energetics Flashcards

(97 cards)

1
Q

two ways to measure energy utilisation

A

direct calorimetry (heat production) and indirect calorimetry (resp. gas exchange).

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2
Q

what do we assume for EE from gas exchange

A

a given small amount and constant amount of protein oxidation, we are working in..

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3
Q

how do we get EE from gas exchange

A

measure both VO2 and VCO2 to know how much cho and fat use.

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4
Q

kj/ LO2 for diff foods

A

carb - 21.1
protein - 19.25
fat - 19.81
alcohol - 20.40
mixed diet - 20.22

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5
Q

RER for protein

A

0.8

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6
Q

average daily energy use gold standard

A

“doubly labeled” water (stable isotopes)

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7
Q

how does double labeled water work? look into this

A

uses rate of water excretion to indicate energy metabolism through stable isotopes. using the excretion rate of the water to calculate co2 production and with assumed or measured RER to calculate EE

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8
Q

advantages and limitations of double labeled water

A

?

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9
Q

what are the effects of exercise on RMR

A

Increased 5-15% with intensive ex. for 24-48 h. if ex is repeated w/in 24-48 h remains elevated.

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10
Q

what are the chronic affects of exercise on RMR mainly due to

A

increase in FFM which needs more energy.

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11
Q

do endurance trained adapt to use less energy

A

they may have an increased efficiency of movement but it is not a large effect on TEE, most trained, in training use more energy regardless.

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12
Q

study on elite Kenyan runners

A

they seemed to have an increased energy expenditure to energy intake. this may have advantageous, economy and reduced heat retention (less fat). but they may have less fuel storage as they are not having enough energy intake BUT this may be overcome by having an extremely dense CHO diet

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13
Q

study on training indivduals EE

A

sleeping in the first 7 weeks were using more EE then went back down to normal or still slighty higher, free living they were had a lower EE so more economical during rest, at training they were using more energy.

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14
Q

what age group does increase in PA no increase TEE

A

older, also not if diet restricted

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15
Q

how can increase in substrate usage and amounts stored affect both performance and health

A

increase amount of fat at moderate then you can save carb for longer.

health - increasing glucose uptake into muscle reduces blood glucose levels and can enhance glycogen storage.

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16
Q

what influences which fuels we use when?

A

training status, duration, intensity, availability, adrenaline.

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17
Q

what influences our fuel selection?

A

energy needed for the task, amount of fuel already in the circulation or storage, contraction (calcium), enzyme acitivity, hormones (SNS - noradrenaline, adrenaline and insulin), aeorbic capacity and blood flow, and transport molecules.

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18
Q

how does the muscle know what it needs?

A

energy charge over the cell, we have indicators telling us what is going on of the energetic state, whether there is ATP there ot not. what is acculumulating around e.g. atp broken down creates adp, then amp, and then phosphate comes from it.

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19
Q

phosphagen (ATP-CP), anaerobic glycolysis, aerobic cho system and fat system. max power, max capacity and o2 requirementrs

A

on your ipad that drawing / table. fat has the highest o2 requiremet and highest capacity but lowest power.

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20
Q

anaerobic glycolysis system information, max power, max capacity and o2 requirement

A

max power 2.4 moles of ATP/min
max capacity 1.6 moles of ATP
o2 requirement 0 mmol o2/atp

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21
Q

aerobic cho system information, max power, max capacity and o2 requirement

A

max power 1.0 moles of ATP/min
max capacity 84 moles of ATP
o2 requirement 0.167 mmol o2/atp

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22
Q

fat system information, max power, max capacity and o2 requirement

A

max power 0.4 moles of ATP/min
max capacity 4000 moles of ATP
o2 requirement 0.177 mmol o2/atp

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23
Q

differences between fat and cho

A

cho is used both anaerobically and aerocbically, cho has a more limited storage, creates less atp/sec but needs less o2 per atp.

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24
Q

difference in cho and fat metabolism with exercise

A

fat increases w exercise duration whereas cho increases with intensity. when we train fat usage increases at any given intensity whereas cho decreases.

