kin334 > MT1 > Flashcards

MT1 Flashcards

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1
Q

what is a Kcal

A

energy needed to increase the temperature of 1kg of water by 1Celcius

1 CAL is 1g of water by 1celcius

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2
Q

how is a Kcal measured (2)

A

direct calorimeter

bomb Calorimeter

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3
Q

is the amount of Kcal measured by calorimeter equate to amount available for humans?

A

no it is only ingested kcals. different from available or metabolizable

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4
Q

what is the Atwater Factor

A

a system that allocates energy values to food by providing an estimate of available energy.

energy value (factor) based on the heat of combustion of each group corrupted for energy losses in digestion, absorption and excretion

proposes that:
CHO: 4kcal/g which has fibre removed before
Fat: 9kcal
protein: 4kcal
ethanol: 7kcal

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5
Q

do macronutrients from different food classes have the same kcals available

A

no

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6
Q

what is the coefficient of digestibility of CHO and fat usually?

A

greater than 90%

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7
Q

how much potential energy is lost in protein?

A

estimated 20% is lost because 15-19% of protein is nitrogen

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8
Q

does insoluble fibre have any energy availability

A

no

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9
Q

does soluble fibre have any energy availability

A

partially fermentation provides some energy.

in Canada classified as 2kcal/g or lower with evidence

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10
Q

what is Atwater specific factors

A

how much energy for macronutrients from different sources

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11
Q

in the food label, what %DV is considered low and high

A

5% or less

20% or more

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12
Q

why might energy availability from mixed meals be different than the sum of it’s parts

A

interaction between the different macronutrients.

ex. dietary fibre can affect the digestibility of fats and carbs

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13
Q

what are the 3 limitations of energy availability estimations

A
  1. specific foods may have different energy availability compared to general Atwater factors
  2. mixed meals energy availability may be different than the sum of it’s parts
  3. EA can change due to other factors like, gut microbiome and obesity
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14
Q

what is the oxidative hierarchy

A

an indicator of a fuel type’s dominance within metabolic pathways. based on the body’s relative storage capacity for the different substrates and on their role in ensuring survival

alcohol
carbs
protein
fat

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15
Q

what to know about CHO intake and oxidation

A

tighty controlled
- brain produces obligatory requirement
-good but limited storage capacity

oxidation is strongly influenced by intake

After eating insulin is released which increases CHO oxidation, storage and decreased fat oxidation

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16
Q

what to know about protein intake and oxidation

A

tightly controlled
-obligatory requirement
-poor capacity to store extra AA

protein intake leads to protein oxidation

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17
Q

what to know about fat intake and oxidation

A

increase in fat consumption does not necessarily increase fat oxidation

small obligatory requirement

huge capacity to store

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18
Q

how are fats stored

A

dietary fats in blood stream with chylomicrons

LPL breaks them down into FA + glycerol

FA then stored in adipose tissue

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19
Q

what to know about alcohol intake and oxidation

A

intake is highly tied to oxidation
-no need for alcohol
-no storage

alcohol suppresses other fuel oxidation

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20
Q

which macronutrients when consumed have good autoregulation

A

auto regulation is the increase oxidation in line with intake

alcohol has perfect
carbohydrates and protein have excellent
fats have poor

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21
Q

from an energy expenditure perspective, does it matter if you absorb kcals from fat vs CHO?

A

Not when in energy balance
- when CHO oxidation increasing, fat oxidization decreasing
- when CHO oxidation decreases, fat oxidization increases

RQ does change to reflect this

when undereating, high fats is more satiating which can increase EI

when over eating, there can be some impact on EE or oxidation of the food consumed

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22
Q

when considering the storage of energy, does macro source matter

A

yes. fat has the highest storage efficiency into adipose tissue

carbs can be stored very efficiently into glycogen but not so much into adipose tissue

