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Flashcards in Week 1 - 3 Deck (71):
1

Lipolysis

Breakdown of Fat stores in adipose tissue to free fatty acids

2

lipogenesis

Storage of fat

3

Glycogenesis

Storage of glucose

4

Glycogenolysis
Rate limiting enzyme

Breakdown of glycogen
glycogen Phosphorylase (Ca++ and adrenaline activates, inhibited by high concentrations of ATP)

5

CHO in kcal/g (energy contribution)

4.1 kcal/g

6

Fats in kcal/g (energy contribution)

9.4 kcal/g

7

protein in kcal/g 9energy contribution)

4.1 kcal/g (only supply's around 5-10% of energy during exercise= gluconeogenesis)

8

where is the majority of the carbs stored in our bodies?

1. Muscle glycogen 2. liver glycogen 3. glucose in body fluids

9

Where is the majority of the Fats stored in our bodies?

1. Subcutaneous and visceral fats 2. inter-muscular

10

Anaerobic metabolism

without oxygen

11

Aerobic

With oxygen

12

Creatine phosphate (ATP-CP system)
rate limiting enzyme

immediate (first 0-1min)
creatine kinase (limited by ATP, stimulated by ADP)

13

Glycolytic (non-oxidative)
rate limiting enzyme ?

1min-5min majority
Breakdown of glucose-- 2 pyruvate molecules or lactic acid.
In sarcoplasm of cell.
Involves a series of enzymatic catalysed, coupled reactions
phosphofructokinase (APT inhibitor)

14

NAD

nicotinamide adenine dinucleotide

15

Oxidative Phosphorylation (aerobic)

1min + if oxygen is present
All the systems function at the same time- just contribute different amounts. In mitochondria.
Involves Krebs cycle and ETC.
Pyruvate is converted to ACetyl CoA when intracellular conditions favour aerobic catabolism of pyruvate.
1 glucose= 2 Acetyl CoA
Oxidative phosphorylation is the process in which ATP is formed as a result of the transfer of electrons from NADH or FADH 2 to O 2 by a series of electron carriers.
Net 38 ATP's produced.

16

NAD

nicotinamide adenine dinucleotide (transport hydrogens
to mitochondria for ATP generation)

17

FAD

flavin adenine dinucleotide (transport hydrogens
to mitochondria for ATP generation)

18

Enzyme used from Pyruvate to Lactate

Lactate dehydrogenase

19

Enzyme used from pyruvate to Acetyl CoA (crebs cycle

Pyruvate dehydrogenase

20

Pyruvate

= lactate + hydrogen ion

21

McArdles

Lack glycogen phosphorylate (glycogen to glucose) Therefore only able to exercise at 50% that of others.

22

Hypoglycaemia

Low blood glucose- feel pain and discomfort alot more.

23

Hypoxia
(what happens to the hydrogen ions)

Low oxygen content in the tissues (VS Hypoximia= low oxygen content in the blood) .
The Hydrogens cannot be carried to mitochondria- then LDH (lactate dehydrogenase) allows NADH to donate its hydrogen ions to pyruvate. Lactate then formed.

24

Key enzymes in glycolysis

Glycogen phosphorylase, PFK (activated by ADP, pi, AMP + a fall in PH, inhibited by ATP and CrP= produce more ATP), LDH, PDH

25

What influences the fate of pyruvate (5)

1. rate of pyruvate production
2. cytosolic redox state
3. mitochondrial density (number and size)
4. oxygen availability
5. activity of LDH (pyruvate to lactase) (more= faster conversion)

26

Aerobic conditions

glycolysis
krebs cycle
electron transport chain (90% of ATP production)

27

1 NADH = ? ATP

3 (NAD enters at a higher level then FAD)

28

FADH= ? ATP

2

29

ETC
rate limiting enzyme

relies on chemical reactions and electrical gradients across the inner mitochondrial membrane; H+ moves from electronegativity to electropositivity .
Hydrogen ions are separated from their electrons by being pumped out the inner membrane then allowed to reunited- this produces energy which allows for the formation of ATP.
It is the positive charge created: this chemical and osmotic potential that provides the E for ATP resynthesis.
cytochrome oxidase (inhibited by ATP)

