CATABOLIC PATHWAYS

Question 1

Muscle contraction and ATP

Answer 1

• Actin + myosin interaction
• Filaments sliding across eachother
• Faster contraction, faster ATP usage
• Maintain ion gradients

Question 2

Type I muscle

Answer 2

Red/slow
* contract slowly
* packed full of mito
* very vascular (good blood supply)

Question 3

Type II muscle

Answer 3

White/fast
* contract rapidly
* fewer mito
* poor blood supply
* packed full of contractile filaments

Question 4

ATP concentration minimum

Answer 4

5 mM
* < 3 mM cells die

Question 5

Sprinting muscle cells use ATP at…

Answer 5

5 mM per second

Question 6

Gentle exercise

Answer 6

↑ ATP synthase
Dissipate the proton gradient
↑ ETC
↑ availability of H/e- strippers
Fuel oxidation can ↑
* Uses fatty acids and glucose

Question 7

Effects of low insulin and high glucagon

Answer 7

• Stim. of glycogen breakdown in liver (Glycogen → glucose → bloodstream)
• Stim. of fat break down in white adipose (Fat → fatty acids → bloodstream)

Question 8

Glucose conservation

Answer 8

• use fatty acids instead
• pyruvate → lactate → liver→ back to glucose

Question 9

Moderate exercise

Answer 9

• Fatty oxidation reach max
• Inhibition on glucose oxidation stops
• Deplete liver glycogen stores

Question 10

Strenuous exercise

Answer 10

Muscle glycogen is now broken down

Question 11

Why is glycogen important?

Answer 11

When glycogen has run out, only FA oxidation can be used for ATP generation
* Power output ↓ when using only fatty acids
* “Hitting the wall”
* No glycogen ≠ sprinting

Question 12

Creatine phosphate (CP)

Answer 12

Instant store of ATP
* < 5 sec supply (15 mM)
* CP + ADP → ATP + Creatine

Question 13

Sprinting

Answer 13

Uses Type II muscle
* Muscle glycogen → G6P → Glycolysis → pyruvate → lactate
* Only 2 ATP
* Build up

Question 14

ATP from glucose

Answer 14

Glucose in blood, glycogen in muscles
* Needs transporters
* Trapped as G6P
* Glycolysis → pyruvate
* PDH catalyses pyruvate → ac-CoA → Krebs

Question 15

ATP from fatty acids

Answer 15

Diffuse into cells
* In cyto - get attached to CoA, can’t diffuse back
* Into mito (carnitine) - **beta-oxidation **
* Produce ac-CoA → Krebs

Question 16

Effects of low insulin and high glucagon

Answer 16

1. Stimulation of glycogen breakdown in liver (Glycogen → glucose → leaves liver to blood stream)
2. Stimulation of fat breakdown in white adipose tissue (Fat → fatty acids → blood stream)

Question 17

Glucose conservation and recycling

Answer 17

Glucose stores (glycogen) are limited
Fatty acids substitute for glucose as a fuel
* Fatty acids prevent glucose from being wastefully oxidised
* Pyruvate → lactate → return to liver → converted back to glucose

Question 18

Gentle exercise

Answer 18

Initially glucose used
* FA takeover (from WAP)
* Glucose still goes into muscle (only goes as far as lactate → gluconeogenesis)

Question 19

Moderate exercise

Answer 19

Rate of FA utilisation ↑ BUT enzymes that catalyse FA oxidation soon reach max capacity
* inhibition on glucose oxidation is removed
* ↓ glucose recycling, ↓ in liver glycogen stores
* AcCoA used faster than made from FA
* PDH NOT inhibited by build up of AcCoA

Question 20

Strenuous exercise

Answer 20

Now limits on speed of oxidation of blood glucose
* Muscle glycogen is now broken down
* Endogenously store

Question 21

Very strenuous exercise

Answer 21

Glycolysis very fast
* Very inefficient
* Now blood lactate levels ↑

Question 22

Sprinting

Answer 22

Uses type IIb muscles
* poor blood supply
* full of contractile filaments, very few mito
* rapid consumption of ATP
* fuel from glycolysis - lots of lactate

Question 23

Buying time until the body gets glycogenolysis going

Answer 23

Creatine phosphate (CP) = instant store of ATP
* But < 5s supply (15 mM)
* Creatine supplements boost CP levels
* CP+ ADP → ATP + creatine