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NME Emma copy and edit > Energy, Metabolism and Exercise > Flashcards

Energy, Metabolism and Exercise Flashcards

1
Q

In patients who have been in a starved or malnourished state, but then starts refeeding, the risk of refeeding syndrome is increased. What key energy molecule is important in refeeding syndrome?

A
  • glucose
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2
Q

In patients who have been in a starved or malnourished state, but then starts refeeding, the risk of refeeding syndrome is increased. What key vitamin is important in refeeding syndrome?

A
  • thiamine, also referred to as vitamine B1
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3
Q

In patients who have been in a starved or malnourished state, but then starts refeeding, the risk of refeeding syndrome is increased. What key electrolytes are important in refeeding syndrome?

A
  • K+
  • Na+
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4
Q

In patients who have been in a starved or malnourished state, but then starts refeeding, the risk of refeeding syndrome is increased. What key mineral is important in refeeding syndrome?

A

Mg+

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5
Q

In patients who have been in a starved or malnourished state, but then starts refeeding, phosphate is important. What syndrome is this important in?

A
  • refeeding syndrome
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6
Q

In refeeding syndrome insulin binds with cells and glucose enters the cell. This can cause phosphate and K+ to flood into the cell causing what?

A
  • hypokalaemia
  • hypophosphatemia
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7
Q

In refeeding syndrome patients can experience high levels of oedema, what drives this?

A
  • Na+ is pumped out of cells
  • H2O follows the Na+
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8
Q

In refeeding syndrome patients can have low phosphate, K+, Mg+ and thiamine (B1) can do what to the heart?

A
  • arrythmias
  • heart failure
  • cardiac arrest
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9
Q

In refeeding syndrome patients can have low phosphate, K+, Mg+ and thiamine (B1) can do what to the lungs?

A
  • respiratory failure due to oedema
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10
Q

In refeeding syndrome patients can have low phosphate, what can this do to the neuromuscular system?

A
  • weakness
  • seizures
  • coma
  • confusion
  • rhabdomyolysis
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11
Q

In refeeding syndrome patients can have low K+, what can this do to the neuromuscular system?

A
  • paralysis (loss of muscle function)
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12
Q

In refeeding syndrome patients can have low Mg+, what can this do to the neuromuscular system?

A
  • ataxia
  • tremors
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13
Q

In refeeding syndrome patients can have low thiamine, what can this do to the neuromuscular system?

A
  • Wernicke-Korsakoff syndrome
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14
Q

The rise of what hormone is responsible for Refeeding Syndrome in patients who start eating having been in the starved state?

A
  • insulin
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15
Q

Which of the following electrolytes and vitamin abnormalities are not seen in Refeeding Syndrome?

1) Hypokalaemia
2) Hypophosphataemia
3) Hypomagnesaemia
4) Low thiamine
5) Hyperphosphataemia

A
  • hyperphosphataemia
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16
Q

In the absorbative phase what happens to glucose once it is absorbed in the liver?

A
  • stored as glycogen
  • stored as triglycerides and amino acids
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17
Q

In the psot-absorbative phase how do we get our energy from the liver?

A
  • Glycogenolysis = break down of glycogen to glucose
  • Gluconeogenesis = breakdown triglycerides and amino to glucose
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18
Q

In the absorbative and post absorbative phase what happens to glucose once it is absorbed by non liver cells?

A
  • absorbative phase = stored as glycogen
  • post absorbative phase = glycogen turned to glucose for energy
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19
Q

In the absorbative and post absorbative phase what happens to fat once it is absorbed by non liver cells?

A
  • absorbative phase = stored as triglycerides
  • post absorbative phase = glycerol and fatty acids provide energy
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20
Q

In the absorbative and post absorbative phase what happens to protein once it is absorbed by non liver cells?

A
  • absorbative phase = stored as proteins
  • post absorbative phase = proteins turned to amino acids for energy
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21
Q

In the absorbative and post absorbative phase what are our many fules for energy?

