid tails of membrane phospholipids)
  • > cells do not contains the means to deal with theses reactive molecules (free radical scavengers, antioxidants; vitamin E and glutathione)
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18
Q

what systems does our body use for control/communication

A

endocrine and neural systems

- > they work together and can activate each other

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19
Q

endocrine system

A
  • > consists of glands that secrete hormones
  • > activation of gland secretion can be used through a variety of chemical messenger pathways, including neural activation
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20
Q

hormones

A

chemical messengers carried via the bloodstream

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21
Q

nervous system hierarch

A

see page 1

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22
Q

components of the control system

A
  1. Reflex arc

2. local control

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23
Q

explain the reflex arc

A

SEE PAGE 2

  • > starts with stimulation of receptor cells (either external or internal specialized cells i.e. thermoreceptors, nociceptor, mechanoreceptor)
  • > signal that is generated travels up the afferent pathway (neural pathway) to the integrating centre (brain and spinal cord)
  • > a response is then sent down the efferent neural pathways to the effector cells (muscle, glands, ect) and a change is effected
  • > reflexes include NS and endocrine components
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24
Q

example of a reflex arc

A

thermoregulation

- > see back of page 2

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25
Q

what is local control, give some examples

A
  • > changes in cell activity due to changes to internal or external environments
  • > stimulus results in a response that occurs in the area of the stimulus
  • i.e. local skin damage or exercising muscles
  • > release of metabolic byproducts + waste signals local increase in blood + oxygen delivery to the exercising muscles
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26
Q

How do chemical messengers and receptors work together for control/system balance

A
  • > system balance is maintained through a variety of feedback mechanisms involving release/secretion of chemical messengers/neurotransmitters and binding of those chemical messengers/neurotransmitters to specific receptors
  • > chemical messengers can be ions, molecules, hormones, and neurotransmitters, they can be released from a cell and act locally or travel in the blood to a distant site before activation of a process
  • > many chemical messengers can bind to a variety of receptors and will activate different responses depending on the type of receptor found in the effector cell
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27
Q

target cells

A

cell acted on by a chemical messenger

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28
Q

neurotransmitter

A

chemical messengers for communication between…

  • > nerve cell to nerve cell
  • > nerve cell to effector cell
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29
Q

neurohormones

A

chemical messengers released into the bloodstream by neural cells

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30
Q

paracrine agent and autocrine agents

A

*both involved in local response
Paracrine
- > chem mess released by cells that act on neighbouring cells. Rapidly broken down by enzymes so do not enter the blood stream
Autocrine
- > chem mess that acts on the cell that released it
* a messenger can be both para and autocrine; acting on neighbouring cells and the cell that released it

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31
Q

ligand

A

chemical messenger that binds to a specific cell receptor

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32
Q

agonist and antagonist chemical messengers

A

agonist
- > ligand that binds to a receptor and turns on the receptor and elicits a response (usually distinct from the normal ligand for that receptor)
antagonist
- > ligand that binds to a receptor and blocks the normal response

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33
Q

what is a receptor and some of its characteristics

A
  • > receptors (specific membrane proteins) are a “mechanical switch” turned on by binding/presence of a chemical messenger
  • > cells contain many receptors specific for the different chemical messengers
  • > a cell response to a chemical messenger increases as the extracellular concentration of the messenger increases and/or the # of receptors increases
  • > the cellular response will continue to increase until “saturation” (all the receptors are bound to a messenger)
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34
Q

plasma membrane receptor activation can be through

A

1st messengers
- > chemical messengers that reach the cell from the extracellular fluid and bind to their specific receptor
2nd messenger
- > substances that enter or are generated in the cytoplasm in response to receptor activation by 1st messengers

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35
Q

how do we regulate receptors

A

the # of receptors a cell has and the affinity of the receptor for the messenger can be regulated
Down-regulation
- > plas.mem receptor-messenger complexes can be brought into the cell, where it is degraded. Eventually the plas.mem concentration of that receptor decreases and the response associated with that receptor also decreases
Up-regulation
- > # of receptors is increased to try and increase the sensitivity to low concentrations of messengers, i.e. the more receptors a cell has the greater the chance that the messenger will bind to a receptor, initiating a response

