Metabolism of Exercise Flashcards
1
Q
Name 3 types of energy intake
A
- Fats
- Proteins
- Carbohydrates
2
Q
Name 3 types of energy expenditures
A
- Basal Metabolic Rate
- Physical activity
- Thermic effect of food
3
Q
Dysregulation in energy homeostasis could lead to the metabolic syndrome what are the risk factors
A
- Visceral obesity
- Elevated TAGs levels in the blood, low HDL
- Arterial hypertension
- Insulin resistance
- Pro-inflammatory state
4
Q
Dysregulation in energy homeostasis could lead to the metabolic syndrome, what are the 3 causes
A
- Obesity
- Inactivity
- Genetic Factors
5
Q
What 4 effects does exercise have on your metabolism?
A
- Blood distribution (oxygen)
VO2, VCO2 and VO2max - Sources of fuel during exercise
- Metabolic phases of exercise
- Effect of training on metabolism
6
Q
What 4 effects does exercise have on your metabolism?
A
- Blood distribution (oxygen)
VO2, VCO2 and VO2max - Sources of fuel during exercise
- Metabolic phases of exercise
- Effect of training on metabolism
7
Q
During rest or exercise is more blood circulated to the muscle
A
exercsie
8
Q
During exercise where is blood returned for reoxygenation
A
heart
9
Q
Pulmonary Respiration
A
Lungs to blood and blood to lungs
10
Q
Cellular Respiration
A
Blood to tissues and tissues to blood
11
Q
2 main players of respiration movement
A
- O2
- CO2
12
Q
VO2
A
Volume of oxygen used by the body each minute
mL kg-1 min-1
13
Q
VCO2
A
VCO2: Volume of carbon dioxide generated by the body each minute
mL kg-1 min-1
14
Q
VE
A
Volume of air exhaled each minute
mL kg-1 min-1
15
Q
Respiratory Exchange Ratio (RER)
A
VC02/VO2
16
Q
RER around 0.7
A
100% of energy comes from fat
17
Q
RER around 0.85
A
ernergy comes from 50% fat, 50% carbohydrates (glucose)
18
Q
RER around 1
A
100% of energy comes from carbohydrates (glucose)
19
Q
T or F: Prolonged excercise causes muscle to shift from carbohydrate to fat metabolsim
A
T
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
21
Q
T or F: Can high intensity exercise use only carbohydrates
A
No it may use a mix of fats and carbohydrates
22
Q
T or F: Can high intensity exercise use only carbohydrates
A
No it may use a mix of fats and carbohydrates
23
Q
T or F: Carbohydrates are not key in fat metabolism
A
False they are
24
Q
Why are carbohydrates necessary to complete aerobic degradation of fat
A
- Acetyl-CoA are produced by the b-oxidation of FAs
- These newly formed acetyl-CoA need to be metabolized by the TCA cycle in order to generate ATP (oxidative-phosphorylation).
- Pyruvate produced by glycolysis can be used to replenish level of oxaloacetate in the TCA cycle.
25
What happens to aerobic degredation of fat if carbohydrates are low
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.
26
Difference between oxygen deficit and oxygen debt
27
Difference between oxygen deficit and oxygen debt
28
Explain oxygen deficit and EPOC
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
What does creatine phosphate (PCr) do in tissues that consume ATP rapidly
It acts like an energy resevoir for the regeneration of ATP
30
When is creatine phosphate used and what follows it
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
When is creatine phosphate used and what follows it
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
Under steady-state oxygen consumption what oxxurs
The energy required by the working muscle is matched by ATP production (exercise intensity is constant too)
32
Following exercise, what occurs
Oxygen consumption decreases but remains elevated (EPOC = Excess Post-Exercise Oxygen Consumption)
33
At the beginning of recovery after exercise what occurs
The fast component of recovery where oxygen consumption decreases rapidly
34
What 2 things happen during the fast component of muscle recovery
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
What follows the fast component of recovery
The slow component of recovery
36
What happens during the slow component of recovery
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
3 effects of exercise on metabolism
1. Physical capacity (dilation of blood vessels)
2. Angiogenesis
3. Mitochondrial biogenesis
38
a 6 week areobic training program can resul in what 3 metabolic functions
1. Increased VO2
2. Heart rate decreases
3. Increased physical capacity
39
How does training increase physical capacity?
Vasodilation of the blood vessels (remodelling)
40
What is the link between exercise and low blood pressure
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
Nitric oxide cycle
42
Does the urea cycle affect the nitric oxide cycle
No because urea takes place in the liver and the nitric oxide cycle affects the blood vessels (different areas)
43
When we have endothelial dysfunction what occurs
Oxidation of BH4 producing BH2 and superoxide
44
Process of endothelial dysfunction vs regular function
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
When superoxide is formed what happens
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
T or F: ENOS is lower in those who train 4 weeks compared to sedentary animals
False its higher and leads to increased blood flow due to vasodilation
47
Angiogenesis
Formation and differentiation of blood vessels
48
T or F: Increased exercise calls for increased demand of oxygen
True so some muscles may not get enough oxygen
49
Suboptimal oxygen levels could lead to
transient hypoxic conditions
50
Under hypoxic conditions what is increased in expression
HIF-1 (Hypoxia-induced factor-1)
51
HIF-1 leads to increase of
gene transcription involved in angiogenesis
52
What is a primary target of HIF-1
VEGF (Vascular endothelial growth factor)
53
Function of VEGF
recruits endothelial cells to the hypoxic region and stimulates their proliferation to create new blood vessels.
54
T or F: Training decreases mitochondrial density
False, increases
55
Exercises stimulates or inhibits AMPK activity
Stimulates
56
Long term effect of exercise (adiponectin and Ca2+) is
The increase of fatty acid oxidation and mitochondrial biogenesis
57
Mitochondrial biogenesis (AMPK and Ca2+ signalling role)
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
Mitochondrail Biogenesis: PGC-1a signaling
PGC-1a uses peroxisome proliferator-activated receptor (PPAR)-y coactivator 1a is a master regulator of mitochondrial biogenesis.
59
What is 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR)
Intermediate in the generation of inosine monophosphate (IMP).
60
Function of 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR)
able to mimic the effect of AMP in the activation of AMPK.
**Not surprisingly, AICAR is now a banned substance in competitive sports.
61
Overexpression of PGC-1a does what
Improves exercises performance and oxygen uptake and increases expression of key metabolic enzymes (mostly fatty acid oxidation)
62
Overexpression of PGC-1a does what to muscle mass
Increases it (no training required)
63
T or F: PGC-1alpha causes more reliance on fatty acid oxidation compared to carbohydrates
True
64
What does PGC-1alpha do to white adipose tissue
Turns it to brown which is better for energy expenditure, thermogeneis, adipogenesis, and mitochondrial bigogenesis
65
What does PGC-1alpha do to white adipose tissue
Turns it to brown which is better for energy expenditure, thermogeneis, adipogenesis, and mitochondrial biogenesis (UCP-1 = heat generation)
66
Why is exercise so important for weight management
Obesity = increase in leptin and decrease in adiponectin, but when you train you want the opposite
