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BCH3120 > Metabolism of Exercise > Flashcards

Metabolism of Exercise Flashcards

1
Q

Name 3 types of energy intake

A
  1. Fats
  2. Proteins
  3. Carbohydrates
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2
Q

Name 3 types of energy expenditures

A
  1. Basal Metabolic Rate
  2. Physical activity
  3. Thermic effect of food
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3
Q

Dysregulation in energy homeostasis could lead to the metabolic syndrome what are the risk factors

A
  1. Visceral obesity
  2. Elevated TAGs levels in the blood, low HDL
  3. Arterial hypertension
  4. Insulin resistance
  5. Pro-inflammatory state
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4
Q

Dysregulation in energy homeostasis could lead to the metabolic syndrome, what are the 3 causes

A
  1. Obesity
  2. Inactivity
  3. Genetic Factors
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5
Q

What 4 effects does exercise have on your metabolism?

A
  1. Blood distribution (oxygen)
    VO2, VCO2 and VO2max
  2. Sources of fuel during exercise
  3. Metabolic phases of exercise
  4. Effect of training on metabolism
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6
Q

What 4 effects does exercise have on your metabolism?

A
  1. Blood distribution (oxygen)
    VO2, VCO2 and VO2max
  2. Sources of fuel during exercise
  3. Metabolic phases of exercise
  4. Effect of training on metabolism
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7
Q

During rest or exercise is more blood circulated to the muscle

A

exercsie

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8
Q

During exercise where is blood returned for reoxygenation

A

heart

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9
Q

Pulmonary Respiration

A

Lungs to blood and blood to lungs

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10
Q

Cellular Respiration

A

Blood to tissues and tissues to blood

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11
Q

2 main players of respiration movement

A
  1. O2
  2. CO2
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12
Q

VO2

A

Volume of oxygen used by the body each minute
mL kg-1 min-1

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13
Q

VCO2

A

VCO2: Volume of carbon dioxide generated by the body each minute
mL kg-1 min-1

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14
Q

VE

A

Volume of air exhaled each minute
mL kg-1 min-1

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15
Q

Respiratory Exchange Ratio (RER)

A

VC02/VO2

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16
Q

RER around 0.7

A

100% of energy comes from fat

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17
Q

RER around 0.85

A

ernergy comes from 50% fat, 50% carbohydrates (glucose)

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18
Q

RER around 1

A

100% of energy comes from carbohydrates (glucose)

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19
Q

T or F: Prolonged excercise causes muscle to shift from carbohydrate to fat metabolsim

A

T

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20
Q

Under high intensity conditions (exercise), muscle will shift from [blank] to [blank] and is called [blank]

A

shift from fat to carbohydrate and is called the crossover concept

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21
Q

T or F: Can high intensity exercise use only carbohydrates

A

No it may use a mix of fats and carbohydrates

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22
Q

T or F: Can high intensity exercise use only carbohydrates

A

No it may use a mix of fats and carbohydrates

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23
Q

T or F: Carbohydrates are not key in fat metabolism

A

False they are

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24
Q

Why are carbohydrates necessary to complete aerobic degradation of fat

A
  1. Acetyl-CoA are produced by the b-oxidation of FAs
  2. These newly formed acetyl-CoA need to be metabolized by the TCA cycle in order to generate ATP (oxidative-phosphorylation).
  3. Pyruvate produced by glycolysis can be used to replenish level of oxaloacetate in the TCA cycle.
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25
Q

What happens to aerobic degredation of fat if carbohydrates are low

A
  1. Reduced rate of glycolysis leads to reduced level of pyruvate.
  2. Reduced conversion of pyruvate to oxaloacetate (to replenish TCA cycle).
  3. TCA cycle slows down
    Only few acetyl-CoA coming from the b-oxidation of FAs can enter the TCA cycle.

**This is why our body try to keep a small reserve of carbohydrates in our muscle.

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26
Q

Difference between oxygen deficit and oxygen debt

A
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27
Q

Difference between oxygen deficit and oxygen debt

A
28
Q

Explain oxygen deficit and EPOC

A
  1. At the beginning of the exercise (first 5 minutes), the uptake of oxygen increases
  2. The uptake of oxygen is lagging in comparison to the oxygen requirements.
  3. ATP production relies heavily on ATP-phosphocreatine cycle and anaerobic glycolysis.
    This is the oxygen deficit phase
29
Q

What does creatine phosphate (PCr) do in tissues that consume ATP rapidly

A

It acts like an energy resevoir for the regeneration of ATP

30
Q

When is creatine phosphate used and what follows it

A

Creatine phosphate will be used within the first minute of exercise to regenerate the ATP pool and it will be followed by anaerobic metabolism.

30
Q

When is creatine phosphate used and what follows it

A

Creatine phosphate will be used within the first minute of exercise to regenerate the ATP pool and it will be followed by anaerobic metabolism.

