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physiology lecture > exam 2- muscle physiology, endocrine, reproductive > Flashcards

exam 2- muscle physiology, endocrine, reproductive Flashcards

1
Q

what are the three types of muscle?

A

cardiac, skeletal, smooth

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2
Q

characteristics of cardiac muscle

A

striated (sarcoma), involuntary

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3
Q

characteristics of skeletal muscle

A

striated (sarcoma), voluntary

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4
Q

characteristics of smooth muscle

A

involuntary (no sarcoma)

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5
Q

the 4 properties of muscle are:

A

contractatility, excitability, extensibility, elasticity

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6
Q

contractility

A

the ability to generate force by contracting

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7
Q

excitability

A

the ability to respond to a stimulus (this is often from a motor neuron)

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8
Q

extensibility

A

stretch beyond resting length without being damaged

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9
Q

elasticity

A

ability to return to resting length after being stretched

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10
Q

what is the primary function of all muscle?

A

to generate force

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11
Q

what is the secondary function of skeletal muscle?

A

to maintain posture, stabilize joints, generate heat (shivering)

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12
Q

how are skeletal muscles attached to bones?

A

via tendons

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13
Q

what causes joint movement?

A

muscle tension on the tendon

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14
Q

origin of the muscle

A

the part of the muscle that is closer to the body. this part remains immobile during the action

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15
Q

insertion of the muscle

A

the part of the muscle that is farther from the body. this part moves during the action

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16
Q

what is the tendon connected to?

A

the bone on one end, and epimysium on other end

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17
Q

structure of the muscle, from smallest part to biggest:

A

muscle cell (fiber), endomysium (between the cell fibers), fasicle (wraps a group of fibers), perimysium (wraps the fasicles in groups), epimysium (wraps around the perimysium) and is attached to tendon, which is attached to bone

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18
Q

what does a parallel arrangement of fascicles tell you?

A

works for range of motion

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19
Q

what does a pennate arrangement of fascicles tell you?

A

works for power. you can fit more muscle cells into a space that is pennate vs parallel. more muscle cells = more force = power

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20
Q

where is calcium stored in the myofiber?

A

sarcoplasmic reticulum

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21
Q

what is the importance of the t-tubule in the myofiber?

A

propogates action potentials into the interior of the cell

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22
Q

what is the sarcomere?

A

it is the functional unit of muscle contraction. it gives rise to the striated appearance of cardiac and skeletal muscles

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23
Q

z-disk

A

protein structure that serves as a point of attachment for the thin myofilament. from one z-disk to another = one sarcomere

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24
Q

m-line

A

in the middle. a protein structure that acts as a place of attachment for the thick myofilaments

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25
Q

a-band

A

the length of the thick myofilament

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26
Q

what is the largest protein in the body?

A

titin

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27
Q

what is the thin myofilament made out of?

A

actin, wrapped in tropomyosin

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28
Q

h-band

A

the length from the end of one thin myo to the start of the next thin myo

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29
Q

what happens in the sarcomere as the muscle contracts?

A

thin filaments slide between thick filaments. the distance between the z-disks shortens. the I-band (which is the part that is thin filament between z-disks of dif. sarcomeres) completely disappears. the h-band shortens. the a-band does not shorten

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30
Q

sliding filament mechanism

A

imagine the thin myofilament (purple helix balls) above the thick myofilament (green stripes with heads). the myosin head is ATPase and has an ATP bonding site. it is currently in the kinked position. as ATP binds, myosin undergoes hydrolysis and the head extends to a non-kinked postion. the ATP has now turned into inorganic phosphate and ADP. the actin binding site has binded the myosin head to the actin on the thin myofilament. the connection that was just made is called a cross bridge.

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31
Q

power stroke mechanism

A

now that the myosin head is binded to the actin, inorganic phosphate may leave. the action of inorganic phosphate leaving is called a power stroke. it brings it back to kinked position, but still bonded to the actin. the sarcomere shortens as the thick myofilament pulls the thin closer to the middle

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32
Q

how do we regulate muscle contraction?

A

when the muscle is relaxed, tropomyosin blocks the binding site on actin, remember, tropomyosin is the string that is attached and runs the span of the thin myofilament. troponin can displace tropomyosin, therefore exposing the actin active site and allow for cross bridge attachment. calcium will bind to troponin, which causes a conformational change, which is what allows for the active actin site to be exposed

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33
Q

how are calcium levels regulated?