30

Krebs Cycle
Rate limiting enzyme

TCA= CAC
1 glucose= 2Acetyl CoA
1 Acetyl CoA= 3 NADH (takes 3 pairs of H) + 1 FADH2 (takes 1 pair of H) + 1 ATP (converted from GTP) + 2CO2.
Isocitrate dehydrogenase (inhibited by ATP)

31

Beta oxidation

process of converting Fatty acids to Acetyl CoA.
Happens inside mitochondria

32

Oxidation of fat

fat can only be burned in oxygen
FFA transported in Blood (by Carnitine)-- FFA activation (attached to CoA- needs ATP)-- Beta oxidation-- Krebs cycle and ETC= ATP

33

Protein metabolism

During prolonged exercise- protein used as a fuel source
glucagon and cortisol= catabolic hormones. Break down protein in liver- strips of nitrate (urea).

34

Muscle fibre types

Type 1= endurance
Type 2a
type 2b

35

Type I

slow oxidative= endurance= slow twitch
Red fibres- high mitochondria density, high ion
slow to fatigue
relatively small in size, slow to contract
high oxidative capacity

36

Type IIa

fast oxidative glycolytic
'fast fibres' but share many characteristic of type 1.

37

Type IIb

Fast glycolytic (ablity to use glucose as a source Vs oxidative = ability to use fat) = white fibres = fast twitch
relatively large in size, fast to contract + fatigue quickly
low fatigue resistance
high motor unit strength

38

Sprint

All the fibres are activated at the same time

39

Endurance training

increase capacity for oxidative metabolism in the type 1 and type 2a muscle fibres

40

Spring and resistance training

elicit adaptations in the type 2a and especially the type 2b muscle fibres. (never increase the number of fibres= determined at birth)

41

EPOC

excess post exercise oxygen consumption (still breathing hard even after exercise is finished).
There is also an oxygen deficit at the start of exercise.

42

Contributing factors to EPOC

increase in heart rate, breathing, temp (~3 degrees following long bout of aerobic exercise.
lactate removal
restoration of tissue oxygen
Elevated Hormones e.g. EPH (adrenaline) = High metabolic rate, high glycogenolysis, high rate and force of heart contractions
resynthesis of PC in muscles.

43

Increase in total body expenditure

by 15-25%

44

1Kcal

amount of heat required to raise 1 g of water by 1 degree.

45

RER used?

respiratory exchange ratio
Volume of carbon dioxide produced in expired air/ number that equates to oxygen consumed.
Used to estimate % contribution of CHO or fat to energy metabolism during exercise.
high RER = High CHO % = high intensity of exercise
Low RER = High FAT % = low exercise intensity
- during prolonged sub maximal exercise that lasts for two hours the RER gradually increases.

46

Measure energy expenditure/ fuel utilisation

a. Direct calorimetry (measuring the bodies heat production, heat= measure of metabolic rate) 40% -ATP 60% heat.
b. indirect calorimetry (energy metabolism is dependent on the utilisation of oxygen)

47

Fuel selection

dependent predominantly on intensity and duration

48

cause of shift from Fats to CHO

1. recruitment of fast fibres (glycolytic enzymes)
2. Increasing blood levels of adrenaline

49

CVS function

1. delivers oxygen nutrients
2. Removes carbon dioxide, oxygen, lactate
3. transports hormones and other molecules
4. temperature balance and fluid regulation
5. Acid- base balance
6. immune function

50

Q

Cardiac output

51

cardiac output

Q= HR * VS
(L/min)
amount of blood heart pumps each min as a function of heart rate and stroke volume
Increases will endurance training

52

Stroke Volume

Amount of blood ejected by each beat
increases with exercise intensity up to 40-60% VO2 max
Plateaus after 60% as the rest time between beats decreases significantly- there is not enough time for ventricle to fill.
biggest improvement during training

53

Max HR

highest HR achieved during exhausting exercise
- highly reproducible
- declines with age
estimate: 220-age
better estimate: 208- (0.7 * age in years)

