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MEH > Lecture 20 > Flashcards

Lecture 20 Flashcards

1
Q

What fuel supplies are normally available in the blood?

A

Glucose
-preferred fuel source (most glucose stored as glycogen, little free glucose in the blood)
Fatty Acids
-stored as triacylglycerol in adipose

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2
Q

Which cells can’t use fatty acids as fuel?

A

RBC’s, brain, CNS

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3
Q

What fuel sources are available under special conditions?

A

Amino acids
-some muscle protein can be broken down (proteolysis) to provide amino acids for fuel
-converted to glucose/ketone bodies
-used directly as a fuel via oxidation
Ketone bodies
-fatty acids converted to ketone bodies in the liver
-used when little glucose available
Lactate
-product of anaerobic metabolism in muscle
-liver can convert it back to glucose (Cori cycle) or utilised as a fuel for TCA cycle

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4
Q

Which hormones determine the availabiliy of fuel molecules in the blood?

A

Insulin: lowers fuel concentrations in the blood

Glucagon/adrenaline/growth hormone/cortisol (anti-insulin hormones): increase concentrations in blood

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5
Q

Which glucose store can be made available to tissues such as the CNS?

A

Glucose stored in the liver

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6
Q

What is hypoglycaemia and its symptoms?

A

Blood glucose <3 mmol/L
Symptoms: trembling, weakness, tiredness, sweating, sickness, tingling around lips, palpitations, changes in mood, slurred speech, staggering walk
(can be confused with intoxication)
Leads to unconsciousness and death as CNS is starved of glucose

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7
Q

What is hyperglycaemia and its symptoms?

A

Blood glucose >7 mmol/L
Symptoms: nervous/cardio/renal systems affected, glucose in urine, polyuria, polydipsia, increased glycation of plasma proteins such as lipoproteins leading to altered function, abnormal metabolism of glucose to harmful products

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8
Q

What are the effects of feeding?

A

Absorption of glucose, AA’s, and lipids from gut into bloodstream
Stimulates endocrine pancreas to release insulin

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9
Q

What are the actions of insulin?

A
  • increases glucose uptake and utilisation by muscle/adipose tissue
  • promotes storage of glucose as glycogen in liver/muscle
  • promotes AA uptake and protein synthesis in the liver/muscle
  • promotes lipogenesis and storage of fatty acids as triacylglycerols in adipose tissue
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10
Q

What are the effects of fasting?

A

As blood glucose concentration falls, insulin secretion is depressed. Reduces uptake of glucose by adipose/muscle and stimulates glucagon secretion

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11
Q

What are the actions of glucagon?

A
  • glycogenolysis in liver to maintain blood glucose for brain and glucose dependent tissues
  • lipolysis in adipose tissue to provide fatty acids
  • gluconeogenesis to maintain supply of glucose to the brain
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12
Q

When does starvation begin?

A

Fasting beyond 10 hours

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13
Q

What is the body’s response to starvation?

A
  • blood glucose falls to 3.5 mmol/L and is maintained by glucagon (stimulates breakdown of hepatic glycogen)
  • these stores only last a few hours so continuing reduction in glucose stimulates pituitary to release ACTH so blood cortisol is increased
  • cortisol stimulates gluconeogenesis and makes gluconeogenic substances available by breakdown of protein and fat
  • glucagon also stimulates gluconeogenesis
  • both hormones increase amounts and activities of key enzymes in the gluconeogenic pathway in liver cells
  • lipolysis occurs at high rate as insulin falls due to rise in lipolytic enzymes (glucagon/cortisol/GH) so free fatty acids rise to 2mmol/L and these are metabolised
  • fatty acids are oxidised in the liver to produce ketone bodies which can be used as a fuel for the brain (this reduces the need for gluconeogenesis and spares body protein)
  • ketone bodies rise from 0.01 mmol/L to 6-7 mmol/L
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14
Q

What are some gluconeogenic substrates?

A

Alanine

Glycerol

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15
Q

What is the normal plasma concentration of fatty acids?

A

0.3 mmol/L

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16
Q

Can fatty acids be used a fuel for the brain?

A

No, they are attached to albumin so can’t bypass the blood brain barrier

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17
Q

What are 2 vital adaptations to starvation?

A
  • brain becomes able to use ketone bodies as fuel, reducing its glucose requirement from 140g to 40g per day
  • kidneys begin to contribute to gluconeogenesis
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18
Q

How does the fact that the brain uses ketone bodies effect gluconeogenesis?

A

It reduces the need for breakdown of protein for gluconeogenesis so it falls to 30%
-urinary nitrogen excretionfalls from 12 g/day to 4g/day

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19
Q

Why must the protein content of a diet of a starved person be increased gradually?