A

this is the process of excitation-contraction coupling

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34
Q

motor unit

A

each motor neuron plus the muscle fiber it makes contact with

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35
Q

neuromuscular junction

A

where contact is made between motor neurons and muscle fibers

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36
Q

characteristics of motor neurons

A

they are all or none, meaning that when the motor neuron is activated, ALL of the muscle fibers that it is connected to become depolarized. depolarization is what allows for muscle contraction

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37
Q

innervation ratio

A

motor neuron : muscle fiber
eye muscles 1:20
calf muscles 1:2000
some things need more/bigger movements and power

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38
Q

how is an action potential generated?

A
  1. the motor neuron action potential drives down the axon. 2. because of the depolarization from the last step, the voltage gated calcium channels open and calcium enters. 3. calcium forms into ACh vesicles which get released and bind to acetylcholinesterase. 4. the ACh binding opens ion channels. 5. sodium enters through the opened channels. 6. the positive charge from sodium travels as a local current through the muscle plasma membrane. 7. this charge go through voltage gated sodium channels, which propogate action potentials
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39
Q

steps of excitation-contraction coupling

A

(in somatic motor neuron). somatic neuron gets activated.

ACh gets released

(in sarcolemma) ACh binds to nicotinic ACh receptors, opens ligand gated channels. sodium diffuses in, producing a depolarizing stimulus of the muscle membrane. an action potential is produced.

(in transverse tubules) action potential are conducted about the tubules. action potentials open the voltage gated calcium channels.

(in sarcoplasmic reticulum) calcium release channels open. calcium diffuses out into sarcoplasm

(in myofibrils) calcium binds to troponin, stimulating contraction

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40
Q

what must happen for muscle relaxation?

A

action potentials must stop. calcium release channels close. calcium gets pumped back into SR via calcium atpase pumps

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41
Q

what is a twitch

A

single contraction of muscle. the muscle quickly contracts and relaxes

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42
Q

what is on the twitch graph

A

action potential, calcium concentration, force

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43
Q

what is a tetanus

A

there is a high frequency of action potentials that lead to the max amount of force a muscle can generate. muscle is stimulated repeatedly. no relaxation between action potentials.

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44
Q

what does the length tension relationship describe?

A

the relationship between the size of the sarcomere and the ability to generate force

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45
Q

what is the optimal amount of overlap?

A

2.0-2.25 um

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46
Q

what happens when the percentage of rest length is shorter than the optimal amount of overlap?

A

at 1.65, steric hinderance causes a disrupted spacing sue to maximal overlap

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47
Q

what happens when the percentage of rest length is too long?

A

there will be no overlap. no overlap means the thin and thick can’t reach each other, which means that there is no chance of creating cross bridges, meaning no force can be generated

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48
Q

what are the types of muscle contractions?

A

isometric & isotonic (which branches into concentric and eccentric)

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49
Q

isometric contraction

A

muscle length remains constant. you are generating max force. the load is greater than the force. this is like trying to push a parked car.

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50
Q

concentric contraction

A

active shortening. think CONcentric = CONcise
the muscle shortens with contraction. the force of the contraction exceeds the load. this is when you’re curling a dumbbell and you are lifting your arm up

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51
Q

eccentric contraction

A

active lengthening. think Eccentric = Elongating
the muscle lengthens with contraction. the load may exceed the force of contraction. this is when you are curling a dumbbell and your arm is going down

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52
Q

what are the determinants of isometric force?

A

activation frequency, motor unit recruitment, muscle size, sarcomere length

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53
Q

activation frequency

A

this is how fast the action potentials are being generated (think twitch vs tetanus). a higher activation frequency= more calcium being released from SR, which allows for more cross bridge formation, which allows for higher force

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54
Q

motor unit recruitment

A

this dictates how much force is being generated. not every movement needs to be a big movement. if you’re flicking something you will recruit more motor units than if you are pushing something

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55
Q

force velocity curve. velocity = distance the muscle shortens / time

A

as the load increases, the velocity decreases. this makes sense. you can shorten and extend your muscle quicker when you are curling 5lbs compared to 200 lbs

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56
Q

when does the force velocity curve show the maximum shortening velocity?

A

at 0 load

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57
Q

when does the force velocity curve show the maximum isometric tension?

