Chapter 4: Fats

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66 Terms

1
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When are fats the primary energy source?

at rest and low-mod intensity exercise

2
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What are fats?

  • carbon, hydrogen and oxygen

  • 9 kcals/g

3
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What are the classifications of fats?

  • TGs: 3 fatty acids + glycerol, most common dietary lipid

  • Phospholipids: glycerol + 2 FAs + phosphate group, cell membranes, water and fat soluble

  • sterols - cholesterol

4
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Where are TGs stored?

adipose tissue, muscle tissue and liver

5
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When will someone rely more on muscle TG’s?

during exercise because it’s immediately available

6
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How do TG’s provide protection?

  • add cushioning

  • insulator (thermal/electrical)

  • myelin sheath - sheath on nerves

7
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What vitamins are stored/carried in fats?

  • A, E, D, K

  • fats are necessary for absorption of certain nutrients (bioavailability)

8
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What are the functions of fats/TG’s?

  • energy source

  • energy reserve

  • provides protection

  • vitamin carrier

  • satiety in diet

9
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What are the different lengths of fatty acid chains and why is it important?

The longer the chain, the more ATP can be produced

  • short-chain fatty acid (SCFA): 2-4 carbons

  • medium-chain fatty acid (MCFA): 6-10 carbons

  • long-chain fatty acid (LCFA): 12+

10
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What are saturated and unsaturated fats?

saturated: no double bonds, saturated with hydrogens, solid at room temp

unsaturated: mono- (1 carbon double bond) and poly- (2+ carbon double bonds), liquid at room temp

11
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What are phospholipids and their functions?

  • glycerol backbone, 2 FAs + phosphate

  • function: cell membrane, transporters

12
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What is the recommended intake of fats?

fat: 20-35% of total calories

saturated: 5-6%

trans: <1%

13
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What is HDL cholesterol?

  • good cholesterol

  • high density lipoproteins

  • higher protein content

  • cholesterol from blood stream delivers to liver

14
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What is LDL cholesterol?

  • low-density lipoproteins

  • bad cholesterol

  • delivers cholesterol to cells

  • can accumulate in arterial walls, trigger inflammatory response, fibrous cap can then rupture

15
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What is VLDL cholesterol?

  • very low-density lipoproteins

  • lipoprotein lipase digests some of the TG forming intermediate density lipoprotein (IDL)

  • IDL then converted to HDL or LDL in liver

16
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Where is fat mobilized from during exercise?

  1. muscle

  2. adipose tissue

  3. blood lipoproteins

  4. exogeneous

17
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What limites the amount and source fat is utilized from?

fitness leve, type of exercise, I + D, avaible fat reserves in muscle, ability to mobilize and transport FA’s (limited if dehydrated, cold and low on CHO), composition of pre-event meal, availability of CHO

18
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What does c-AMP PK do?

activates HSL

19
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What activates lipolysis?

  • exercise

    • ~0.2 - 0.4 mmol/L at rest

    • increases 10-20 fold during exercise

      • I + D

      • rate of lipolysis (during exercise) exceeds need for FAs for oxidation by muscles

20
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What is the rate limiting step in fat metabolism (lipolysis)?

HSL bc it can be inhibited by various factors

21
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What is the fate of glycerol after lipolysis?

  • goes to liver

  • gluconeogenesis or re-esterified with FAs to make TGs

22
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What happens to FFAs when TGs breakdown?

  • blood (passive or active)

    • then bound to albumin and transported to working muscles

  • re-esterification

    • intracellular recycling

    • extracellular recycling

23
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When is re-esterification high?

at rest and recovery

24
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What factors affect re-esterification?

  • albumin not available - malnutrition or blood loss

  • blood flow through tissue is low - cold, dehydrated, etc

  • transport sites of albumin are full

  • high lactate levels - decrease FFA mobilization to increase re-esterification

25
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What is re-esterification and when is it low and high?

reutilization of the FFAs by fat cells through a futile cycle

  • high during rest and recovery

  • low during exercise

26
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What is the difference between lipolysis and beta oxidation?

  • lipolysis is break down of TGs into FAs and glycerol

  • oxidation: metabolism of fat to make ATP in presences of O2, electron transport chain, oxidizes FAs in Acetyl-CoA

27
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What are the 4 factors that hormonal responses during lipolysis depend on?

intensity, duration, fitness level, nutritional statue

28
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What are catecholamines and which ones are the strongest stimulators for lipolysis?

  • hormones and neurotransmitters

  • epinephrine and norepinephrine

    • stimulate breakdown of stored fat and CHO

    • blood levels increase dramatically within seconds

29
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What other hormones influence lipolysis?

GH (growth hormone), cortisol, TSH (thyroid stimulating hormone)

30
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What does insulin do in lipolysis?

  • strongest inhibitor

  • decreases phosphorylation of HSL (by inhibiting cAMP)

31
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What is the strongest regulator of lipolysis?

BG

  • increase BG = suppresses lipolysis (independent of insulin)

32
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What affects how much fat is stored in muscle?

  • muscle fiber type (type 1 stores more fat bc energy system)

  • nutritional status

  • type PA performed

33
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What is the process of fat oxidation?

  1. FAs bound to albumin, transported to muscle, FABP transports FA’s into muscle

  2. Once in cytoplasm

    1. re-esterified and stored as TG

    2. transported to mitochondria

  3. used by mitochondria, first activated by acyl-CoA (outside mitochondria)

  4. Activated FA transported across mitochondria with CPT1 and CPT2

34
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What is CPT1?

brings fatty acid across outer membrane of mitochondria

35
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What is CPT2?

brings fatty acids across inner membrane mitochondria

36
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What are 2 different ways increasing BG inhibits fat use?