A
  • absorbative = glucose
  • post absorbative phase = triglycerides
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22
Q

Human metabolism oscillates between the fed and fasting states. A ratio between which 2 hormones in the blood determines the metabolic switch between glucose and triglyceride metabolism in the fed and fasted states?

A
  • molar ratio of insulin to glucagon in the blood
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23
Q

In the fed and fasted state (6-12 hours post meal) what are the insulin and glucagon levels?

A
  • fed = HIGH insulin / LOW glucagon ratio
  • fasted = LOW insulin / HIGH glucagon ratio
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24
Q

What is the definition of the fasted state?

A
  • 6-12 hours post meal
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25
Q

Following food intake insulin release is stimulated from beta cells of the pancreas, which in turn inhibits glucagon (which normally is slowly secreted). What is the normal ratio of insulin to glucagon in the fed state?

A
  • high insulin to glucagon ratio of 4 : 1
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26
Q

Following food intake insulin release is stimulated from beta cells of the pancreas, which in turn inhibits glucagon (which normally is slowly secreted). There is a high insuline:glucagon ratio of 4:1. This affects metabolims in what 3 tissues, and 1 tissue that remains unaffected?

A
  • affected = liver, adipose tissue and muscle
  • unaffected = brain
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27
Q

Once glucose has been absorbed by the liver in the fed state, what are the 3 main things that could happen to it?

A

1 - stored as glycogen

2 - enter glycolysis and produce energy

3 - enter glycolysis and produce fatty acids

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28
Q

Once glucose has been absorbed by the liver in the fed state, it can be stored as glycogen, enter glycolysis and produce energy or enter glycolysis and produce fatty acids. What happens to the fatty acids produced here?

A
  • undergo lipogenesis
  • fatty acid and triglyceride synthesis from glucose or other substrates
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29
Q

Once glucose has been absorbed by the liver in the fed state, it can be stored as glycogen, enter glycolysis and produce energy or enter glycolysis and produce fatty acids. Fatty acids then undergo lipogenesis, where fatty acid and triglyceride area synthesised from glucose or other substrates. Some triglycerides can be stored in the liver, but those that leave the liver, leave using what?

A
  • very low density lipoproteins
  • travel around body for energy or to be stored as adipose tissue
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30
Q

Once glycerol from triglycerides has been absorbed by the liver in the fed state, what happens to it?

A
  • imported into lipogenesis
  • used to make triglycerides
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31
Q

Once amino acids from triglycerides have been absorbed by the liver in the fed state, what happens to them?

A
  • can enter the citric acid cycle and used to make energy
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32
Q

In the fed state blood glucose levels rise and are absorbed by skeletal muscle. Which GLUT transporter facilitates glucose uptake by skeletal muscle?

A
  • GLUT-4
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33
Q

In the fed state blood glucose levels rise and are absorbed by skeletal muscle via the GLUT-4 receptors. What are the 2 things that can happen to glucose uptake by skeletal muscle?

A

1 - stored as muscle glycogen

2 - glycolysis and produce energy

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34
Q

In the fed state blood fatty acid levels rise and are absorbed by skeletal muscle. Whis is the 2 ways in which fatty acids can be absorbed?

A
  • in the diet via chylomicrons
  • via VLDL from the liver
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35
Q

In the fed state blood fatty acid levels rise and are absorbed by skeletal muscle. Fatty acids can be absorbed via the diet in chylomicrons and through VLDL from the liver. What then happens to the fatty acids once they enter the skeletal muscle cells?

A
  • oxidised via β-oxidation (produce energy)
  • acetyl CoA is produced that can enter the citric acid cycle and produce energy
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36
Q

In the fed state blood amino acid levels rise and are absorbed by skeletal muscle. What 2 things then happens to the amino acids once they enter the skeletal muscle cells?

