MEH > Lecture 20 > Flashcards

Lecture 20 Flashcards

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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?

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A

Maternal insulin
Oestrogens
Progesterone
Placental lactogen

25
What is the role of insulin in pregnancy?
Maternal concentration increases as pregnancy proceeds to promote storage and uptake of nutrients (as fat in adipose tissue)
26
What are the effects of foetal-placental hormones?
Anti-insulin. Oppose the actions of insulin
27
What are some examples of hormones of the placental origin?
- human placental lactogen - progesterone - corticotropin releasing hormone
28
What are the metabolic changes during the first half of pregnancy?
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
What are the metabolic changes during the second half of pregnancy?
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
What happens to maternal ketogenesis during pregnancy?
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
What is gestational diabetes?
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
How does the mother meet increased demand for insulin?
Pancreatic beta cell hyperplasia and hypertrophy | Rate of insulin synthesis in beta cells increases
33
What does the metabolic response to exercise ensure?
- 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
What does the magnitude/nature of metabolic response to exercise depend on?
- 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
Which muscles do the energy requirements of exercise usually effect?
Skeletal and cardiac muscles rather than respiratory muscles
36
How does the BMR change during exercise?
Resting: 4 kJ/min of energy Marathon: 80 kJ/min of energy 100m sprint: 200 kJ/min of energy
37
Where does the energy for muscle contraction come from?
Hydrolysis of ATP
38
Rate of ATP turnover:
Rest: 0.06 mmol/sec/kg Marathon: 1.2 mmol/sec/kg Sprint: 3 mmol/sec/kg
39
What is the ATP concentration in muscle?
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
How is ATP initially regenerated?
From creatine phosphate | Creatine phosphate + ADP = ATP + creatine
41
What are the major fuel molecules?
Stores: glycogen (300g in muscle, 100g in liver), and triacylglycerols Circulating fuel molecules: glucose and free fatty acids
42
How long do glycogen stores last?
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
What is the glycogen store of the liver for?
Prevent hypoglycaemia and associated impairment of CNS function -could provide muscle with enough glucose for 18 mins of low intensity exercise
44
What are the advantages of using glycogen rather than circulating glucose?
- 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
What limits anaerobic metabolism of glucose in muscle?
Build up of lactate and H+ | -H+ build exceeds buffering capacity of muscle cells and impairs their function producing fatigue
46
How does H+ impair muscle function?
- inhibition of glycolysis - interferes with actin/myosin interaction - causes sarcoplasmic reticulum to bind Ca2+ (inhibits contraction)
47
What factors limit the use of fatty acids by muscle?
- 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
How much glucose/free fatty acids are in the extracellular fluid?
12g glucose (180 kJ) 4g fatty acids (100 kJ) Enough energy for 4 mins of marathon runnning
49
What are the metabolic responses to short duration high intensity exercise?
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
What are the metabolic responses to medium duration intensity exercise?
- 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
What is the metabolic response to marathon running?
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
Which fuel molecules are used in the marathon?
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
When is eating carobohydrates to increase glycogen stores most effective?
After exercise, as exercise promotes storage of glucosen as muscle glycogen rather than conversion to lipid
54
What controls the metabolic reponses during a marathon?
-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
What are the biochemical causes of fatigue?
- depletion of muscle glycogen - accumulation of H+ in muscle - dehydration
56
What is a whole body response to prolonged exercise?
- 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
What is a whole body response to training?
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
What are the benefits of exercise?
- 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
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