54

Factors that increase stroke volume

1. preload (amount of blood in left ventricle, increase the stretch)= more blood = greater the stroke volume
the greater the stretch the greater the following force of contraction
= franck starling mechanism
2. endurance training (HR at given intensity reduces)
- due to a dampening in the effect of the aerobic responce (= more used to exercise= less stress causes lower concentration of stress hormones in blood= lower HR)
3. more plasma in trained individual= Greater V of blood and a dampening of the stress hormones

55

Franck Starling mechanism

the greater the stretch = the greater the force of contraction

56

Fick principle

estimated amount of oxygen that the body uses during exercise.
VO2= Q * (a-v)O2 dif
(a-v)O2 = how much oxygen is extracted by the muscles.
improves with training= capillarisation

57

MAP

mean arterial pressure
Q * total peripheral resistance (vasoconstriction= necessary for venous return)
increases proportional to exercise intensity

58

RPP

rate pressure product
= HR * SBP (systolic blood pressure)

59

Cardiovascular drift

HR drifts upwards during continuous sub-maximal exercise (constant work rate).
- been associated with an increase in core temperature
- loss of water from the blood (dehydration)= lower volume of blood = the heart has to work hard = gradual increase in the concentration of circulating hormones.
to keep the cardiac output constant HR has to drift up to keep SV constant.

60

Blood

Plasma (55-60%)+ formed elements (= RBC + white blood cells= hematocrits)(40-45%)

61

Plasma

55-60 % of blood
• Can decrease by 10% with dehydration in the heat
• Can increase by 10% with training, heat acclimation
• 90% water, 7% protein, 3% nutrients/ions/etc

62

Blood viscosity

Thickness of blood
increases as hematocrits increase
decreases as plasma increases
twice as viscose as water

63

VO2 max

maximal oxygen uptake
upper limit of a persons ability to increase oxygen uptake
good indicator of cardiorespiratory endurance and aerobic fitness
differs: sex (lower in women then men), body size, age (decreases with age) , training
ml of O2 / kg/ min
_ reached within 8-18 months of heavy endurance training.

64

Adaptations to endurance training

1. left ventricle can increase in size (hypertrophy)
2. increase in SV (increase in plasma, decrease in HR (parasympathetic tone= increase in filling time= frank starling mechanism)
3. increase in ventricular mass = increases contractibility (frank- starling mechanism)
4. Q increases (increase in SV) = increase in plasma
5. VO2 max increases
6. muscles ability to extract oxygen increases = increase capillary network (= related to the oxidative capacity of the fibre= 4.1/ type 1, 3.4/ type IIa, 2.3/ type IIb + increase in size of mitochondria + increased amount of enzymes responsible for metabolism
7. Blood volume increases= fights dehydration/ less viscous= reducing strain
8. Increased capacity of the muscles to use fat as a fuel during exercise ( delays onset of fatigue by sparing glycogen deprivation)

65

Everything is reversible

central adaptations are not as reversible as peripheral adaptations= harder to improve central adaptations.

66

Respiratory exchange ratio of 0.75

suggests that the person is at rest

67

EPOC

exercise post oxygen consumption

68

Crossover concept

Describes the shift from fat to CHO metabolism as exercise intensity increases
- Due to:
- Recruitment of fast muscle fibers - ↑ glycolytic enzymes; few mitochondria and few lipolytic enzymes to break down fat.
- Increasing blood levels of epinephrine - increase muscle glycogen breakdown

69

Lactate threshold

1.) The point at which blood lactic acid rises systematically during incremental exercise
- Appears at ~50-60% VO2 max in untrained subjects
- At higher work rates (65-80% VO2 max) in trained subjects
2.) Also called:
- Anaerobic threshold
- Onset of blood lactate accumulation (OBLA)
- Blood lactate levels reach 4 mmol/L

70

Explanation for the lactate threshold

1.) Low muscle oxygen (hypoxia)
2.) Accelerated glycolysis
- NADH produced faster than it is shuttled into mitochondria
- Excess NADH in cytoplasm converts pyruvic acid to lactic acid
3.) Recruitment of fast-twitch muscle fibers
- LDH isozyme in fast fibers promotes lactic acid formation
4.) Reduced rate of lactate removal from the blood

71

Creatine kinase

creatine phosphate rate limiting enzyme