A

1 - reformed into proteins for muscle growth and repair

2 - turned into acetyl CoA and enter citric acid cycle for energy

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37
Q

In the fed state blood glucose levels rise and are absorbed by adipose tissue via GLUT-4 receptors. What 2 things then happens to the glucose once they enter the adipose cells?

A

1 - enter glycolysis creating acetyl CoA that can then be used in lipogenesis to form triglycerides

2 - transformed into glucose-3-phosphate and can be used to form triglycerides

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38
Q

In the fed state blood fatty acid levels rise and are absorbed by adipose tissue. Whis is the 2 ways in which fatty acids can be absorbed?

A
  • in the diet via chylomicrons
  • via VLDL from the liver
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39
Q

If glycerol is released from skeletal muscle and adipose tissue, where will it then travel to?

A
  • liver
  • used in gluconeogenesis
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40
Q

In the fed state blood glucose levels rise and are absorbed by the brain. What 2 GLUT receptors are involved in glucose absorption in the brain?

A
  • GLUT-1
  • GLUT-3
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41
Q

In the fed state blood glucose levels rise and are absorbed by the brain via GLUT-1 and 3 receptors. What then happens to the glucose that has been absorbed by the brain?

A
  • enters glycolysis for energy only
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42
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is reduced from beta cells, and glucagon secretion from alpha cells of the pancreas is increased. What is the normal ratio of insulin to glucagon in the fasted state?

A
  • liver switches from a glucose-utilizing to a glucose-producing organ
  • low insulin to glucagon ration (ratio = 0.8 : 1)
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43
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is released from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). What does this do to glycogen synthesis, glycogenolysis (breakdown of glycogen for energy) and gluconeogenesis?

A
  • glycogen synthesis = reduced
  • glycogenolysis = increased
  • gluconeogenesis = initiated
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44
Q

Only when glycogen stored drop below what % does gluconeogenesis get turned on?

A
  • 20%
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45
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). GLUT-2 glucose receptors on liver have a low affinity of glucose and the liver no longer absorbs glucose but rather becomes what?

A
  • producer of glucose
  • exporter of glucose
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46
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). GLUT-2 glucose receptors on liver have a low affinity of glucose and the liver no longer absorbs glucose and becomes and exporter of glucose. What 2 things are turned on in the liver cells only?

A

1 - glycogenolysis

2 - gluconeogenesis

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47
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). What happens to protein in the liver?

A
  • broken down to amino acids to fuel gluconeogenesis
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48
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). What happens to triglycerides in the liver?

A
  • triglycerides undergo lipolysis
  • fatty acids from lipolysis used to produce energy via b-oxidation
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49
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). What happens in adipose tissue to glucose?

A
  • reduced glucose taken up by GLUT-4 receptors
  • glycolysis is severely reduced
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50
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). What happens in adipose tissue to triglycerides?

A
  • neuroadrenalin stimulates B3 receptors on adipose tissue
  • triglycerides broken down into fatty acids and glycerol
  • fatty acids used as energy
  • glycerol sent to liver for gluconeogenesis
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51
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). In skeletal muscle the energy switches from glucose to what?

A
  • B oxidation is switched on
  • fatty acids are used as energy
  • glycolysis is inhibited
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52
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). In skeletal muscle what happens to proteins?

A
  • broken down to amino acids
  • carbon skeletons can be used for energy or exported to the liver in the form of alanine
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53
Q

In the fasting (post absorpative state), which is normally 6-12 hours following a meal, insulin secretion is release is decreased from beta cells, and glucagon secretion from alpha cells of the pancreas is increased, leaving a low insulin/high glucose ratio (0.8:1.0). Does this affect the brain?

A
  • no
  • GLUT-1 and 3 unaffected as have high glucose affinity
  • brain cannot swithc to fatty acid for energy as they cannot pass the blood brain barrier
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54
Q

If we do not eat for over 12 hours this is classed as the starved state. What happens to the insulin and glucagon ratio here?

A
  • chronic LOW insulin:HIGH glucagon
  • 0.4:1 ratio
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55
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). What happens to thyroid hormones and why is this important?

