Carbohydrate Metabolism Flashcards

(67 cards)

1
Q

Why are carbohydrates the preferred fuel in high-intensity exercise?

A
  • More efficient than fat (uses less oxygen)
  • Main fuel source during high-intensity exercise
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2
Q

What limits the use of carbohydrates during exercise?

A

Limited muscle and liver glycogen stores

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3
Q

How do athletes manage carbohydrate availability?

A
  • Maximise glycogen stores by fuelling before and refuelling after exercise
  • Use exogenous carbs (like energy bars) during exercise
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4
Q

What happens to muscle glycogen at 30% VO₂max?

A
  • Mostly type I muscle fibres used
  • Glycogen depletion is slow, stores remain high in Type II fibres
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5
Q

How does muscle glycogen change at 60% VO₂max?

A
  • Both type I and type II fibres recruited
  • Glycogen use increases and plateaus as exercise continues
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6
Q

What occurs to muscle glycogen during 120% VO₂max (maximal effort)?

A
  • Heavy use of both type I and II fibres
  • Rapid glycogen depletion causes early exercise termination
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7
Q

How does a high-carb diet affect muscle glycogen and exercise duration + what’s this relationship?

A

Increases muscle glycogen stores + extends exercise performance time

  • Linear
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8
Q

What is glycogen supercompensation?

A

After low glycogen levels, a high-carb diet leads to greater glycogen uptake and storage

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9
Q

How does exercise intensity affect fuel source preference?

A

Higher intensity → more reliance on muscle glycogen and blood glucose

  • Less fat oxidation due to higher oxygen cost
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10
Q

Why is fat less efficient than carbohydrates as a fuel?

A

Requires more oxygen for oxidation (~5.5% more than carbs)

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11
Q

What are the three main monosaccharides?

A

Glucose, fructose, galactose

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12
Q

Which monosaccharide is commonly used in sports nutrition and which uses a different transport system?

A

Glucose is in most sports products

Fructose uses a different intestinal transport system

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13
Q

What are common disaccharides?

A

Maltose, sucrose, lactose

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14
Q

What is maltodextrin and why is it used?

A

Oligosaccharide (8–12 glucose units) with a high GI

  • Less sweet → more tolerable in sports nutrition
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15
Q

What are the two types of polysaccharides?

A

Amylopectin (starch) and amylose

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16
Q

Why does amylopectin have a higher glycaemic index than amylose?

A

Amylopectin has more branches → breaks down faster → higher GI

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17
Q

Where does glucose come from in the fasted state?

A

From liver glycogen breakdown → released into blood

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18
Q

What is the primary destination of glucose in the fasted state + where else does it go?

A

The brain, to support normal function

  • adipocytes
  • muscles
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19
Q

Which glucose transporters are active in the fasted state?

A

Liver & brain: GLUT-2

Muscle: GLUT-4

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20
Q

What happens to plasma glucose concentration in the fed state?

A

Increases from ~4–5.5 mmol/L to ~6–8 mmol/L

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21
Q

Why does plasma glucose conc increase in a fed state?

A

Now getting an influx of glucose from the small intestine as we have ingested food

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22
Q

How does insulin affect glucose uptake in the liver during the fed state?

A

Increases glucose uptake for storage

  • Reduces glycogen breakdown
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23
Q

How does insulin affect muscle glucose uptake?

A

Promotes translocation of GLUT-4 to cell membrane → increases glucose uptake

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24
Q

What effect does insulin have on adipocytes?

