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HLTH331 > Week 2: Energy balance, body composition, disease > Flashcards

Week 2: Energy balance, body composition, disease Flashcards

1
Q

Energy IN

A

Food consumption

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2
Q

Energy OUT

A
  1. Basal metabolic rate (BMR)
  2. Exercise activity thermogenesis (EAT)
  3. Non-exercise activity thermogenesis (NEAT)
  4. Thermic effect of food (TEF)
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3
Q

% of total daily energy expenditure from BMR

A

65

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4
Q

% of total daily energy expenditure from NEAT

A

20

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5
Q

% of total daily energy expenditure from EAT

A

10

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6
Q

% of total daily energy expenditure from TEF

A

5

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7
Q

Resting energy expenditure (RER)

A

Amount of energy required by the body in the resting condition (less accurate)

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8
Q

Basal metabolic rate

A

Amount of energy needed to maintain basic life metabolic processes at rest (more accurate)

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9
Q

Factors that affect BMR

A
  1. Sex
  2. Diet
  3. Pregnancy
  4. Age
  5. Fat free mass
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10
Q

Sex and BMR

A

Females have lower BMR

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11
Q

Age and BMR

A

Lower BMR as you age

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12
Q

Fat free mass and BMR

A

More muscle you burn more calories

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13
Q

Thermic effect of food

A

Energy cost during food digestion, absorption and storage

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14
Q

Non-exercise activity thermogenesis (NEAT)

A

Portion of daily energy expenditure resulting from spontaneous physical activity that is NOT the result of voluntary exercise ex. fidgeting

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15
Q

Exercise activity thermogenesis (EAT)

A

Calories burned when engaging in purposeful physical activity

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16
Q

Metabolic equivalent of task (MET)

A

Ratio of the rate of energy expended during an activity to the rate of energy expended at rest

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17
Q

What is 1 MET?

A

Amount of O2 consumed while sitting at rest

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18
Q

Measuring energy expenditure

A

Indirect and direct calorimetry

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19
Q

Indirect calorimetry

A

Wear a mask that measures ratio of consumption of O2 and release of CO2

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20
Q

Direct calorimetry

A

Measures heat dissipation

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21
Q

Calorie

A

Energy required to increase temp of 1 g of water by 1 degree celcius

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22
Q

Obesity

A

Progressive chronic disease characterized by abnormal or excessive fat accumulation that impairs health

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23
Q

Body mass index (BMI)

A

Universal definition of overweight and obesity

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24
Q

BMI equation

A

Mass (kg)/height (m2)

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25
Q

BMI- underweight

A

<18.5

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26
Q

BMI- normal weight

A

18.5-24.9

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27
Q

Overweight

A

25.0-29.9

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28
Q

BMI- obese class I

A

30-34.9

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29
Q

BMI- obese class II

A

35.0-39.9

30
Q

BMI- obese class III

A

> 40

31
Q

BMI limitations

A
  1. Body composition
  2. Fat distribution
  3. Ethnic groups and age
32
Q

Direct methods of measuring BMI

A

MRI, CT, DXA

33
Q

Indirect methods of measuring BMI

A

Lab based: hydrostatic weighing, BodPod
Field methods: Skin folds, BIA

34
Q

Subcutaneous adipose tissue

A

Makes up 80% of total body fat
Energy storage, adrenergic stimulation and endocrine regulation

35
Q

Visceral adipose tissue

A

Makes up 5-20% of total body fat
Protects organs

36
Q

Negative impacts of visceral body fat

A

Secretes proinflammatory cytokines
Increased risk of metabolic and cardiovascular disease

37
Q

Theories regarding how visceral adipocytes mediate insulin resistance

A
  1. Pro-inflammatory cytokines
  2. Spillover hypothesis
  3. Portal hypothesis
38
Q

Pro-inflammatory cytokines

A

Alter hepatic function, insulin sensitivity, cytokine production

39
Q

Spillover hypothesis

A

When SAT reaches its limit for expansion, excess energy is stored as VAT resulting in the overdevelopment of ectopic fat stores and metabolic perturbations