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36
Q

characteristics of up/down regulation

A
  • > both up and down regulation can be controlled through protein synthesis since receptors are proteins
  • > with down regulation, synthesis of the protein/receptor is slowed or stopped
  • > with up regulation, synthesis of the protein/receptor is increased
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37
Q

how are chemical messengers and receptors competitive and specific

A

see page 5 and 6 for example

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38
Q

define signal transduction

A

conversion of the signal from the chemical messenger to cellular response

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39
Q

what are the 2 classes of messengers

A

Lipid(fat) soluble (lipophilic)
- > chemical messengers bind to receptors in cytosol; messenger crosses the membrane lipid bilayer and into the interior of the cell
- > SLOW RESPONSE, takes time to cross barrier
- > i.e. hormone
Lipid-insoluble (lipophobic)
- > chemical messengers that bind to receptors on the plasma membrane
- > receptors are a part of this pathway
- > fast response pathway

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40
Q

classes of lipid-insoluble chemical messengers

A

Ion channels
Protein kinases
Protein Phosphatases
JAK/STAT

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41
Q

what are ion channels

A

the simplest mechanism for turning on cellular response; often used for the initiation/transfer of electrical signals

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42
Q

protein kinases

A
  • > transmembrane proteins, where the extracellular side contains the receptor and the intracellular side contains the enzyme(protein kinase) which is activated by the binding of the messenger
  • > once enzyme is activated, it can phosphorylate (add P from ATP) cytosolic proteins, plasma membrane proteins and itself
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43
Q

protein phosphatases

A

these are enzymes that basically do the opposite of protein kinases
- > they de-phosphorylate proteins

44
Q

JAK/STAT

A

Janus Kinase/Signal Transducers and Activators of Transcription

  • > are associated with specific receptors and act together as a unit
  • > is the principle signalling pathway for cytokines and growth factors
  • > jak/stat activity stimulates cell replication, differentiation, migration and apoptosis (cell death) (the replication/death gives kinase the name janus because of the 2 faced roman god)
45
Q

the activation of jak kinases

A

the different jak kinases are activated together resulting in tyrosine kinase activation and phosphorylation of the receptor and transcription factor substrates that are latent in the cytoplasm until activation

46
Q

characteristics of G-proteins

A
  • > most complex of the receptor classes as at least 2 chemical messengers are required for full cellular response
  • > G-proteins bind to guanine and are found throughout the cell, although we are interested in primarily the plasma membrane G-proteins
  • > there are at least 16 different plasma membrane G-proteins
47
Q

Explain how G-proteins go from the inactive state to the active state

A
  • > in the inactive state, GP bind to guanoside diphosphate
  • > 1st CM (hormone, neurotransmitter) binds to a receptor on the cells plasma membrane, activating that receptor, which in turn interacts and activates a GP by causing the release of GDP
  • > the activated GP binds with GTP then interacts with another plasma membrane protein (called the effector protein)
  • > once GP and effector protein interact, a 2nd chemical messenger can be released from the effector protein into the interior of the cell, resulting in a cellular response OR the action of the effector protein can be the alternation in membrane potential (opening/closing of ion channels)
    SEE PAGE 9 FOR DIAGRAM
48
Q

what are the advantages to the 2nd messenger system

A

(2 chemical messengers = 1 response)

  • > main advantage is signal amplification
  • 1 signal mol (CM or ligand) can result in multiple second messenger molecules created through “amplifier” enzyme activity - this results in a large cell response
  • 1 first messenger molecule binding to 1 receptor can ultimately result in 1,000,000 final phosphorylated products
49
Q

amplifier enzymes in the 2 messenger system

A
  • > adenylate cyclase
  • > guanylate cyclase
  • > phospholipase C
50
Q

Classes of effector/amplifier proteins and G Protein Interactions

A
  1. G-proteins, adenylyl/adenylate cyclase and cAMP
  2. G-proteins and guanylyl cyclase
  3. Phospholipase C, diacylglycerol (DAG) and inositol triphosphate (IP3)
  4. G-proteins and ion channels
  5. Receptors and neurotransmitters
51
Q

what is adenylyl cyclase and what happens when it is activated

A
  • > it’s an effector/amplifier protein located in the membrane
  • > once activated, it converts cytosolic ATP into cAMP
  • > cAMP is a 2nd M which diffuses through the the cell and triggers a sequence of events that leads ultimately to desired cellular response through phosphorylation of a wide variety of different proteins and alters ion channels SEE PAGE 10
52
Q

how is the g-proteins and guanylyl cylcase pathway activated

A

with the chemical messenger/neurotransmitter, NO (nitric oxide)