A
  • thyroid hormones are decreased
  • causes a decreases in metabolic rate
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56
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). Thyroid hormones are decreased, which subsequently reduces metabolic rate. What becomes the primary energy source and what is produced?

A
  • fatty acids are energy source
  • ketones are produced
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57
Q

What are ketones?

A
  • carbon containg molecules
58
Q

Where can ketones be produced and by what?

A
  • in liver mitochondria
  • made by acetyl CoA
59
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). Are there any glycogen stores in the liver after 24 hours of fasting?

A
  • no
60
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). After 24 hours there are no glycogen stores in the liver, so what does the liver depend on to maintain plasma glucose?

A
  • gluconeogenesis
  • lactate, glycerol, alanine and from fat / protein breakdown
61
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). After 24 hours there are no glycogen stores in the liver so the liver bcomes dependent on gluconeogenesis to maintain plasma glucose. What other organ becomes an important site of gluconeogenesis?

A
  • kidneys
62
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). After 24 hours there are no glycogen stores in the liver so the liver bcomes dependent on gluconeogenesis to maintain plasma glucose. Amino acids contribute to this, but can become toxic to the liver in high doses. What does the liver synthesise to remove the amino acids from the liver?

A
  • urea
  • excreted through urine
63
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). After 24 hours there are no glycogen stores in the liver so the liver bcomes dependent on gluconeogenesis to maintain plasma glucose. What happens to glycolysis and glycogen synthesis during starvation?

A
  • both are inhibited
64
Q

If we do not eat for over 12 hours this is classed as the starved state. There will be chronically LOW insulin:HIGH glucagon ratio (0.4:1). After 24 hours there are no glycogen stores in the liver so the liver bcomes dependent on gluconeogenesis to maintain plasma glucose. Oxaloacetate is a substrate for gluconeogensis, meaning acetyl CoA cannot be converted into citrate and enter the citric acid cycle. What does that then leave an abundance of in the liver and whatis this converted into?

A
  • acetyl CoA is abundant in the liver during fasted state
  • converted into ketone bodies
65
Q

What are the 2 ketone bodies that are generally used by all tissues for energy?

A

1 - acetoacetate

2 - β-hydroxybutyrate

66
Q

The liver is able to make the 3 key ketones in the body during the fasted state. The 2 ketone bodies that are generally used by all tissues for energy are acetoacetate and β-hydroxybutyrate, but which organ cannot use these as an energy source?

A
  • liver
67
Q

Once ketones have been absorbed by cells and used for energy, what do they become, and what is the fate of this molecule?

A
  • turned back into acetyl CoA
  • then enter the cirtric acid cycle for energy
68
Q

In adipose tissue in the starved state (>12 hours) does glucose enter the adipose tissue through the GLUT-4 receptors?

A
  • very little as insulin is low
69
Q

In adipose tissue in the starved state (>12 hours) glucose entry into adipose tissue through the GLUT-4 receptors is low as insulin levels are low. What does adipose tissue switch to in this instance?

A
  • lipolysis (breakdown of triglycerides)
  • fatty acids used for energy and released into plasma where fatty acid plasma levels can increase 10 fold
  • glycerol leaves adipose tissue and is used in the liver for gluconeogenesis
70
Q

Lipolysis is the breakdown of triglycerides into glycerol and fatty acids. Can fatty acids be used as energy by all tissues?

A
  • no
  • cannot cross the blood brain barrier, so not in the brain
71
Q

In skeletal muscle in the starved state (>12 hours) does glucose enter the skeletal muscle through the GLUT-4 receptors?

A
  • very low levels as insulin is so low
72
Q

In skeletal muscle in the starved state (>12 hours) what is the primary and secondary energy source for muscle contraction?

A
  • primary = fatty acids from lipolysis
  • secondary = ketones
73
Q

In skeletal muscle in the starved state (>12 hours) what happens to proteins?