A

Increases glucose uptake into fat cells

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25
Where is insulin secreted from?
Pancreas
26
Is gastric emptying a limiting factor for carbohydrate use during exercise?
Rehrer et al. (1992) - found no difference in oxidation rates despite different gastric emptying speeds - Suggests gastric emptying is not the limiting factor
27
What are the two key transporters for glucose absorption in the intestine?
SGLT-1: transports glucose with sodium into intestinal cells GLUT-2: transports glucose from cells into bloodstream
28
What is the saturation limit of the SGLT-1 transporter?
Saturated at ~1.0–1.2 g/min - Limits glucose absorption to ~60 g/hour
29
How can athletes increase carbohydrate intake beyond 60 g/hour during exercise - what's the ratio?
Add fructose, which uses a different transporter - Old = 2:1 (glucose:fructose) - New = 1:0.8 (e.g. 60g glucose : 48g fructose)
30
Which transporter is responsible for fructose absorption into the intestine?
GLUT-5 moves fructose into the intestinal wall GLUT-2 transports it into the bloodstream
31
What limits exogenous carbohydrate oxidation during exercise?
Saturation of transport proteins, mainly SGLT-1 - remember its at 1-1.2 g/min
32
Why is using multiple transportable carbohydrates beneficial during exercise?
Allows use of both SGLT-1 (glucose) and GLUT-5 (fructose) - Increases total carbohydrate uptake without causing GI distress
33
How does glucose enter muscle cells from the bloodstream?
Via GLUT4 transporters
34
What happens to glucose after entering the muscle cell?
Rapidly phosphorylated by hexokinase into glucose-6-phosphate (G6P) - G6P then enters glycolysis or undergoes glycogenesis
35
What's the concentration of glucose like in a myocyte (muscle cell)
Very low because its phosphorylated rapidly
36
What triggers GLUT4 translocation to the muscle cell membrane?
Exercise and insulin both trigger GLUT4 movement towards cell wall to increase glucose uptake
37
Briefly outline how insulin initiates GLUT4 translocation
1. Insulin binds to receptor → activates IRS-1 (insulin receptor substrate -1) 2. IRS-1 activates PI3-kinase (by creating a docking protein for it) 3. PI3K activates PDK, which activates Akt 4. Akt causes GLUT4 to translocate to membrane
38
Which increases glucose uptake more—insulin or exercise?
Exercise increases uptake more due to much higher blood flow (but has low A-V difference) Insulin has a greater A–V difference, but lower blood flow - compensatory effect means that blood flow leads to greater increase in glucose uptake
39
Does muscle glucose uptake limit exogenous carbohydrate oxidation?
No — Hawley et al. (1994) - Infusion of glucose to 10 mmol/L increased oxidation rates
40
What is the possible + main limiting factor for exogenous carbohydrate oxidation?
- Gastric emptying DOES NOT limit - Muscle glucose uptake DOES NOT limit - Intestinal CHO absorption DOES limit
41
How can exogenous carbohydrate oxidation be assessed during exercise?
Using stable isotope tracers (e.g. ¹³C-labelled carbs) in a drink - ¹³C mixes with endogenous stores (mostly ¹²C), and CO₂ samples are analysed to determine usage
42
Why must athletes deplete carbohydrate stores before tracer studies?
To minimise endogenous ¹³C interference - Ensures all measured ¹³CO₂ comes from the drink, not stored glycogen or hidden ¹³C (e.g. from corn-based food)
43
What technique analyses expired air in tracer studies?
Gas Chromatography Isotope Ratio Mass Spectrometry (GC-IRMS) - Measures δ¹³C: the ratio of ¹³C to ¹²C, reported in parts per thousand - Reference: Pee Dee Belemnite (PDB) standard
44
What were the three test conditions in the stable isotope study of CHO intake?
1. Glucose at 1.2 g/min (rate-limiting) 2. Glucose at 1.8 g/min (above rate limit) 3. Glucose + fructose mix (1.2 g glucose + 0.6 g fructose = 1.8 g total)
45
What did the tracer study reveal about exogenous CHO oxidation?
Glucose alone: no increase above 1.2 g/min → saturation + rate-limiting step Glucose + fructose: higher exogenous oxidation, as both transport systems (SGLT-1 and GLUT-5) are used
