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ANATOMY > ENERGY METABOLISM > Flashcards

ENERGY METABOLISM Flashcards

1
Q

energy to work conversions

A

1 calorie is the amount of energy needed to heat 1g of water by 1 degree celcius
1kcal=4.184 kilojoules

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2
Q

what are the 2 laws that define calorimetry

A
  1. first law of thermodynamics
  2. hess’s law of heat summation
    -they justify the used of indirect calorimetry to measure energy expenditure
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3
Q

what is hess’s law of heat summation

A

it states that the heat released from a change of reactions is dependent only on the end by products. so if the by products of oxidation are the same; irrespective of if the reaction occured in vitro or in vivo; then we can determine the heat released

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4
Q

what is bomb calorimetry

A

this is when a sample of food is burned with oxygen to mimick oxidation in the body
-the energy released can be determined by the raise in temperature

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5
Q

what is the RER

A

the respiratory exchange ratio which calculates VCO2/VO2 at the level of the mouth
-RQ is used interchangeably but measures gas exchange at the tissue level

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6
Q

what are the different RER values for the different sources of food

A

carbs RER=1
protein RER= 0.85
fat RER= 0.70

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7
Q

how do we go from RER to EE

A

RER=VCO2/VO2
-so the first step is to determine the CO2 produced
-done so using doubly labelled water

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8
Q

what is doubly labelled water

A

-it is a non radioactive isotope of H2O18
- the O18 rapidly diffuses between the oxygen in water and the oxygen in carbon dioxide and so when CO2 is expelled; so is the O18 isotope
-so we can measure the amount of CO2 produced by looking at the difference between the 2 isoforms because only 2H2 will be left in the body
- so now we have determined the VCO2

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9
Q

how do we then determine RER and VO2

A

-we can replace RER with the food quotient which determines the VO2:VCO2 ratio when ALL food eaten is oxidised
-so now we have VO2
EE= VO2 X MINUTES X CALORIC EQUIVALENT

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10
Q

what are the assumptions and sources of error for indirect calorimetry

A
  1. that gas exchange happens in a non acidotic steady state environment and so there is no time delay for the production of CO2
  2. some unaccounted for energy loss from proteins like hair and nails and also solutes lost in sweat
  3. all O2 is used to oxidise degradable fuels and so all CO2 evolved is thus recovered
  4. errors in the caloric equivalents for CO2, O2 and nitrogen
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11
Q

what is the relationship betwen FFM and EE

A

the greater your fat free mass the greater your REE/BMR

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12
Q

what is the different EE for the different tissue types

A

-vital organs like heart, liver, brain etc all contribute the least to body mass but have the highest EE of all the tissues
-skeletal muscle in lean individuals contributes the most to body mass and second highest contributor to EE
-skeletal muscle has a greater EE than adipose tissue so obese individuals will thus have a lower EE because they have less skeletal muscle

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13
Q

what are some factors that affect your BMR

A

age- declines with age
smoking and caffeine- increase BMR
gender-males genetically have more skeletal muscle so a greater REE
height - increases with height

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14
Q

what are some ways to measure EE

A
  1. doubly labelled water
    2.accelerometers
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15
Q

components of daily energy expenditure

A
  1. BMR/REE-50-70%
    2.TEF=10%
    3.TEE=20-35%
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16
Q

what is TEF

A

this is the energy required to absorb and digest a meal
-the higher the better because it means you are using more of the calories in that meal to digest it/ burning more calories and so fewer calories left over to contribute to body mass essentially

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17
Q

what is the TEF for the different food groups

A

carbs=5-10%
fats=0-5%
proteins=20-30%

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18
Q

what is the relationship between habitual exercisers and TEF

A

habitual exercisers have a greater TEF after a meal
ie; greater EE post meal

19
Q

what are the 2 components of the TEF

A
  1. facultative - wastage of energy after a high caloric meal
  2. obligatory -this is all the energy required to digest, absorb and break down the food
20
Q

what is adaptive thermogenesis

A

this is the process by which heat is produced in response to changing environments or changes in diet
- so when ADP is not produced when the cell is still in a high energy state; then ATP is not going to be produced
- so no phosphorylation is going to occur
-so the proton gradient is dissipated by other means which causes an increase in ETC and O2 consumption
ie; oxidation and phosphorylation are uncoupled

21
Q

where has adaptive thermogenesis been found

A

in BAT
-has thermogenin which allows energy to be produced as heat
-but the energy loss is very insignificant to have any major affect on energy balance