A
  • proteolysis (breakdown of protein)
  • stimulated by noradrenaline and cortisol
  • carbon skeletons used for for net glucose synthesis in the form of alanine
  • alanine then returns to the liver for gluconeogensis
74
Q

In skeletal muscle in the starved state (>12 hours) protein is degraded for energy in a process called proteolysis. What limits the degree of proteolysis and therefore muscle wasting?

A
  • ketones
75
Q

In the brain during the starved state (>12 hours) GLUT-1 and 3 continue to take up glucose due to their high affinity, which can then enter glycolysis. But what else can contribute to energy for the brain in the starved state?

A
  • ketones
76
Q

What should always be the primary route of nutrients?

A
  • orally
77
Q

Enteral feeding refers to intake of food via the gastrointestinal GIT. What is a Ryles tube?

A
  • an example of nasogastric feeding tube
  • a tube is fed through the nose and into the stomach
  • ryles tubes can drain and feed
78
Q

What are the 2 methods that can help determine if the nasogastric tube is located in the stomach?

A
  • X-ray to confirm location
  • aspirate contents and measure pH (_<_5.5)
79
Q

What is a nasojejunal feeding tube?

A
  • tube fed from nose to jejunem
80
Q

A nasojejunal feeding tube must pass through the stomach, the pyloric sphincter and into the duodenum. What 2 methods can be used tpo guide this?

A
  • X-ray
  • endoscopy
81
Q

Nasogastric and nasojejunal feeding tube are both examples of enteral feeding. What is the benefit of nasojejunal over nasogastric?

A
  • doesnt rely on function of stomach
  • gastritis or pancreatic mass impairing duodenum
82
Q

Nasogastric and nasojejunal feeding tube are both examples of enteral feeding. Are these fed continous or intermittently using syringes?

A
  • can be both
83
Q

What is Percutaneous endoscopic gastrostomy (PEG) feeding?

A
  • feeding tube placed through abdomen into the stomach
  • guided by endoscopy
84
Q

Percutaneous endoscopic gastrostomy (PEG) feeding is guided via endoscopy, what is the basic process of how PEGs are inserted?

A
  • endocsopy placed in stomach and needle placed through abdomen into stomach
  • endoscopy pulls wire from needle out through mouth
  • feeding tube is then fed back through mouth, stomach and out through abdominal wall
85
Q

If a PEG cannot be inserted because the patient has a head and neck cancer they may need treatment as there is an obstruction of the oesophagus. In this case a Radiologically Inserted Percutaneous Gastrostomy (RIG) feeding is used. What is this?

A
  • sergery is used to insert the tube in the abdomen
86
Q

What is parenatral feeding?

A
  • nutrients given intravenously
87
Q

Parenatral feeding involves delivery of nutrients intravenously. What is a peripheral and centrally inserted central catheter?

A
  • peripheral = a thin, flexible tube that is inserted into a vein in the upper arm and guided into a large vein
  • central = thin vein guided directly into a large vein
88
Q

Is enteral or parenatal feeding cheaper?

A
  • enteral
89
Q

Does enteral or parenatal feeding have a higher risk of liver damage?

A
  • parenatal feeding
90
Q

Are the bags for enteral or parenatal feeding easier to store (Some care homes won’t give PN)?

A
  • enteral
91
Q

Are Nasogastric and Nasojejunem bags or parental feeding used longer term?

A
  • parenatal
92
Q

Is there a higher risk of infection, sepsis and blood clots with enteral or parenatal feeding?

A
  • parenatal feeding
93
Q

Can enteral or parenatal feeding deliver nutrients quicker?

A
  • parenatal
94
Q

What does the SALT team stand for in hospitals?

A
  • Speech and Language Team (SALT)
95
Q

How much can ATP demand of contracting muscles increase during exercise?

A
  • 100 fold in milliseconds
96
Q

What is the main source of fuel for exercise in skeletal muscle?

A
  • glycogen
97
Q

As well as providing energy for skeletal muscle, ATP also supplies anergy for ATPase. Why is this important?