53
Q

describe the g-protein and guanylyl cyclase pathway

A
  • > similar to adenylyl pathway although not seen in as many cells/tissues as the adenylyl cyclase
  • > the receptor, G-protein and guanylyl cyclase are in the plasma membrane and guanylyl cyclase is also in the cytosol
  • > 2nd messenger in the case is cGMP, which diffuses through the cell activating the cGMP-dependant protein kinase, resulting in a variety of cellular responses including ion channel opening
54
Q

phospholipase C, diacylglycerol and inositol triphosphate pathway

A
  • > here, the receptor activates the G-protein, which in turn activates the effector protein, phospholipase C, located in the plasma membrane
  • > phospholipase C breaks down a plasma membrane phospholipid: phosphatidylinositol biphosphate (PIP2) into 2 components: inositol triphosphate (IP3) and diacylclycerol (DAG)
55
Q

IP3

A
  • > composed of the phospholipid headgroup and PO4
  • > plays an important role in muscle contractions
  • > diffuses through the cell and into the ER (SR in skeletal muscle) where it makes the ER/SR membrane become “leaky” to calcium
  • calcium stored within the ER/SR will be released into the cytosol initiating a variety of cellular responses
  • calcium here can be considered a 3rd messenger in the G-protein pathway
    LIPID SOLUBLE CHEMICAL MESSENGER
56
Q

DAG

A

lipid insoluble

  • > activates the protein kinase C on the plasma membrane
  • > which in turn, results in the phosphorylation of a variety of plasma membrane proteins
  • > often associated with plasma membrane regulation
57
Q

how do G-proteins and ion channels interact

A

Direct G protein gating
- > g proteins can directly cause the opening/closing if membrane ion channels
Indirect G protein gating
- > the 2nd messenger produced through the effector proteins, adenylyl cyclase and guanylyl cyclase, can also open or close ion channels

58
Q

relate Acetylcholine to receptors and neurotransmitters

A
  • > acetylcholine is the major neurotransmitter in the PNS and the brain
  • > receptors can also respond to acetylcholine and either nicotine or muscarine
59
Q

two types of acetylcholine receptors

A

Nicotinic Receptors
- > receptors that respond to acetylcholine and nicotine
Muscarinic Receptors
- > receptors that respond to acetylcholine and muscarine (toxin from certain mushrooms)
SEE PAGE 13

60
Q

nicotinic receptors

A
  • > these receptors contain an ion channel that is permeable to both Na and K
  • due to the larger electrochemical driving force of sodium, opening of these ion channels usually results in depolarization
  • > they are present at neuromuscular junctions (where motor neurons send signals to muscles cells) and are also present in the brain where they are important in cognitive functions and behaviour (including reward pathway)
61
Q

muscarinic receptors

A
  • > these receptors couple with G-Proteins, which alter a number of different enzyme activities and ion channel activity
  • > they are prevalent at cholinergic synapses in the brain and at junctions of where the PNS innervates glands and organs
62
Q

atropine

A

an antagonist of the muscarinic receptors (used to cause pupil dilation) and an antidote for certain nerve gases

63
Q

all the catecholamines are know as ____

A

metabotropic
- > initiate metabolic processes that affect cell function and all use second messengers in their pathways for activation