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25
what are the 4 similarities between cho and fat usage
greater capacity w training break-down products can be used in krebs cycle low e state of the cell enhance release from storage SNS and adren enhance release from storage
26
what is the difference between GLUT1 and GLUT4
GLUT4 can easily uptake glucose into the muscle
27
do both glucose and glycogen feed into glycolysis ?
yes
28
run through glycolysis
glucose into g-6-p into fructose 6-phosphate into fructose 1, 6-bis phosphate into 2 PEP then 2 pyruvate
29
what happens to free glucose to enter glycolysis
acted on by a hexokinase, which loves glucose and then will hook a phosphate onto it.
30
does free glucose stay free for long
no, as hexokinase loves it
31
what happens when a phosphate goes onto a free glucose
it traps it in the muscle, as the muscle is greedy unlike the liver.
32
what is the only way glucose can leave the muscle
as lactate.
33
what are inhibitory things in glycolysis
citrate, hydrogen, PC, ATP, too much g-6-p will feedback and inhibit hexokinase.
34
things that keep glycolysis going
phosphate, ADP, NH4+, AMP, Pi, fructose.
35
why is rate of glycogenesis super important
because of the time constraint when exercisiing.
36
what is the difference between glycolysis and glycogenolysis
?
37
what is the most preferred cho usage
from the muscle storage
38
what is the main enzyme that breaks glucose from the glycogen
phosphorylase, which is inorganic phosphate with no atp. when it breaks it off this is enough energy and then the inorganic will join the glucose.
39
how do we get phosphorylase in its active form?
Before and during exercise, adrenaline and calcium signals “switch on” glycogen phosphorylase through cAMP and kinase cascades. This prepares glucose for ATP production ahead of demand, explaining why heart rate and metabolism rise even before movement begins.
40
NAD and NADH making
we take NAD to NADH in glycolysis, then in the ETC NADH is turned back into NAD.
41
what happens when NADH builds up
when the NAD to NADH and then NADH to NAD equilibrium is out and we get a build up of NADH, it stimulates the lactate dehydrogenase, which takes pyruvate to lactic acid. which is what is happening in anaerobic glycolysis.
42
when do we increase lactate
when increase in energy demands and NADH builds up.
43
what do we do with lactate ?
some lactate will diffuse out of the muscle into the blood, or when you stop exercise you can oxidise this and go in other direction, as we can manage NADH
44
what is a good quantifier of exercise intentoy and anaerobic metabolims
lactate, imeediatly or during exercise
45
where does fat come from
adipose tissue and intermuscular triglycerides
46
what transports fatty acids across sarocolemma
CD36
47
how does training and exercise affect the FFA transporters
it increases it enabling more mobility.
48
why is fat less utilised at high intensities?
rate of atp release from fat < cho. o2 need/atp blood flow reduced to adipose tissue, as IMTGs are limited when we exercise more hydrogen ions which inhibits the ffa into the mitochondria.
49
how does training affect fat metabolism
enhance stores. increases amount of acid binding proteins, carriers. increase amount of enzymes of fat metabolism, enhanced o2 delivery et all (incfreased CV function). increase capillarisation which makes the distance of delivery for adipose to muscle closer.
50
what does insulin do to adipose tissue
enhance the glucose take up, inhibits the release of FFA from triglycerides by inhibiting the enzyme that breaks it off.
51
what does cateclomines do to the liver
increse the release of glucose from the liver. and enhance the breaking off of ffa from triglycerides. inhibit insulin release.
52
what does cateclomines have the biggest effect on, versus glucagon
the liver for c and the mucle for glucagon.
53
what happens after exercise?
decrease SNS and catecholamines. replenishment of substrate stores, slow retunr of CV to resting state EPOC
54
why do HIT sports still need aerobic capacity
for recovery, so they can maximise recovery to rebuild CP.
55
what affects recovery?
energy state, hormones, blood flow, precursors (nutrients), aerobic metabolism and training status
56
How are free fatty acids (FFA) transported in the blood?
FFAs bind to albumin for transport. Lipoprotein lipase in the capillaries helps release FFAs from circulating triglycerides so they can enter muscle.
57
Can fats be metabolised without oxygen?
No. Fats can only be metabolised aerobically (requiring oxygen) inside the mitochondria.
58
what inhibit cAMP
insulin
59
what activates cAMP
glucagon epiinephrine
60
what does cAMP inhibit
glycogen synthase
61
what does cAMP activate
phosphorylase
62
does glycogen synthase increase when glycogen is deplteted
yes
63
how does supercompensation workmwith glycogen depletion
if you do large depletion a lot you dont go back to normal stores you will start to get more.
64
who has more glut-4 untrained or trained
trained
65
other things that influence the rate of glycogen recovery