22
Q

what is shivering thermogenesis

A

this is when the muscles involuntarily contract to generate heat
-they do so by increasing the oxygen consumption by up to 5x the BMR
- the muscles will eventually fatigue

23
Q

what contributes to adaptive thermogenesis in the skeletal muscles

A

protein turnover where old proteins are degraded so new ones can be formed
-contributes to energy expenditure

24
Q

how do skeletal muscles peform adaptive thermogenesis

A

using SERCA and Sarcolipin
-Sln binds to SERCA to modulate its capacity to transport calcium across the SR membrane of the muscles without generating ATP
-so Sln is using SERCA to uncouple calcium transport from ATP hydrolysis

25
Q

what is NEAT

A

non exercise activity thermogenesis
ie; all the energy expended from spontaneous activity

26
Q

what is your EPOC

A

This the excess post exercise oxygen consumption 2 components:
1. fast component
-2 to 3 minutes
-used in the regeneration of ATP stores
2. slow component
-min/hours

27
Q

what are the proposed mechanisms for EPOC

A
  1. increase in temperature loosely couples oxidation and phosphorylation
  2. increase in calcium during exercise may lead to increased oxygen consumption without ATP production
  3. complete uncoupling of oxidation and phosphorylation
28
Q

what is the cost of fat storage

A

-to store excess fat as fat costs around 5% of metabolisable energy
-but to store excess carbs as fat costs around 23% of metabolisable energy
ie; energetically inefficient process

29
Q

how do we store excess carbs as fats

A

-convert the carbs into fat using a process called de novo lipogenesis
-in this process; 2 enzymes called acetyl coA carboxylase and fatty acid synthase will convert malonyl coA and acetyl coA from glucose into palmitate
-energetically inefficient process as it requires ATP
-this process occurs in the liver

30
Q

how do we measure DNL

A

-measure net lipogenesis as the area under the graph; above an RER of 1.
-this means that fat synthesis is surpassing fat oxidation

31
Q

what is the difference between high GI and low GI foods

A

-low GI carbs are slowly broken down and so they slowly release sugar into the blood whereas high GI foods are rapidly broken down and so they quickly release sugar into the blood

32
Q

what is phenotype plasticity

A

this is where the environment has an influence on the development of a phenotype
eg: diet and body weight

33
Q

muscle fiber type and obesity

A

genetically the more type 1 fibers you have; the more lower your % body fat because type 1 fibers are more oxidative

34
Q

define metabolic flexibility

A

the ability of tissue, cells and organisms to rapidly switch substrate oxidation according to changes in nutrient intake and energy demands
-obese individuals are metabolically inflexible; they struggle to oxidise fat even after a high fat meal
- can improve this via exercise

35
Q

what are the metabolic consequences of weight loss

A
  1. lower EE
  2. lower BMR
    3.decline in fat oxidation
36
Q

what are ketogenic diets

A

these are low carb high fat diets where the body will produce an alternative fuel source from fat when glucose is low
-this fuel source is called ketone bodies

37
Q

what is the negative impact of weight cycling

A

people who constantly lose and regain weight end up with a lower TEF

38
Q

what are the consequences of weight loss by caloric restriction only

A
  1. decreased EE and BMR
  2. decreased fat oxidation
  3. increased ghrelin
    4.decreased insulin and leptin
39
Q

neural differences between successful and unsuccessful dieters

A

-see successful dieters have increased neuro behavioural control over external food cues and decreased reward orientated feeding patterns

40
Q

consequences of weight loss relapse

A
  1. decreased insulinaemia
  2. decreased leptinaemia
  3. lowered EE
  4. lowered fat oxidation
41
Q

explain the cross over concept

A

-shows the relative contribution of CHO and fat to TEE
-this is where we see with increased training/power output; an increase in the contribution of carbs whereas an increase in SNS stimulation leads to an increase in the contribution of fat to TEE
-note though that to optimize fat oxidation you should choose the exercise intensity that maximises fat oxidation; not its relative contribution to TEE

42
Q

what are the contributing factors to obesity

A
  1. physical inactivity
  2. unhealthy diet
    3.genetics
  3. nutrition in the womb
  4. nutrition in early life stages
43
Q

what is the thrifty phenotype hypothesis

A

this looks at the level of disparity between the intra and extra uterine environments
-the greater the mismatch; the greater the risk for disease
-this mismatch occurs because during development their are periods of plasticity where the maternal environmental cues may change the expression of genes so as to produce phenotypes that suit the environment of the mother.
-then once the fetus is born and the environment of the mother and now fetus has drastically changed; this leads to increased disease risk

ANATOMY (13 decks)

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