A

at 0 shortening velocity. this makes sense. this is when you cant move (like trying to push a car)

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58
Q

what are the 3 energy systems that create ATP needed for myosin and calcium pumping?

A

phosphagen, glycolytic, aerobic

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59
Q

phosphagenic system

A

is able to generate/resynthesize ATP at the fastest rate possible. but, creates a limited amount of phosphocreatine. this is what is employed during a 10 second sprint. rapidly converts ADP to ATP
look for PCr domination

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60
Q

glycolytic system

A

is able to generate/resynthesize ATP at 80% intensity, which can last a few minutes. this is what is employed in a 400 m swim
look for glycolysis domination

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61
Q

aerobic system

A

is able to generate/resynthesize ATP at a lower intensity, but is virtually unlimited. this is what is employed in marathon runners. occurs in the mitochondria (where glucose and fats are converted to ATP). consumes oxygen. by-product=co2,h20,heat
look for oxidative domination

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62
Q

how do we classify between a slow twitch and a fast twitch fiber?

A

the contraction speed

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63
Q

what type of fiber is a slow twitch?

A

type 1

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64
Q

what type of fiber is a fast twitch?

A

type 2 (2 types of this, 2a & 2x)

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65
Q

what color are slow twitch fibers (type 1)

A

red

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66
Q

do slow twitch fibers have a lot or a little capillaries/myoglobin?

A

Many

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67
Q

do slow twitch fibers have a lot or a little mitochondria?

A

many. high oxidative capacity

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68
Q

are slow twitch fibers resistant to fatigue?

A

yes, they are common in endurance muscles

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69
Q

why are fast twitch fibers called fast?

A

they have a fast contraction time

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70
Q

what is the most predominant type of fast twitch fibers?

A

type 2a

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71
Q

do fast twitch fibers have a lot or a little mitochondria?

A

many, but not as many as slow twitch

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72
Q

are fast twitch type 2 fibers resistant to fatigue?

A

yes

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73
Q

what color are fast twitch type 2x fibers?

A

white, because they lack myoglobin

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74
Q

what do fast twitch 2x fibers store a lot of ?

A

glycogen

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75
Q

do fast twitch 2x fibers have a lot of or a little capillaries and mitochondria?

A

little

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76
Q

what is the function for fast twitch 2x fibers?

A

sprint tasks

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77
Q

type 1 diameter

A

small

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78
Q

type 1 z-line thickness

A

wide

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79
Q

type 1 glycogen content

A

low

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80
Q

type 1 resistance to fatigue

A

high

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81
Q

type 1 capillaries

A

many

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82
Q

type 1 myoglobin content

A

high

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83
Q

type 1 respiration

A

aerobic

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84
Q

type 1 oxidative capacity

A

high

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85
Q

type 1 glycolytic ability

A

low

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86
Q

type 1 twitch rate

A

slow

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87
Q

type 1 myosin ATPase rate

A

low

88
Q

type 2a diameter

A

intermediate

89
Q

type 2a z-line thickness

A

intermediate

90
Q

type 2a glycogen content

A

intermediate

91
Q

type 2a resistance to fatigue

A

intermediate

92
Q

type 2a capillaries

A

many

93
Q

type 2a myoglobin content

A

high

94
Q

type 2a respiration

A

aerobic

95
Q

type 2a oxidative capacity

A

high

96
Q

type 2a glycolytic ability

A

high

97
Q

type 2a twitch rate

A

faster

98
Q

type 2a myosin ATPase rate

A

higher

99
Q

type 2x diameter

A

large

100
Q

type 2x z-line thickness

A

narrow

101
Q

type 2x glycogen content

A

high

102
Q

type 2x resistance to fatigue

A

low

103
Q

type 2x capillaries

A

few

104
Q

type 2x myoglobin content

A

low

105
Q

type 2x respiration

A

anaerobic

106
Q

type 2x oxidative capacity

A

low

107
Q

type 2x glycolytic ability

A

high

108
Q

type 2x twitch rate

A

fastest

109
Q

type 2x myosin ATPase rate

A

highest

110
Q

what type of stem cell is a satellite cell?