A

Reduction in urea synthesis (less proteins broken down, so less ammonia released): decrease in amount and activity of enzymes involved in the process in liver cells
-refeeding syndrome: excess ammonia

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20
Q

What does the body use once all of the fat stores are depleted?

A

Protein, rapidly used up and death follows shortly

-death due to loss of muscle mass including serious respiratory infections due to loss of respiratory muscles

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21
Q

What is the net weight gain by the end of pregnancy?

A

8kg

foetus: 3.5kg, placenta:0.6kg, amniotic fluid:0.8kg, maternal fuel stores: 3kg

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22
Q

What is the rate of transfer across the placenta to the foetus dependent on?

A

Their concentration in the maternal circulation

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23
Q

Why does maternal metabolism channge during pregnancy?

A

To ensure

  • the foetus is supplied with range of nutrients it requires
  • nutrients are supplied at the appropriate rate for each stage of development
  • minimal disturbances to maternal nutrient homeostasis
  • foetus is buffered from any major disturbances in maternal nutrient supply
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24
Q

What hormones are involved in maternal metabolism?

A

Maternal insulin
Oestrogens
Progesterone
Placental lactogen

25
Q

What is the role of insulin in pregnancy?

A

Maternal concentration increases as pregnancy proceeds to promote storage and uptake of nutrients (as fat in adipose tissue)

26
Q

What are the effects of foetal-placental hormones?

A

Anti-insulin. Oppose the actions of insulin

27
Q

What are some examples of hormones of the placental origin?

A
  • human placental lactogen
  • progesterone
  • corticotropin releasing hormone
28
Q

What are the metabolic changes during the first half of pregnancy?

A

Increase in maternal nutrient stores ready for the more rapid growth of the foetus, birth and lactation

  • increasing levels of insulin (increases insulin/anti-insulin ratio) promotes anabolic state
  • increased insulin sensitivity
29
Q

What are the metabolic changes during the second half of pregnancy?

A

Marked growth of placenta and foetus
Keeping the nutrients in the maternal circulation relatively high
-decreased insulin sensitivity
-reducing maternal utilisation of glucose by switching tissues to use fatty acids
-delaying disposal of nutrients after meals
-releasing fatty acids from stores build up during first half
Even though the maternal insulin levels increase, the amount of anti-insulin hormones increases at an even faster rate so the insulin/anti-insulin ratio falls

30
Q

What happens to maternal ketogenesis during pregnancy?

A

The fall in the insulin/anti-insulin ratio stimualtes production of ketone bodies by maternal liver which are used as a fuel by developing foetal brain

31
Q

What is gestational diabetes?

A

Pancreas is unable to respond to metabolic demands of pregnancy and pancreas fails to release the increased amounts of insulin required.

  • this disappears after pregancy as the endocrine pancreas can respond adequately
  • these women are likely to develop diabetes later in life
32
Q

How does the mother meet increased demand for insulin?

A

Pancreatic beta cell hyperplasia and hypertrophy

Rate of insulin synthesis in beta cells increases

33
Q

What does the metabolic response to exercise ensure?

A
  • products of metabolism are removed
  • glucose supply to brain is maintained
  • minimal disturbances to homeostasis by keeping rate of mobilisation equal to rate of utilisation
  • increased energy demands are met by mobilisation of fuel molecules from energy stores
34
Q

What does the magnitude/nature of metabolic response to exercise depend on?

A
  • type of exercise (which muscles)
  • intensity/duration (high intensity with short duration: anaerobic, lower intensity with long duration: aerobic metabolism)
  • physical condition and nutritional status of individual
35
Q

Which muscles do the energy requirements of exercise usually effect?

A

Skeletal and cardiac muscles rather than respiratory muscles

36
Q

How does the BMR change during exercise?

A

Resting: 4 kJ/min of energy
Marathon: 80 kJ/min of energy
100m sprint: 200 kJ/min of energy

37
Q

Where does the energy for muscle contraction come from?

A

Hydrolysis of ATP

38
Q

Rate of ATP turnover:

A

Rest: 0.06 mmol/sec/kg
Marathon: 1.2 mmol/sec/kg
Sprint: 3 mmol/sec/kg

39
Q

What is the ATP concentration in muscle?

A

5 mmol/kg

Last for 2 secs during a sprint, but the ATP concentration doesn’t fall by more than 20% as it is regenerated from ADP

40
Q

How is ATP initially regenerated?

A

From creatine phosphate

Creatine phosphate + ADP = ATP + creatine

41
Q

What are the major fuel molecules?

A

Stores: glycogen (300g in muscle, 100g in liver), and triacylglycerols
Circulating fuel molecules: glucose and free fatty acids

42
Q

How long do glycogen stores last?