timing of intake, amount of cho, type of cho, muscle damage inflammation and muscle fibre type
66
muscle fibre type fastest for glycogen recovery
fast twitch initially quicker
67
can the liver release glucose into the blood
yes, unlike the muscle
68
what is gluconeogenesis and where does this happe
in the liver and the breaking down of glycogen into glucose
69
what do different hormones do to the release of glucose from the liver
glucagon increase insulin decrease carecholamines increase (both directly via phosphorlylase and indicrelty by inhibiting insulin)
70
how is the muscle and liver different for cho in terms of enzymes
the liver has seperate enzymes for glucose and fructose whereas skeletal muscle has one for both
71
liver cho enzymes
glucokinase and fructokinase
72
skeletal muscle cho enzymes
hexokinase
73
hexokinase afinity for cho
lower affinity for fructose than glucose.
74
what loves glucose more hexokinase or glucokinase
hex, therefore some of it gets phosphorlated but most will go into the general.
75
does the liver or the muscle have an ezyme to split glucose and phosphate
the liver that is why it can leave.
76
what are the transporters that can take lactate out of the muscle cell
monocarboxylate (MCT1, MCT2, MCT4)
77
fates of lactate
oxidised in low energy demanding cells, llike next door of a hard working fast muscle fibre it could go to another slow and be used there. or go into the blood stream and be taken up by another organ. if it goes into the liver it can be converted into pyruvate and then do glycogenesis (Cori cycle)
78
why is insulin not always necessary to transport glucose
as in exercise muscle contraction stimulates uptake glucose into muscles, independent of insulin. the liver doesnt need insulin to take glucose up and low insulin allows fatty acid oxidation to proceed.
79
fatty acids regulatory on glucose metabolism and vice versa
have to have regulation due to the small reserve stores in the muscle and liver, therefore cannot have both activated at one time. there are obligatory requirements for glucose in some tissues. it is effected by the use of the two, atp and the relative availability.
80
what is the cross point of fatty acids and glucose
acetyl-CoA
81
main points of the glucose - fatty acid cycle
primarily fat metabolism inhibiting glucose utilisation. acetyl-coa inhibits pyruvate dehydrogenase, meaning the pyruvate coming fromg lucose cant be turned into acetyl-coa, inhibiting PKF. which builds up fructose-6-phosphate inhibitiing hexokinase. high ffa in the blood inhibits glucose uptake
82
does the glucose-fatty acid cycle function during exercise
yes, but likley due to other mechanisms that we switch between the two. the inhibitory mechanisms are overrridenn
83
why would increase in fat oxidation reduce cho usage in exercise
Increased fat oxidation → lower ADP, AMP, Pi → reduced phosphorylase activation → less glycogenolysis.
84
why do we switch to CHO usage in high intensity and how?
glucose metabolism will block fat metabolism. the acetylcoa from pyruvate binds carnitine, which blocks it from bringing fatty aicds into the mitochondria.
85
what burns in whose flame
fat burns in carbohydrates flame.
86
why do we need both pyruvate and fatty acid for Krebs cycle
beta oxidation leads to acetylCoA, which can enter thekrebs cycle ultimately oxidised to co2. but acetylcoa needs oxaloacetate (OAA) to form citrite. which OAA is formed from pyruvate
87
what happens when we do not get enough OAA from pyruvate.
ketone synthesis, which is an alternative pathway in the liver.
88
what is ketone body production influenced by...
fasting, starving, exercise (long duration), low cho availabilityanf rate of fatty acid release relative to utilisation.
89
why can we get ketosis post exercise sometimes
when we exercise we have an increase in catecholamines and these can sometimes stay around after exercise which cause a build up of fatty acids in the liver, which causes a build up of acetylcoa without glucose.
90
what happens to the ketone bodies and where are they made
made in the liver, can go into the blood stream and they are volatile so can be expried in the lungs, or excreted in the urine, taken up in the tissue, if they have oxilcate they can be used for energy.
91
What are the three main ketone bodies?
Acetoacetate, β-hydroxybutyrate, and acetone.
92
How do ketones regulate fat metabolism?
They inhibit lipolysis by suppressing hormone-sensitive lipase and promoting insulin release.
93
What happens if ketone levels get too high?
Can cause fatigue, headache, nausea — mild ketosis or, in extreme cases, ketoacidosis.
94
Are ketones a major energy source?
No — they are a backup energy source during fasting or carbohydrate restriction.
95
how does glucose indirectly inhibit fat metabolism
actiavtes insulin in the pancreas which inhibits HSL.
96
what can ketone bodies do to glucose
can inhibit glucose usage in the brain.
97
other functions of the liver
making glucose from other substances. converting some amino acids to others detoxifying pharmaceuticals, alcohol and other environmental toxins.