A
  • provides immediate source of energy for action and myosin binding
98
Q

At rest how much ATP does skeletal muscle have as dry weight?

A
  • approx 27 mmol of ATP per kg dry weight
99
Q

At rest skeletal muscle has approx 27 mmol of ATP per kg dry weight. Furing vigourous exeecise, how long would this last?

A
  • 4 seconds
100
Q

What are the 3 systems that can be used during and aerobic and anaerobic exercise?

A
  • anaerobic = ATP phospocreatine

lactic acid (anaerobic glycolysis

  • aerobic = electron transport chain
101
Q

What is creatine phosphate, also known as phosphocreatine?

A
  • first top up when ATP is low
  • product of substrate-level phosphorylation
  • ADP + creatine phosphate = ATP + creatine
  • following contraction ADP is recylced
102
Q

How long can creatine phosphate, also known as phosphocreatine last for?

A
  • may be enough for a 100-200 metre sprint
  • around 16 seconds
103
Q

Glucose-1-phosphate is the first step of glycolysis. What are the 2 enzymes that can be involved at this step and what do they do?

A
  • phosphorylase = breaks down glycogen
  • glycogen synthase = makes glycogen
104
Q

The full glycolytic pathway and oxidative phosphorylation require oxygen to function optimally. What happens to blood flow durin exercise?

A
  • local mediators and β-adrenergic stimulation of vascular smooth muscles
  • increased blood flow to working muscles
  • ensures oxygen is present in muscles for Glycogenolysis (break down of glycogen)
105
Q

The full glycolytic pathway and oxidative phosphorylation require oxygen to function optimally. During exercise local mediators and β-adrenergic stimulation of vascular smooth muscles and increase blood flow to working muscles. This ensures oxygen is present in muscles for Glycogenolysis (break down of glycogen). However, ensuring a continous supply of O2 is dependent on what?

A
  • type and duraiton of exercise
106
Q

During exercise what is able to allosterically bind with phosporylase and initiate glycogen breakdown?

A
  • AMP
  • it is a marker of low ATP
107
Q

During exercise AMP, a marker of low ATP is able to allosterically bind with phosporylase and initiate glycogen breakdown. What else can activate phosporylase?

A
  • increased Ca2+ in contracting muscle
  • cortisol, neuradrenalin
108
Q

During exercise AMP, a marker of low ATP is able to allosterically bind with phosporylase and initiate glycogen breakdown. In addition increased Ca2+ in contracting muscle and stress hormones such as cortisol and neuradrenalin can activate phosporylase. But what do all of these do to glycogen synthase?

A
  • inhibit glycogen synthase
109
Q

Glucose-6-phosphate is able to activate glycogen synthase and encourage the synthesis of glycogen. During exercise is glucose-6-phosphate high or low?

A
  • low during exercise
  • glycogen synthase is inhibited
110
Q

Phosphofructokinase 1 (PFK-1) is an important enzyme in glycolysis, responsible for converting fructose-6-phosphate into fructose 1,6 biphosphate. During exercise if AMP is high, what is this able to do?

A
  • AMP (marker of low glycogen) allosterically binds to PFK-1
  • PFK-1 activity is increased
111
Q

Glycolysis generates 2 ATP and 2 NADH, and although the ATP can be used for energy, the NADH cannot enter the electron transport chain. What does lactate dehydrogenase do to pyruvate and the 2 NADH during intense exericse?

A
  • creates 2 molecules of lactate
  • leaving 2 NAD+
112
Q

Glycolysis generates 2 ATP and 2 NADH, and although the ATP can be used for energy, the NADH cannot enter the electron transport chain. Lactate dehydrogenase is able to take 1 NADH and add it to the 3 carbon pyruvate creating lactate 2 times, giving 2 lactate. Why does this cause pain in the muscles if lactate continues to build up?