31
Q

Under steady-state oxygen consumption what oxxurs

A

The energy required by the working muscle is matched by ATP production (exercise intensity is constant too)

32
Q

Following exercise, what occurs

A

Oxygen consumption decreases but remains elevated (EPOC = Excess Post-Exercise Oxygen Consumption)

33
Q

At the beginning of recovery after exercise what occurs

A

The fast component of recovery where oxygen consumption decreases rapidly

34
Q

What 2 things happen during the fast component of muscle recovery

A
  1. Muscle ATP and creatine phosphate stocks are replenished
  2. Remaining lactate is converted back to glucose
    **Takes about 3 minutes for 100% recovery
35
Q

What follows the fast component of recovery

A

The slow component of recovery

36
Q

What happens during the slow component of recovery

A
  1. Body temperature, redistribution of ions in the muscle, rehydration, replenishment of glycogen reserves are all reset
  2. Elevated VO2 may last for up to 60 minutes.
37
Q

3 effects of exercise on metabolism

A
  1. Physical capacity (dilation of blood vessels)
  2. Angiogenesis
  3. Mitochondrial biogenesis
38
Q

a 6 week areobic training program can resul in what 3 metabolic functions

A
  1. Increased VO2
  2. Heart rate decreases
  3. Increased physical capacity
39
Q

How does training increase physical capacity?

A

Vasodilation of the blood vessels (remodelling)

40
Q

What is the link between exercise and low blood pressure

A

Nitric oxide is over-expressed as you train and will travel to the smooth muscle to sGC and converts GTP to cGMP to cause vasodilation (stops contraction)

41
Q

Nitric oxide cycle

A
42
Q

Does the urea cycle affect the nitric oxide cycle

A

No because urea takes place in the liver and the nitric oxide cycle affects the blood vessels (different areas)

43
Q

When we have endothelial dysfunction what occurs

A

Oxidation of BH4 producing BH2 and superoxide

44
Q

Process of endothelial dysfunction vs regular function

A

Dysfunction = decreased arginine and BH4 = superoxide produced which produced hydrogen peroxide and peroxynitrite = toxic (dotted line in picture = will not occur)
Regular = produces NO and citrulline regularly

45
Q

When superoxide is formed what happens

A

Superoxide reacts with NO to cause oxidation of heme group of sGC (Fe2+ to Fe3+) which will deactivate the enzyme causing no production of cGMP and will cause vasoconstriction

46
Q

T or F: ENOS is lower in those who train 4 weeks compared to sedentary animals

A

False its higher and leads to increased blood flow due to vasodilation

47
Q

Angiogenesis

A

Formation and differentiation of blood vessels

48
Q

T or F: Increased exercise calls for increased demand of oxygen

A

True so some muscles may not get enough oxygen

49
Q

Suboptimal oxygen levels could lead to

A

transient hypoxic conditions

50
Q

Under hypoxic conditions what is increased in expression

A

HIF-1 (Hypoxia-induced factor-1)

51
Q

HIF-1 leads to increase of

A

gene transcription involved in angiogenesis

52
Q

What is a primary target of HIF-1

A

VEGF (Vascular endothelial growth factor)

53
Q

Function of VEGF

A

recruits endothelial cells to the hypoxic region and stimulates their proliferation to create new blood vessels.

54
Q

T or F: Training decreases mitochondrial density

A

False, increases

55
Q

Exercises stimulates or inhibits AMPK activity

A

Stimulates

56
Q

Long term effect of exercise (adiponectin and Ca2+) is

A

The increase of fatty acid oxidation and mitochondrial biogenesis

57
Q

Mitochondrial biogenesis (AMPK and Ca2+ signalling role)

A

1) Increase in Ca2+ activates CaMK (calcium/calmodulin depndent kinase) which increased PGC-1a expression
2) AMPK increases when AMP/ATP ratio increases so AMPK targets PGC-1a
**Adiponection = long term activator wheras Ca2+ and AMP = immediate activators

58
Q

Mitochondrail Biogenesis: PGC-1a signaling

A

PGC-1a uses peroxisome proliferator-activated receptor (PPAR)-y coactivator 1a is a master regulator of mitochondrial biogenesis.

59
Q

What is 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR)

A

Intermediate in the generation of inosine monophosphate (IMP).

60
Q

Function of 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR)

A

able to mimic the effect of AMP in the activation of AMPK.
**Not surprisingly, AICAR is now a banned substance in competitive sports.

61
Q

Overexpression of PGC-1a does what

A

Improves exercises performance and oxygen uptake and increases expression of key metabolic enzymes (mostly fatty acid oxidation)

62
Q

Overexpression of PGC-1a does what to muscle mass

A

Increases it (no training required)

63
Q

T or F: PGC-1alpha causes more reliance on fatty acid oxidation compared to carbohydrates

A

True

64
Q

What does PGC-1alpha do to white adipose tissue

A

Turns it to brown which is better for energy expenditure, thermogeneis, adipogenesis, and mitochondrial bigogenesis

65
Q

What does PGC-1alpha do to white adipose tissue

A

Turns it to brown which is better for energy expenditure, thermogeneis, adipogenesis, and mitochondrial biogenesis (UCP-1 = heat generation)

66
Q

Why is exercise so important for weight management

A

Obesity = increase in leptin and decrease in adiponectin, but when you train you want the opposite

BCH3120 (36 decks)

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