A

multipotent. it is restricted to muscle cells

111
Q

Duchenne Muscular Dystrophy

A
  • most common form of dystrophy
  • it is recessive and linked to the x (which is why its more common in boys)
  • the mutation lies in the dystrophin gene, which is the gene that provides structural stability to the cell membrane
112
Q

symptoms of DMD

A
  • symptoms may first appear at ages 2-3
  • muscle weakness in legs and pelvis due to muscle mass loss
  • pseudo hypertrophy (it looks like the muscles are getting bigger, but really fat fibrotic tissue is replacing the muscle)
  • life expectancy is 30 due to paralysis
113
Q

how are cardiac muscle cells joined together?

A

by gap junctions

114
Q

how does action potential travel through cardiac muscle cells?

A

by gap junctions

115
Q

how do the cells behave in a cardiac muscle cell?

A

as one unit (syncitium)

116
Q

how does EC coupling in the heart happen?

A

via calcium induced calcium release

117
Q

do smooth muscle cells have sarcomeres?

A

no, not striated

118
Q

what is the ratio of actin to myosin in smooth muscle cells?

A

16:1 (more thin myos than thick myos). hence not an every other pattern that we can see in the cardiac and skeletal muscles

119
Q

what are the actin filaments attached to in smooth muscles?

A

dense bodies (en vez de zdisk)

120
Q

do smooth muscles have more or less opportunity to form cross bridges?

A

more, they have more actin

121
Q

the steps of smooth muscle contraction are:

A
  • stimulated by a rise in intracellular calcium
  • this calcium then binds to calmodulin
  • this calcium-calmodulin complex activates the myosin light chain kinase
  • this makes the myosin heads be phosphorylated
  • then, myosin heads bind to the actin
  • relaxation will occur when calcium decreases
122
Q

what is endocrinology

A

the branch that is concerned with glands that secrete hormones into the blood

123
Q

what does impaired endocrine function lead to?

A

higher morbidity and mortality. someone with diabetes has a higher risk for many other damages and concerns

124
Q

what are the 6 endocrine glands?

A

pancreas
hypothalamic-pituitary
thyroid-parathyroids
adrenals
male gonads
female gonads

125
Q

what are the 2 communication systems that are used for maintaining the body’s homeostasis?

A

nervous system and endocrine system

126
Q

what is the functional unit of the endocrine system?

A

a gland cell

127
Q

what is the chemical messenger of the endocrine system?

A

hormone

128
Q

what is the mode of transmission for the endocrine system?

A

circulation (via blood)

129
Q

what is the reaction time for the endocrine system?

A

minutes-days

130
Q

analogy you can use for the endocrine system and how it affects the body

A

is it like the wifi connection. it affects every device it is connected to.

131
Q

what is a hormone

A

a chemical messenger from a ductless gland

132
Q

where do endocrine hormones travel?

A

in the blood to communicate with their target cells in every corner of the body

133
Q

what are the 4 things that can happen to a hormone that is circulating in the blood?

A
  1. excreted in urine or feces
  2. inactivated by metabolism
  3. activated by metabolism
  4. binds to receptor of target cell and create a cellular response
134
Q

what does the concentration of the hormone in blood reflect?

A

the secretion rate by the gland cell, the excretion rate, and activation rate

135
Q

how do we group endocrine hormones?

A

based on its polarity, either polar (hydrophilic) or non-polar (hydrophobic)

136
Q

hydrophilic (polar) hormones

A

catecholamine
peptide/protein

137
Q

hydrophobic (non-polar) hormones

A

thyroid
steroid
vitamin D

138
Q

where are hydrophilic hormones stored?

A

secretory vesicles. released after stimulation

139
Q

how do hydrophilic hormones travel in the blood?

A

free of proteins. hydrophilIC they get the ICK

140
Q

what do hydrophilic proteins bind to?

A

trans-membrane receptor proteins. they cant make it through the plasma membrane, so must be trans membrane

141
Q

how are catecholamine hormones secreted?

A

by sympathetic neurons and adrenal medulla: dopamine, norepinephrine, and epinephrine

142
Q

synthesis of catecholamine:

A

tyrosine > tyrosine hydroxylase > dopa > tyrosine hydroxylase > dopamine > tyrosine hydroxylase > norepinephrine > tyrosine hydroxylase > epinephrine

143
Q

2 pathways for catecholamine

A

1) ACh gets secreted into the ganglion. it binds to the nicotinic receptor on the post ganglionic neuron. norepinephrine gets released in the nerve ending

2) ACh gets secreted into the adrenal medulla. norepinephrine and epinephrine get released into the blood vessel/stream

144
Q

is the half life of catecholamine short or long? why?