A
  • lowers pH and burns
113
Q

Glycolysis generates 2 ATP and 2 NADH, and although the ATP can be used for energy, the NADH cannot enter the electron transport chain. Lactate dehydrogenase is able to take 1 NADH and add it to the 3 carbon pyruvate creating lactate 2 times, giving 2 lactate. Lactate and NAD+ can then be recycled, but how does this occur?

A
  • lactate travel to the liver
  • lactate then goes through gluconeogenesis to create glucose
  • glucose can then be released into blood and taken up by GLUT-4 in skeletal muscle
  • this is called the Cori Cycle
114
Q

Although the liver can recylce lactate it requires a lot of energy to do this. How many ATPs are required?

A
  • 6 ATPs
115
Q

When we exercise anaerobically and there is a reduced blood flow to working muscles, is lactate able to be recyled by the liver?

A
  • no
  • it is trapped in muscle causing pain
116
Q

When we exercise adrenalin is released. How does this affect insulin and glucagon levels?

A
  • insulin decreases
  • glucagon increases promoting gluconeogenesis
117
Q

When we exercise adrenalin is released, which reduces insulin levels. Is this bad for skeletal muscle when it comes to glucose uptake?

A
  • no
  • GLUT-4 receptors are activated by muscle contractions
118
Q

When we exercise adrenalin is released, which reduces insulin levels. Skeletal muscle do not need insulin as muscle contraction stimuates GLUT-4 receptors increasing glucose uptake. Why is the reduction in insulin important for glucose production, especially in relation to the liver?

A
  • insulin inhibits gluconeogenesis
  • low insulin means more gluconeogenesis
119
Q

What is fatigue?

A
  • inability to maintain desired power output
120
Q

What causes fatigue?

A
  • rate of ATP utilization exceeds its rate of synthesis
  • accumulation of pyruvate and lactic acid in the contracting muscle result in a decline in force generated
  • decrease in muscle pH
  • glycolysis inhibited by H+ from lactic acid
121
Q

In addition to glycogen as an energy source during exercise, we can also use fatty acids. However, was is the main problem when using fatty acids for exercise?

A
  • dependent on O2 supply
  • fatty acids can only enter the citric acid cycle and ATC
  • no O2 means no ATP fro fatty acids
122
Q

At rest what is the main energy source for skeletal muscle?

A
  • fatty acids that can enter the citric acid cycle
  • glucose from the diet can provide energyy, but normally turned into glycogen
123
Q

For a short sprint, what are the 2 energy supplies?

A

1 - phosphocreatine

2 - anaerobic glycolysis (lactic acid)

124
Q

In a marathon, what are the 3 energy supplies, and roughly the proportions they contribute?

A

1 - oxidative phosphorylation = 70%

2 - fatty acids from adipose tissue = 20%

3 - glycogen in liver (glucose) = 10%

125
Q

During a sprint catecholamines (adrenaline/noradrenaline) are released for instant activity (fight/flight). What do catecholamines do for energy metabolism?

A
  • stimulate glycogen breakdown in muscle anaerobically to lactate
  • phosphocreatine is converted to creatine with the transfer of Pi to ADP to form ATP
126
Q

During a sprint catecholamines (adrenaline/noradrenaline) are released for instant activity (fight/flight). Catecholamines stimulate glycogen breakdown in muscle anaerobically to lactate and phosphocreatine is converted to creatine with the transfer of Pi to ADP to form ATP. What happens to blood flow and lactate levels during a 100m sprint though?

A
  • blood flow is reduced and lactic acid increases, impairing nerves and causing pain
  • lactic acid can eventually move to the liver and be used for gluconeogenesis to produce glucose
127
Q

During a middle distance event, what is the energy source in skeletal muscle?

A
  • aerobic oxidation of glycogen makes up 30% of the ATP
  • lactate can contribute up to 65% of ATP required
  • phosphocreatine to the ATP contributes 5%
128
Q

In the early phases of a marathon, what is the main energy source in skeletal muscle?