46
What is glycogenesis and where does it occur?
The process of storing glucose as glycogen - Occurs in liver and muscle cells for future energy needs
47
What conditions are required for glycogenesis to occur?
- Glucose must be in the cell - Insulin must be elevated to promote uptake - Key enzyme: Glycogen synthase
48
What happens to liver and muscle glycogen after an overnight fast?
Liver glycogen slightly decreases Muscle glycogen remains relatively unchanged
49
Outline the key steps in glycogen elongation
1. Glucose → G6P (via hexokinase) 2. G6P → G1P (via phosphoglucomutase) 3. G1P + UTP → UDP-glucose (catalysed by UDP-glucose pryophosphorylase) 4. UDP-glucose added to other glucose molecules by glycogen synthase
50
Why is glycogen highly branched?
Can only be stored as branches of glucose polymers - More branches = more end points = faster breakdown - Enhances rapid access to stored glucose during exercise
51
How are branches formed in glycogen?
1. Glycogen synthase only forms straight bonds 2. SO a branching enzyme breaks an α-1,4 bond 3. Reattaches part of the chain to form an α-1,6 glycosidic bond 4. Branching starts after ≥11 glucose residues in a chain
52
Where does fructose metabolism occur and why?
In the liver, not muscle - Muscle lacks fructokinase, needed to convert fructose → fructose-1-phosphate
53
Outline the metabolic pathway of fructose in the liver
1. Fructokinase → fructose-1-phosphate 2. F1P→ dihydroxyacetone phosphate (DAP) + glyceraldehyde by aldolase enzyme 3. Used for gluconeogenesis, glycolysis, or converted to fatty acids
54
Why is fructose metabolism considered unregulated?
Fructose bypasses key regulatory steps (unlike glucose) - Leads to uncontrolled entry into pathways → ↑ FA production + triglyceride storage if consumed excessively - sport aspect = provides different way of getting carbs to muscles
55
What happens when glucose is co-ingested with fructose?
Fructose-derived F1P shifts glucokinase receptor protein's affinity towards F1P and away from G6P - This frees up glucose phosphorylation, enhancing liver glycogen storage
56
What are the approximate metabolic fates of fructose-derived triose phosphates?
50% → glucose (gluconeogenesis) 15–20% → glycogen 25% → pyruvate (oxidised / converted to lactate)
57
How does insulin regulate glycogen synthase?
1. Insulin activates Akt 2. Akt inactivates GSK-3 (glycogen synthase kinase-3), reducing phosphorylation 3. Result: ↑ glycogen synthase activity
58
How does adrenaline affect glycogen synthase and metabolism?
1. Activates PKA 2. PKA ↓ glycogen synthase (inhibits glycogenesis) 3. ↑ lipolysis and ↑ glycogenolysis
59
How quick is muscle glycogen storage post ingestion?
Very quickly - 4 hours post ingestion to maximally store glycogen - due to increase glycogen synthase activity by insulin
60
What is glycogenolysis?
The breakdown of glycogen into glucose - want to convert branched glycogen into a straight one
61
What are the end products of glycogen breakdown?
~90% → glucose-1-phosphate ~10% → free glucose
62
What enzyme initiates glycogen breakdown?
Glycogen phosphorylase cleaves α-1,4 bonds forming G1P
63
How is G1P used after it's formed?
Converted to G6P by phosphoglucomutase - G6P used in glycolysis (muscle) or glucose metabolism (liver)
64
What happens when only 4 glucose units remain at a branch point?
Breakdown stops - Glucan transferase moves 3 to the main chain - Debranching enzyme releases the last unit as free glucose
65
What is the purpose of glycogenolysis during intense exercise?
Provides rapid energy, especially in events like 800m run or 2000m rowing - Highly active in skeletal muscle
66
How does adrenaline stimulate glycogenolysis?
1. Adrenaline attached to receptor on cell membrane 2. Activates G-protein 3. Activates adenylate cyclase which converts ATP → cAMP 4. Activates PKA which activates phosphorylase kinase which activates glycogen phosphorylase 5. This converts glycogen to G1P
67
How fast can glycogenolysis occur + why?
Within 1 second - cAMP cascade is slow, but... - Ca²⁺ acts as allosteric activator of phosphorylase kinase → speeds process