A

short. there are enzymes in the blood that are destructive. because ceta travels in the blood by itself, it gets destroyed quickly

145
Q

what does catecholamine do

A

bind trans-membrane receptor proteins (G protein coupled receptors) > activate enzymes (adenylyl cyclase) and produce 2nd messengers (cAMP) > evoke a rapid response

146
Q

examples of peptide/protein hormones

A

insulin, prolactin

147
Q

how are peptide/protein hormones synthesized?

A

via transcription-translation

148
Q

where are peptide/protein hormones stored?

A

secretory vesicles

149
Q

what are the 3 transmembrane receptors for peptide hormones?

A

GPCR, tyrosine kinase, JAK

150
Q

example of GCPR (g coupled protein receptor) for peptide hormone

A

glucagon-R, ACTH-R

151
Q

example of tyrosine kinase receptor for peptide hormones

A

IGF 1-R, insulin-R

152
Q

example of JAK kinase receptor for peptide hormones

A

GH-R, Leptin-R, PRL-R

153
Q

GPCR (peptide hormone)

A

generation of second messenger

154
Q

tyrosine kinase receptor (peptide hormone)

A

autophosphorylation - none for JAK (he aint got JAK shit)

155
Q

what do GPCR, TKR, and JAK all lead to?

A

activation of cellular kinase and cellular response

156
Q

summary of catecholamines:

A
  • hydrophilic
  • secreted by neurons and adrenal medulla
  • synthesized through enzymatic reactions from tyrosine
  • stored in secretory vesicles
  • secreted in response to secretagogue (stimulus)
  • binding and activating G-protein coupled receptors
  • evoke a rapid response in a target cell
157
Q

summary of protein/peptide hormones:

A
  • hydrophilic
  • synthesized through transcription translation (think- this process ends in protein production, duh)
  • stored in secretory vesicles
  • secreted in response to secretagogue (stimulus)
  • binding and activating transmembrane receptors (GCPR, TKR, or JAK)
  • evoke a rapid response in a target cell
158
Q

examples of hydrophobic hormones

A

thyroid, steroid, vitamin D (these cannot be stored, meaning they are made on demand)

159
Q

how do hydrophobic hormones circulate in the blood?

A

mostly protein-bound. small amount of free hormones

160
Q

what does the free hormone do and why is it important?

A

it diffuses across the PM of the target cell. it is the only one that can do this. they modulate the rate of transcription

161
Q

what do hydrophobic hormones do?

A

bind and activate their specific intracellular receptor proteins and change the rate of transcription of their target genes

162
Q

how are thyroid hormones (T3&T4) secreted?

A

via thyroid gland

163
Q

how are thyroid hormones created?

A

from enzymatic reactions from tyrosine, which requires iodine ingestion

164
Q

what do thyroid hormones do in plasma?

A

bind liver-produced proteins
(thyroxine-binding globulin)

165
Q

what do thyroid hormones do in target cells?

A

bind intracellular thyroid hormones receptors and alter transcription

166
Q

what do thyroid hormones do in the liver?

A

they are modified. they become hydrophilic and get excreted

167
Q

T4 thyroid hormone

A

most abundant
most stable
pro-hormone form

168
Q

T3 thyroid hormone

A

most potent. the active hormone. you want to convert T4 to T3

169
Q

how are steroid hormones secreted?

A

by:
adrenal glands
ovaries
testes

170
Q

how are steroid hormones made?

A

from cholesterol

171
Q

what is the rate limiting enzyme for steroid hormones?

A

P450 SCC

172
Q

what do steroid hormones do in plasma?

A

bind liver produced binding globulins

173
Q

what do steroid hormones do in target cells?

A

bind their specific intracellular receptor proteins

174
Q

what do steroid hormones do in the liver?

A

become modified, hydrophilic, excreted

175
Q

summary of thyroid hormones:

A
  • hydrophobic
  • synthesis involves enzymatic incorporation of iodide onto tyrosine
  • not stored (made on demand)
  • bind intracellular receptors, ligand-induced transcription factors
  • slow cellular response that involves changes at transcription translation
  • metabolized for increased solubility and excreted
176
Q

summary of steroid hormones:

A
  • hydrophobic
  • synthesis involves enzymatic reactions from cholesterol
  • not stored (made on demand)
  • bind intracellular receptors, ligand-induced transcription factors
  • slow cellular response involving changes at transcription translation
  • metabolized for increased solubility and excreted
177
Q

summary of vitamin D:

A
  • hydrophobic
  • synthesis involves enzymatic activation to 1,25-dihydroxy-vitamin D
  • not stored (made on demand)
  • bind intracellular receptors, ligand-induced transcription factors
  • slow cellular response involving changes at transcription translation
  • metabolized for increased solubility and excreted
178
Q

what are the catecholamine hormones?