40
Q

Ectopic fat

A

Storage of fat in tissues other than adipose tissue such as the liver, heart, muscle and pancreas
Interferes with organ function and is associated with insulin resistance

41
Q

Portal hypothesis

A

Liver is directly exposed to FFA and cytokines released from visceral fat tissue leading to development of hepatic insulin resistance and T2D

42
Q

Waist circumference of men

A

More likely to accumulate visceral fat leading to a greater risk of CVD (android obesity)
>102cm =increased risk

43
Q

Waist circumference of women

A

Gynoid obesity
>88cm = increased risk

44
Q

Why has obesity increased?

A

Energy in increased
NEAT has decreased

45
Q

Why has energy in increased ?

A

Bigger portion sizes
Easier access

46
Q

Why has NEAT decreased?

A

Occupations involving less PA and more sitting

47
Q

Set point theory

A

Human body has a predetermined weight or fat mass set point range; there are compensatory physiological mechanisms that resist deviation from set point

48
Q

Factors that alter set point

A
  1. Genetics
  2. Epigenetics
  3. Obesogens
  4. Diet and PA
  5. Disease
49
Q

Unregulated zone

A

When we are sedentary there is a mismatch btwn energy intake and energy expenditure resulting in high body weight

50
Q

Regulated zone

A

When we increase energy expenditure our energy intake can increase while our body weight actually declines

51
Q

Obligatory thermogenesis

A

Necessary accompaniment of all metabolic processes involved in maintenance of body in living state
- decreased metabolically active tissue
- reduced energy cost of movement
- decreased postprandial response

52
Q

Adaptive thermogenesis

A

Physiologicial mechanisms employed to maintain weight
Underfeeding associated fall in resting and and non-resting energy expenditure independent of changes in FFM and FM

53
Q

Spendthrift phenotype (compensators)

A

Subjects who respond to overfeeding with increased spontaneous PA
(less susceptible to obesity)

54
Q

Thrifty phenotype (non-compensators)

A

Subjects who do not respond to overfeeding with increased NEAT
(more susceptible to weight gain)

55
Q

Hard gainers

A

People who can eat whatever they want and not gain weight bc when they overeat their NEAT increases (ex. fidgeting can burn an extra 600kcals a day)

56
Q

Why is protein important for maintaining weight?

A

Thermogenic effects
Promotes fat loss
Nutrient dense
Poor lipogenic substance
Preserves lean tissue
Increased satiety

57
Q

Roles of insulin

A
  1. Stimulates glucose uptake from blood into tissues (lowers blood glucose)
  2. Stimulates glycogen formation
  3. Suppresses release of fatty acids from adipose tissue
  4. Inhibits production of ketones in liver
58
Q

Glucagon

A

Promotes an increase in blood glucose levels and stimulates glycogen breakdown

59
Q

Carbs effect on insulin secretion

A

Potent effect

60
Q

Protein effect on insulin and glucagon

A

Elevates both

61
Q

Fat effect on insulin

A

NO effect

62
Q

Carbohydrate insulin model- a calorie is not just a calorie

A

Dietary quality can change hormonal responses to shift partitioning of calories consumed in meal toward deposition of fat tissue, causing few calories to remain available in the blood stream for the rest of the body, driving hunger and overeating

63
Q

Study 1- Insulin secretion

A

Only decreased in RC diet

64
Q

Study 1- fat oxidation

A

Only increased w RC diet

65
Q

Study 1- body fat loss

A

More cumulative body fat loss with RF diet

66
Q

Study 1- energy expenditure

A

Only decreased in RC diet

67
Q

Final conclusion of study 1

A

The effects of the RC and RF diet are statistically insignificant and therefore a calorie is just a calorie

68
Q

Study 2- conclusions

A

Ultra-processes diet caused increased ad libitum (eat whatever) energy intake and weight and fat mass gain

69
Q

Summary of the two studies

A

Both increased carbs and fats increase weight
Refined carb intake may accelerate weight gain

70
Q

When is a calorie just a calorie

A

When it comes to weight loss

HLTH331 (9 decks)

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