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23
Q

how much of TDEE is TEF/DIT usually

A

10% if in energy balance

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24
Q

EEA is split into which two variables

A

thermic effect of exercise

non exercise activity thermogenesis

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25
how does doubly labeled water work
water that has both the hydrogen and oxygen partially or completely replaced with uncommon isotopes to measure TDEE -oxygen 18 -deuterium 25% replacement of BW would be toxic the difference between the loss of O18 and deuterium reflects EE (CO2 production) requires RQ estimate and thus diet record
26
what is the difference between BMR and RMR
BMR is extremely strict and involves -dark thermoneutral room -awake after 8 hour sleep - 12 hour fasting - controlled phase of menstrual cycle ---> higher BMR in luteal - no exercise 12 hour - reclined position --> postural muscle relaxed RMR is less strict and does not require sleeping in facility before testing
27
define RMR
resting metabolic rate energy required to sustain basic life function at rest
28
how much does RMR increase with each celcius increase in body temp
12%
29
what is the difference between obligatory and facultative thermogenesis
obligatory is the energy required to digest, absorb and metabolize nutrients or BMR thermogenesis Facultative thermogenesis is regulated heat production that increases in response to cold exposure to maintain body temperature -shivering -brown fat
30
how does FM influence RMR
increase FM increase RMR
31
explain the adaptive thermogenesis effect of diet induced weight loss
RMR and BW are linear related so the expectation is that a decrease in BW will result in a linear decrease in RMR. But often the drop in RMR is much greater when compared to drop in BW.
32
how does chronic or acute exercise affect RMR
research is inconsistent but there are some conclusions 1. increase FFM = greater RMR 2. EPOC makes assessment of true RMR difficult
33
describe the impact of EPOC on EE
EE is mostly increasing the first few hours but can persist for up to 48 hours If EPOC can last up to 48 hours then despite being rested and in a post absorptive state, RMR will be acutely elevated with exercise -5% increase RMR
34
what influences TEF/DIT
DIT is proportional to energy and protein content
35
is it true that adults with obesity have bunted DIT
no
36
how much of DIT is thought to be obligatory
50-75%
37
what is facultative DIT
dissipation of excess energy. can be blocked by SNS
38
how does Beta/adrenergic blocking change RMR and DIT
decreasing RMR -decreases non-obligatory DIT -decrease facultative thermogenesis 12 % decrease
39
how does aging effect DIT
ageing lowers DIT
40
what is 1 MET
1 Metabolic equivalent time 1 MET = 3.5 mlO2/kg/min
41
how was the MET determined
a single 70kg 40year old man
42
does 1 MET really mean Resting metabolic equivalent for all people
no. one size does not fit all and 3.5 ml/kg/min is likely an overestimation
43
how much variability does age and body composition account for MET variability
60% body comp 14% age
44
weight gain in an overfeeding study is most related to which factor and how
inversely related to change in NEAT
45
what is PAL
physical activity level (PAL) = TEE/BMR higher the number the more active
46
what is set point theory
set point theory hypothesizes that the body has an internal control mechanism that is a set point that regulates metabolism to maintain a certain body fat active feedback system
47
what is settling point theory
settling point theory proposes that weight gain and loss in most humans is mostly related to patterns of diet and PA that people 'settle' into as habits. no active feedback system
48
how does body fat change with age
increase
49
what is the issue with set point theory
doesn't explain why set points have been increasing over the last 50 years contradicted by studies showing refeeding that results in greater fat and body mass also does not take into account habits and environment
50
what is the the issue with settling point theory
doesn't take into account the biological relation of weight control
51
what is satiation
sensations that govern meal size and duration and contribute to cessation of eating
52
what is orexigenic
stimulating effect on appetite ex. Ghrelin
53
what is the most common way to measure appetite and is it good
visual analogue scales (VAS) correlation between VAS and EI is moderate to weak
54
what is the role of the brain in regulating fat stores
brain integrates signals from meals and fat stores to regulate EI and EE to maintain stable fat stores eating food inhibits rewarding properties of food starving, increases reward and decreases satiety
55
what to know about leptin
protein synthesized and secreted from adipose tissue proportional to fat mass leads to decrease food intake and weight loss