A

dopamine
norepinephrine
epinephrine

179
Q

what are the thyroid hormones?

A

T3
T4

180
Q

what are the steroid hormones?

A

estrogen
progesterone
testosterone
DHT
androstenedione
cortisol
aldosterone
DHEA

181
Q

what is the vitamin D hormone?

A

calcitriol

182
Q

the hormone __________ is derived from cholesterol

A

cortisol

183
Q

which hormones is hydrophilic and circulates free of proteins in the plasma?

A

TSH (thyroid stimulating hormone)

184
Q

which hormone is synthesized by trasncription-translation process?

A

insulin

185
Q

a patient with a lower sensitivity to insulin would require _______ insulin for the same response

A

more

186
Q

T/F
receptors for all of the hormones are proteins

A

true

187
Q

this modified amino acid is an example of a catecholamine

A

epinephrine

188
Q

this hormone is derived from cholesterol

A

aldosterone, cortisol

189
Q

this hormone’s receptor leads to the changed production of cAMP

A

epinephrine, TSH

190
Q

this hormone is carried in plasma by liver produced binding globulins

A

aldosterone, cortisol, thyroid hormone

191
Q

this hormone is not a steroid but acts on intracellular receptors

A

thyroid hormone

192
Q

this hormone’s receptor is a transcription factor

A

aldosterone, cortisol, thyroid hormone

193
Q

this hormone is hydrophilic and circulates free in plasma

A

insulin, epinephrine, prolactin, TSH

194
Q

T/F
an estrogen priming which increases the synthesis of the receptor for progesterone is required for progesterone effects. this is known as additive effects

A

false

195
Q

T/F
a prolonged presence of a hormone at a high concentration may decrease its receptors in target cells. this is known as down-regulation

A

true

196
Q

compared to a normal subject, a person with type 2 diabetes mellitus has lower sensitivity to insulin and requires __________ insulin for the same response

A

more

197
Q

what do blood glucose levels do after each meal?

A

they peak

198
Q

what hormone do insulin and glucagon belong to?

A

peptide

199
Q

is glucagon an alpha or beta cell

A

alpha

200
Q

is insulin an alpha or beta cell

A

beta

201
Q

how many kcal/g for carbohydrate?

A

4

202
Q

how many kcal/g for fat?

A

9

203
Q

how many kcal/g for protein?

A

4

204
Q

where is energy stored? (3 places)

A

fat
carbohydrate
protein

205
Q

what is anabolism?

A

the building up/storing of energy

206
Q

what is catabolism?

A

the breaking down/releasing of stored energy

207
Q

what is carbohydrate stored as?

A

stored as glycogen in the liver and muscle

208
Q

what is fat stored as?

A

stored as triglyceride in adipocytes
*most abundant
*most efficient

209
Q

where is protein stored?

A

muscle. *remember that this is only available for long term fasting

210
Q

timeline of absorptive state

A

(fed state) 4 hours after meal

211
Q

timeline of post-absorptive phase

A

(fasting state) period 4 hours after meal until next one

212
Q

what is happening with energy in the absorptive phase?

A

use energy, store energy

213
Q

what is happening with energy in the fasting state?

A

mobilize and release energy

214
Q

levels of glucose, insulin, and glucagon during the fed state

A

glucose: high
insulin: high
glucagon: low

215
Q

what does insulin do for anabolism and catabolism?

A

stimulates anabolism
inhibits catabolism

216
Q

anabolism process

A

building blocks -> organic macromolecules
this is stimulated by elevated levels of insulin

217
Q

what does the combo of high insulin and low glucagon promote and inhibit?

A

promotes anabolism
inhibits catabolism
*this makes sense, this combo is seen during the absorptive (fed) state, and this is when energy gets used/stored. you wouldnt be breaking it down (catabolism) while youre eating

ended on pg 129 of notes

physiology lecture (4 decks)

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