A

Aerobic conditions: completely oxidised to CO2, lasts for 60 mins of low intensity exercise
Anaerobic conditions: end product is lactic acid, lasts 2 minutes
(more ATP produced in aerobic conditions and less used up)

43
Q

What is the glycogen store of the liver for?

A

Prevent hypoglycaemia and associated impairment of CNS function
-could provide muscle with enough glucose for 18 mins of low intensity exercise

44
Q

What are the advantages of using glycogen rather than circulating glucose?

A
  • availability not affected by blood supply
  • no need for membrane transport into muscle cells
  • produces G-6-P without using ATP (glycogen phosphorylase uses Pi)
  • mobilisation is rapid due to highly branched structures for enzyme attack
45
Q

What limits anaerobic metabolism of glucose in muscle?

A

Build up of lactate and H+

-H+ build exceeds buffering capacity of muscle cells and impairs their function producing fatigue

46
Q

How does H+ impair muscle function?

A
  • inhibition of glycolysis
  • interferes with actin/myosin interaction
  • causes sarcoplasmic reticulum to bind Ca2+ (inhibits contraction)
47
Q

What factors limit the use of fatty acids by muscle?

A
  • rate of fatty acid release
  • limited capacity of blood to transport fatty acids
  • rate of fatty acid uptake into muscle cells
  • fatty acid oxidation requires more oxygen/moles of ATP produced than glucose
  • fatty acids can only be metabolised under aerobic conditions
48
Q

How much glucose/free fatty acids are in the extracellular fluid?

A

12g glucose (180 kJ)
4g fatty acids (100 kJ)
Enough energy for 4 mins of marathon runnning

49
Q

What are the metabolic responses to short duration high intensity exercise?

A

Rapid response confined to skeletal muscle tht works anaerobically.

  • muscle ATP and CP are used
  • muscle glycogen is rapidly mobilised
  • G-6-P is metabolisedvia glycolysis to provide ATP from ADP at substrate level phosphorylation
  • glycolysis occurs anaerobically producing lactate and H+
  • build up of H+ produces fatigue
50
Q

What are the metabolic responses to medium duration intensity exercise?

A
  • initial sprint uses muscle ATP and CP and anaerobic glycogen metabolism
  • middle phase where ATP is produced aerobically from glycogen in muscle
  • final burst relies on anaerobic metabolism of glycogen and produces lactate
51
Q

What is the metabolic response to marathon running?

A

Carbohydrate stores are insufficient and muscle cells have to oxidise fatty acids

  • muscles work aerobically and use all types of fuel molecules
  • origin and type of fuel changes as exercise proceeds
52
Q

Which fuel molecules are used in the marathon?

A

Major fuel: glycogen (many runners eat carbohydrate rich diets to increase their glycogen stores)

  • increased utilisation of circulating blood glucose (but this stays constant as the glucose used by muscles is replaced by glucose released by liver)
  • blood glucose may eventually fall due to limited substrates for liver gluconeogenesis
  • fatty acids can be used as a source of energy due to aerobic conditions
53
Q

When is eating carobohydrates to increase glycogen stores most effective?

A

After exercise, as exercise promotes storage of glucosen as muscle glycogen rather than conversion to lipid

54
Q

What controls the metabolic reponses during a marathon?

A

-insulin levels fall due to adrenaline and NA secretion
-adrenaline/NA/GH increase rapidly
-glucagon/cortisol levels increase gradually
Causing
-increased glycogenolysis in liver
-increased gluconeogenesis in liver
-increased lipolysis

55
Q

What are the biochemical causes of fatigue?

A
  • depletion of muscle glycogen
  • accumulation of H+ in muscle
  • dehydration
56
Q

What is a whole body response to prolonged exercise?

A
  • increased fuel consumption by muscles
  • increased ATP production and utilisation by muscles
  • increased heat production
  • increased delivery of O2 to muscles (vasodilation of arterioles)
  • increased removal of CO2, H+, lactate from muscles
  • increased CO
  • redistribution of blood away from gut and kidneys to muscles
  • changes in breathing (increased rate and depth)
57
Q

What is a whole body response to training?

A

Long term adaptations to improve capacity for physical work (effect cardio/skeletal systems rather than resp)
Are reversible
-heart beats slower for same CO
-more 2,3-BPG in blood lowering affinity of Hb for oxygen
-increased GLUT4 in cell membranes of muscles
-increased storage of glycogen
-increased number and size of muscle fibres
-increased vascularisation of muscles
-increased myoglobin content of muscles (store more O2)
-more mitochondria and enzymes

58
Q

What are the benefits of exercise?

A
  • body composition changes (increaed muscle, reduced adipose)
  • glucose tolerance improves (how well your cells take up glucose)
  • insulin sensitivity of tissues increases
  • blood triglycerides decrease (low LDL/LDL, high HDL)
  • lowers BP
  • psychological effects (well-being)

MEH (22 decks)

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