64
Q

list the catecholamines

A

dopamine
norepinephrine
epinephrine

65
Q

how are catecholamines formed

A
  • > they’re all formed from the AA tyrosine, and all three follow the same 2 initial steps for synthesis (tyrosine then enzyme 1 turns it into L-Dopa)
  • > which catecholamine is formed is based off which enzymes are present in the cell
    SEE PAGE 14
66
Q

what are the 2 main classes of receptors for norepinephrine and epinephrine

A
  1. Alpha-adrenergic receptors

2. Beta-adrenergic receptors

67
Q

alpha-adrenergic receptors

A
  • > alpha-2 acts pre-synaptically to inhibit norepinephrine release from the adrenergic terminal
  • > alpha-1 acts post synaptically to either stimulate or inhibit activity at the different types of potassium channels
  • A-1 are found in most sympathetic target organs except the heart
68
Q

beta-adrenergic receptors

A
  • > act via stimulatory G proteins to increase cAMP in the post-synaptic cell
  • > beta-1 and beta-3 are found in the least number of body systems while the B2 is the most prevalent form of beta-adrenergic receptors
69
Q

serotonin

A
  • > produced from the AA tryptophan
  • > generally has excitatory effects of pathways involved in the control of muscles and inhibitory effects on pathways involved in sensations
  • > serotonergic neuron activity is low or absent during sleep and at its highest activity during alert wakefulness
70
Q

neurons that release serotonin

A

serotonergic
- > serotonergic pathways also function in the regulation of food intake, reproductive behaviour, emotional states (mood and anxiety)

71
Q

Selective Serotonin Re-Uptake Inhibitors (SSRIs)

A
  • > this class of drugs (includes prozac and zoloft) keeps serotonin levels high extracellularly (in the CNS) by preventing reabsorption of serotonin
  • > deficiency in CNS seratonergic activity may be a cause of moderate to severe depression
72
Q

What does NO do

A

nitric oxide

  • > in the CNS, NO acts as a neurotransmitter and regulates synaptic plasticity (remodelling/formation+deletion of neural pathways) and plays a role in the sleep-wake cycle and in hormone secretion
  • > also plays a role in both neural cell protection and death with physiological levels of NO providing neural protection, and higher levels of NO resulting in neural cell death
73
Q

nitric oxide synthases (NOS)

A

class of enzymes that regulate synthesis of NO

74
Q

NO release, and over production/poor regulation

A
  • > NO release results in activation of G-protein guanylyl cyclase activity
  • > NO over production/poor regulation has been implicated in neurodegenerative disorders like Alzheimers and Parkinsons, especially when ROS are present as well
75
Q

How many skeletal muscles are in the adult body

A

660

76
Q

skeletal muscles make up what percentage of body weight

A

45%

77
Q

epimysium

A

connective tissue that surrounds the entire muscle

78
Q

perimysium

A

membrane that binds fibres (cells) into fascicles

79
Q

endomysium

A

(basal lamia/basement membrane)

first outer “membrane” of individual muscle cells

80
Q

sarcolemma

A

plasma membrane of cell

81
Q

myofibrils

A

several types of proteins arranged in parallel structures

- > proteins that make up myofibrils each play a specific role in muscle contraction

82
Q

contractile proteins of the sarcomere

A

myosin
- > makes up 1/2 of myofibrillar proteins
actin
- > 1/5 of total proteins

83
Q

Regulatory proteins of the sarcomere

A

tropomyosin & troponin

regulate contraction

84
Q

Structural proteins/components of the sarcomere

A
  1. C protein
  2. M-Line proteins
  3. Z-line/Z-disc
  4. tintin
  5. actinin
  6. spectrin
  7. desmin
  8. dystrophin
    Thick and thin filaments
85
Q

c- protein

A

part of thick filament (myosin)

- > hold tails of myosin in correct arrangement

86
Q

tintin

A

links the ends of thick filaments to z-disc

87
Q

M-Line proteins

A

m-line = myomesin

- > keep thick and thin filaments in proper arrangement

88
Q

actinin

A

attaches actin filaments at z-disc

89
Q

desmin

A

links z-discs of adjacent myofibrils together

90
Q

spectrin

A

plasma membrane proteins

91
Q

dystrophin

A

structural and functional roles

- > reinforces the sarcolemma allowing muscle fibres to withstand stresses and stains of contraction and stretching

92
Q

z-line/z-disc

A

defines the 2 ends of the sarcomere

93
Q

Muscular dystrophy (MD)

A

progressive deterioration of the skeletal muscles through disruption in formation of DYSTROPHIN
- > normal dystrophin levels help reinforce the sarcolemma, allowing for normal stress and string to not cause damage to the cell membrane