  1. increase in BG = increase in insulin and inhibits HSL (lipolysis)

  2. increase BG = elevated malonyl-CoA that inhibits CPT1 (fat oxidation)

37
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What is carnitine?

  • conditionally essential

  • does not affect fat oxidation

38
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What does maximizing fat oxidation do?

  • helps prevent fatigue and improve performance

    • glycogen stores are limited

39
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What are some limitations of fat oxidation?

  • lipolysis and mobilization of FA’s from adipose tissue

  • transportation of FA’s within muscle and to the muscle

  • uptake of FA’s across muscle membrane

  • lipolysis/fat mobilization FA’s from intramuscular triacylglycerol pools

  • regulation FA movement across mitochondrial membrane

40
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When does most fat use occur?

untrained people max is 60-65% VO2max vs trained people 45-50% VO2max

41
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Is there a way to enhance fat mobilization during exercise?

eat enough carbs

42
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Do high fat diets work to improve performance?

no

but increased mobilization and oxidation of fat and may spare MG

43
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What are the benefits of caffeine?

  • CNS stimulation: alters perception of effort, improve neural activation of muscle

  • affect sk. muscle by altering enzymes/systems regulating CHO breakdown

  • altered metabolism

    • increase epinephrine = increase fat mobilization (lipolysis), decrease CHO use

    • lacks support

44
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What is caffeine’s effect on performance?

  • moderate does 3-9mg/kg 1 hr prior = enhanced endurance performance

  • TTE protocols show greatest impact

  • direct caffeine different than drink

  • response differs based on use

45
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Why does caffein work to improve performance?

  • not one physiological mechanism

  • primary effect on CNS

46
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What is carnitine?

  • “fat burner”

    • required to transport FA’s into mitochondria

47
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What should fat consumption look like after exercise?

  • normal dietary recommendations

    • 20-35% fat

    • focus on unsaturated

  • CHO and pro predominate

48
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Is a single high-fat meal prior to exercise beneficial?

  • not beneficial

    • GI distress (bloating, diarrhea, stomach cramping)

    • fullness

49
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Why is fat considered a calorie-dense nutrient?

it has the highest concentration of calories per gram of any macronutrient

50
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What are trans fats and why should they be avoided?

  • hydrogenation: addition of H to unsaturated fats take on saturated properties

  • increase risk for heart disease, diabetes and metabolic syndrome

51
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What are sources of saturated fats?

animal products

52
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What is total cholesterol?

HDL+LDL+TG

53
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Why is HDL considered the “good” cholesterol and how can we increase it?

  • removes other cholesterol from blood stream and reduces risk of heart disease and stroke by working against plaque buildup in arteries

  • aerobic exercise regularly, choose healthier fats (mono and polyunsaturated fats), include high fiber foods

54
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Why is LDL considered “bad” cholesterol?

  • carries cholesterol to cells

  • collects in walls of blood vessels causing plaque buildup leading to narrowing of arteries

    • increases risk of heart disease, stroke and peripheral artery disease

55
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What are the steps of fat metabolism (lipolysis)?

  1. exercise starts: release epinephrine, binds to cell membrane

  2. epinephrine stimulates production of phospo-HSL (active form)

  3. final FA split off by MGL

  4. glycerol not used is released into blood (marker of lipolysis) - substrate for hepatic gluconeogenesis

56
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What are the four sources of fat for energy metabolism?

  • muscle TGs

  • adipose tissue

  • blood lipoprotein/fat in blood

  • exogenous

57
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What factors do the amount and source of fat depend on?

  • fitness level

  • available fat reserves in muscle

  • intensity

  • duration

58
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What are the steps of fat metabolism during exercise?

  1. epinephrine stimulates lipolysis and breakdown TGs

  2. transport FAs out of adipocyte to blood, to muscle and then transported in muscle to mitochondria

    • if TG is in muscle it goes directly to mitochondria

  3. then starts Krebs cycle

59
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What is the role of epinephrine and insulin in lipolysis?

  • epinephrine: stimulates HSL/lipolysis - HSL breaks off FA from TG

  • insulin: inhibits HSL/lipolysis - stopes HSL break odd of FA from TG

60
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What is the role of albumen in fat metabolism?

protein that transports free fatty acids in the blood

61
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What are two possible fates of FFAs after they are cleaved off of glycerol?

  • blood: then bound to albumin and transported to working muscles

  • re-esterification: intracellular recycling, extracellular recycling

62
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How/why does the rate of appearance (Ra) of glycerol and FFAs change in the blood as we go from rest to exercise? How might RER change and why?

within 20 minutes of exercise, huge jump of glycerol and continues to increase, end of exercise it drops

more fat we use the lower RER is but RER goes up

63
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Why is insulin a strong inhibitor of lipolysis and why does this “make sense”?

  • it prevents FFAs from cleaving off of glycerol

  • it makes sense because it maintains blood glucose because glycerol can be converted to glucose and that would raise blood glucose levels

64
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How could you demonstrate that a training program increases and individual’s fat use as an energy source?

do baseline test and measure RER, train them for X amount of weeks and then test them at same workload and if RER decreases that demonstrates an increase in fat use

65
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When might an individuals fat use be hindered and why?

anything that limits blood flow and O2 delivery bc it limits the aerobic system relying more on glycolysis so less fat use and more carb use

66
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Ho can exercise training improve fat use?

  • more mitochondria

  • bigger mitochondria

  • increase aerobic pathway enzymes