Muscle contraction and ATP
- Actin + myosin interaction
- Filaments sliding across eachother
- Faster contraction, faster ATP usage
- Maintain ion gradients
Type I muscle
Red/slow
* contract slowly
* packed full of mito
* very vascular (good blood supply)
Type II muscle
White/fast
* contract rapidly
* fewer mito
* poor blood supply
* packed full of contractile filaments
ATP concentration minimum
5 mM
* < 3 mM cells die
Sprinting muscle cells use ATP at…
5 mM per second
Gentle exercise
↑ ATP synthase
Dissipate the proton gradient
↑ ETC
↑ availability of H/e- strippers
Fuel oxidation can ↑
* Uses fatty acids and glucose
Effects of low insulin and high glucagon
- Stim. of glycogen breakdown in liver (Glycogen → glucose → bloodstream)
- Stim. of fat break down in white adipose (Fat → fatty acids → bloodstream)
Glucose conservation
- use fatty acids instead
- pyruvate → lactate → liver→ back to glucose
Moderate exercise
- Fatty oxidation reach max
- Inhibition on glucose oxidation stops
- Deplete liver glycogen stores
Strenuous exercise
Muscle glycogen is now broken down
Why is glycogen important?
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
Creatine phosphate (CP)
Instant store of ATP
* < 5 sec supply (15 mM)
* CP + ADP → ATP + Creatine
Sprinting
Uses Type II muscle
* Muscle glycogen → G6P → Glycolysis → pyruvate → lactate
* Only 2 ATP
* Build up
ATP from glucose
Glucose in blood, glycogen in muscles
* Needs transporters
* Trapped as G6P
* Glycolysis → pyruvate
* PDH catalyses pyruvate → ac-CoA → Krebs
ATP from fatty acids
Diffuse into cells
* In cyto - get attached to CoA, can’t diffuse back
* Into mito (carnitine) - **beta-oxidation **
* Produce ac-CoA → Krebs
Effects of low insulin and high glucagon
- Stimulation of glycogen breakdown in liver (Glycogen → glucose → leaves liver to blood stream)
- Stimulation of fat breakdown in white adipose tissue (Fat → fatty acids → blood stream)
Glucose conservation and recycling
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
Gentle exercise
Initially glucose used
* FA takeover (from WAP)
* Glucose still goes into muscle (only goes as far as lactate → gluconeogenesis)
Moderate exercise
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
Strenuous exercise
Now limits on speed of oxidation of blood glucose
* Muscle glycogen is now broken down
* Endogenously store
Very strenuous exercise
Glycolysis very fast
* Very inefficient
* Now blood lactate levels ↑
Sprinting
Uses type IIb muscles
* poor blood supply
* full of contractile filaments, very few mito
* rapid consumption of ATP
* fuel from glycolysis - lots of lactate
Buying time until the body gets glycogenolysis going
Creatine phosphate (CP) = instant store of ATP
* But < 5s supply (15 mM)
* Creatine supplements boost CP levels
* CP+ ADP → ATP + creatine