A
  • fatty acids
129
Q

10 minutes into the marathon progresses, what is the main energy source in skeletal muscle?

A
  • muscle glycogen and glucose from the liver provide ATP through glycolysis
130
Q

10 minutes into the marathon progresses, what does adrenalin and AMP stimulate?

A
  • glycogen breakdown
131
Q

10 minutes into the marathon progresses, in addition to stimulating glycogenolysis, what else is adrenalin able to stimulate?

A
  • fatty acids mobilisation from adipose tissue
  • helps liver maintain blood glucose
132
Q

A marathon requires around 700g of glycogen, but muscle and liver combined contain only 500g. After 2 hours into the marathon, glycogen levels are almost entirely depleted. What happens to blood glucose levels and what does this do?

A
  • blood glucose falls significantly
  • 90% of liver glycogen used
  • insulin levels fall and glucagon secretion is increased
133
Q

A marathon requires around 700g of glycogen, but muscle and liver combined contain only 500g. After 2 hours into the marathon, glycogen levels are almost entirely depleted. As blood glucose falls, glycogen stores drop below 90%, insulin levels fall and glucagon is increased. What becomes the main energy supply?

A
  • fatty acids
  • only sufficient ATP for 50% for maximum power output and pace falls off as glycogen depleted – known as ‘hitting the wall’.
  • ketone bodies may also be used by muscle
134
Q

2 hours into the marathon, glycogen levels are almost entirely depleted. As blood glucose falls, glycogen stores drop below 90%, insulin levels fall and glucagon is increased. Fatty acids becomes the main energy source of energy, supported by ketones. What else will the liver do in an attempt to maintain blood glucose levels?

A
  • maintain gluconeogenesis through lactate, glycerol and muscle amino acids
135
Q

At the end of the marathon what could happen to the patient, relating to blood glucose levels that is common in patients with diabetes?

A
  • hypoglycaemia
  • symptoms include confusion, lack of cognitive function, lactic acidosis and exhaustion may occur
136
Q

Substrate level phosphorylation (SLP) SLP is where ATP is generated through the transfer of phosphate from a donor molecule to ADP, providing us with ATP. In the ATP-Phosphocreatine (PC) pathway what is the substrate in this?

A
  • phosphatase removes phosphate from PC
  • phosphate added to ADP leaving just creatine
137
Q

Substrate level phosphorylation (SLP) SLP is where ATP is generated through the transfer of phosphate from a donor molecule to ADP, providing us with ATP. In the ATP-Phosphocreatine (PC) pathway phosphatase removes phosphate from PC and adds it to ADP leaving just creatine. How many molecules of ATP can be generated from one phosphocreatine?

A
  • 1 phosphocreatine = 1 ATP
138
Q
A
139
Q

What does a low insulin to glucagon mean? e.g. 0.8

A

fasting state/post absorbative

  • Reduced insulin: glucagon ratio activates glycogenolysis and gluconeogenesis (from lactate, alanine, glycerol) via cAMP production in response to glucagon
  • The reduced insulin:glucagon ratio also inhibits glycogen, fat synthesis and liver glycolysis
140
Q

What does an increase in the insulin to glucagon ratio indicate?

A
  • FED/ABSORPTIVE STATE: High concentrations of nutrients lead to an increase in the insulin:glucagon ratio
  • High blood glucose means it enters the liver and is converted to glycogen and TGs à secreted as VLDL. Some enters TCA cycle.
141
Q

What happens to brain glucose intake when insulin is not being secreted?

A

•Continues to take up glucose because of the high affinity of Glut1 and Glut3 transport system and independence from insulin

142
Q

What does a very low insulin to glucagon ratio mean? e.g. 0.4

A

the starved state, •No glucose enters liver → glycogen stores depleted within 24 hours

•Plasma glucose dependent on gluconeogenesis from lactate, glycerol & alanine from fat / protein breakdown. The kidney becomes an important source of gluconeogenesis

Ketone bodies will be produced

NME Emma copy and edit (61 decks)

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