94
Q

thick filaments

A
  • > composed mainly of myosin
  • > 2 heavy myosin chains
  • > 4 light myosin chains
95
Q

thin filaments and its regulatory proteins

A

composed mainly, but not only, actin

  • > also contains troponin and tropomyosin (thin filament contains both regulatory proteins)
  • > troponin is found in 3 different forms
  • troponin-t (TN-T) which binds to tropomyosin
  • troponin-C (TN-C) which binds to calcium
  • troponin-I (TN-i) that binds to actin
96
Q

Explain skeletal muscle development during embryonic development and early childhood

A
  • > muscle fibres are formed during embryo development by the fusion of undifferentiated, mono-nucleated cells (myoblasts; muscle mitosis), into a singular, cylindrical multi-nucleated fibre/cell
  • > skeletal muscle cells differentiation is complete around the time of birth and the fibres continue to grow in size until adulthood
97
Q

how do satellite cells affect muscle growth

A
  • > satellite cells (undifferentiated stem cells), lie between the sarcolemma and basement membrane and can respond to strain, injury, or become active and undergo mitotic proliferation
  • > with mitosis, daughter cells form and differentiate into myoblasts that can either fuse to form new fibres or fuse with damaged fibres to help reinforce and repair those fibres
  • > many hormones and growth factors regulate satellite cell activity
98
Q

muscle hypertrophy

A

a response to exercise

- > also triggers satellite cell activity and increase the size of individual fibres

99
Q

explain the single-filament mechanism for muscle contractions

A

single sarcomere in a single fibre/cell

  • > shortening of the skeletal muscle cell/fibre = contraction
  • > shortening of the sarcomere produced by movement of thick and thin filaments so that they overlap
  • > overlap of thick and thin due to movements by cross-bridges
  • > during fibre shortening, cross-bridges move in an arc forcing thin filaments to the centre of the sarcomere
100
Q

cross bridges

A

connections between the thick filament proteins, myosin; and the thick filaments, actin
- > 1 cross-bridge stroke only moves the thin filaments a tiny distance therefore, many cross-bridge strokes are required

101
Q

Explain thick filaments work in the cross bridge cycle

A
  1. ATP binds to ATPase on the myosin head
  2. ATPase breaks ATP to ADP + Pi, releasing energy
  3. Energy is transferred to myosin, producing an energized for of myosin
  4. Energized myosin attaches to actin
  5. Movement of cross bridges/globular head forces thin filament (actin) to the centre of the sarcomere
  6. Actin/myosin complex releases ADP and Pi
  7. New ATP binds to myosin, causing the release of actin (new ATP to reset the cycle)
102
Q

explain thin filaments at rest, during the cross bridge cycle

A

IN RESTING MUSCLE

  • > actin and myosin are prevented from attaching due to 2 proteins on the surface of actin
  • troponin and tropomyosin
  • > tropomyosin partially blocks myosin binding site on actin
  • > TN-T holds tropomyosin in place, helps maintain blockage of actin-myosin binding site along with TN-I, which binds to actin
103
Q

explain what happens to the thin filaments during activity; cross bridge cycle

A
  • > Ca binds to troponin-C (TN-C)
  • this causes a conformational change to troponin, moving tropomyosin away from the myosin binding site on actin
  • the removal of Ca will cause tropomyosin to again block the myosin binding site on actin, stopping contractions
104
Q

explain the path of calcium during the cross-bridge cycle

A
  • > Ca is stored within the Sarcoplasmic reticulum of muscle cells
  • > the release of Ca is due to an action potential, generated from neural input
  • > initial release of Ca from the SR results in the opening of Ca channels, increasing the amount of Ca released into the muscle cell
  • > neural input releases Ca from the lateral sacs of the SR
  • > Ca diffuses into cytosol of the muscle cell and binds to TN-C, initiating opening of the myosin
105
Q

what is an action potential

A

rapid alterations in membrane potential

106
Q

action potentials in skeletal muscle cells

A

occur due to the opening of Na channels in plasma membrane (sarcolemma)
- > this leads to a relatively large influx of Na (End-plate potential; EPP)

Human Physiology 2 (3 decks)

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