56
why is leptin and leptin medication not widely used
most obese are leptin resistant not deficient
57
in what situations could leptin treatment be useful
leptin deficiency weight loss resulting in insufficient leptin. threatment could help with maintenance
58
what to know about insulin
peptide secreted from beta cells of pancreas rise when glucose load crosses blood brain barrier and reduces appetite or increase EE
59
what is the change in result when insulin is injected into brain vs peripheral
brain = satiety and weight loss peripheral =. hunger weight gain
60
what happens to insulin as weight is lost
decreases
61
what to know about ghrelin
peptide synthiszed in stomach stimulate GH orexigenic
62
what to know about PYY
secreted from small and large intestine released after feeding and leads to reduced food intake
63
what to know about GLP1
glucagon like peptide 1 inhibits glucagon release and stimulate insulin release which lowers blood glucose cosecreted with PYY in response to nutrients in gut and inhibits feeding slows gastric emptying
64
what is incretin
increase in the amount of insulin released when glucose levels are normal or particularly when they are elevated ex. GLP1
65
what to know about CCK
gut hormone that inhibits feeding stimulates digestion of fat, secreted by duodenum may synergies leptin action
66
what is energy availability
amount of dietary energy remaining after exercise, available for other physiological functions such as growth
67
how much is low, moderate and adequate energy availability
68
what is the difference between intentional and unintentional LEA
intentionally is restricting energy intake for BW concerns unintentionally is not increasing EI to account for higher training
69
why might LEA's impact on performance be minimal or seemingly nonexistent
some sports where there is a tremendous effect of body weight on performance.
70
what did New Zealand rowing show about LEA
encouraged to eat more --> many wins
71
define obesity
disease in which excess BF has accumulated such that health may be adversely affected
72
difference between the types of diabetes
type 1: destruction of beta cell. No or insufficient insulin release type 2: insulin resistance + insufficient insulin gestational diabetes: glucose intolerance during pregnancy
73
what are the 4 different means of diagnosing T2 diabetes
FPG >7mmol/L (fasting plasma glucose/ 8hour fast) -easy -unstable -high day to day variability HBa1c > 6.5%. (average blood sugar over 2-3 months) -low day to day variability -convenient -cost 2hPG in a 75g OGTT >11.1mmol/L 2hr plasma glucose after 75g oral glucose tolerance test -unstable -high day to day variability -unstable -uncomfortable -cost random PG > 11.1mmol/L
74
how does being overweight or obese effect risk of T2D
doubles risk 5-10% of population have T2D 10-20% overweight/obese have T2D
75
what are the two mechanisms that link high adipose tissue and T2D
increase FFA leads to detrimental impact on insulin uptake by liver and increased gluconeogensis. Pancreas then has to make more insulin because of increased glucose production increases insulin resistance of muscle. increases in insulin release leads to eventual b-cell failure and hyperglycaemia
76
what is the Canadian standard for hypertension
140/90 american standards are lower 130/80
77
compare percentages of people with hypertension between normal and overweight/obese
16% normal 40% overweight/obese
78
what is the difference between primary and secondary hypertension
primary is when there is no underlying cause -90 to 95% of all causes secondary is caused by other conditions affecting the kidney, arteries or diseases
79
what are the pathways that adipocytes increase BP or lead to hypertension
Leptin increases SNS activation leading to hypertension FFA -Increases inflammation and arterial stiffness -effects kidney function angiotensinogen -altered kidney function other endocrine signals that lead to inflammation and arterial stiffness
80
what is adiponectin and what does it do
secreted only by adipocytes and is inversely proportional to %body fat. - fat loss increases adiponectin concentrations -adiponectin increases insulin sensitivity
81
how is metabolic syndrome defined (5)
a combination of factors Elevated waist circumference -NA>europe>asia elevated TG reduced HDL-C Elevated BP Elevated FPG (resting plasma glucose)
82
how does the risk of cancer change when obese
40 BMI increases cancer 52% men 62% women
83
how does obesity effect the risk for osteoarthritis
obesity is the number one preventable risk factor -NOT PURELY MECHANICAL -->b/c found also in hands and fingers possibly due to inflammatory environment and sedentary
84
how to calculate Kcal from METS
kcal = METS x BW(kg) x hr
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