L3.1 Lipid Metabolism Flashcards
How are fats broken down?
- Fats can only be oxidised aerobically
- Lipoprotein lipase → breaks down circulating trigly (<10% during exercise)
Relationship of exercise (not intensity) and durationon fat oxidation?
- After exercise → muscles able to clear trigly more (↑oxidation)
- ↑duration → ↑lipolysis > ↑FA uptake > FA oxidation
What is the relationship between usage of FA from adipose tissues and muscles?
- Reciprocal relationship between FA from adipose & FA from muscles
- ↑use of FA from adipose → ↓ use of FA from muscles
What are the 3 triglyceride lipases?
- 1) Adipose tissue triglyceride lipase (ATGL) – trigly to bigly
- 2) Hormone sensitive lipase (HSL) – bigly to monogly
- 3) Monoglyceride lipase (MGL) – monogly to gly & FA
- ATGL and HSL can be phosphorylated ∴ are the regulatory steps
How is adipose tissue lipolysis regulated?
- ATGL & HSL
- Β-adrenergic stimulation (↑Adrenaline → ↑HSL → ↑lipolysis)
- ↓ Insulin (during exercise)
- Adipose tissue blood flow (↓during exercise - ↓release of FA into bloodstream)
- FFA/Albumin ratio (albumin binds FA → transports hydrophobic FFA through hydrophilic membrane)
- Caffeine → ↑FA (Spares glycolysis)
How is muscle lipolysis regulated?
- ATGL & HSL(main)
- Β-adrenergic stimulation
- ERK (kinase responds to Ca2+) → simulates mobilisation of fats
- AMPK inhibits HSL activation (still ?)
- ↑Blood glucose → ↑oxidation of triglyceride
- Plasma FFA availability (↑availability → ↑lipolysis)
What are the determinants of muscle FA uptake?
- FA transporters
- [FA] (for conc gradient)
- Ability of muscles to oxidise FA
- Carnitine (helps FA across membrane) & CPT (combines carnitine & FA)
- Β-oxidative capacity in mito (HAD enz involved in 1st step oxidation of FA)
What are the methods of muscle FA uptake by transporters?
1) Simple diffusion
2) CD36 & FABP → enhances diffusion gradient, facilitates FA uptake
3) Long chain FA uptake via FATP
What is the effect of carnitine during exercise?
- ↑Acetylcarnitine, ↓carnitine (at high intensities)
- Carnitine combines with acetyl-CoA to form acetylcarnitine
- Prevents overwhelming the TCA cycle from high levels of glycolysis during high intensities
- Carnitine combines with acetyl-CoA to form acetylcarnitine
- *↑carnitine → ↑FA uptake → ↑ Fat burn
- ↑HAD in muscles → burn more fats, ↑fat oxidation
- ∴↓FA going into adipose tissue
Why does an increase in exercise intensity rely less on fats and more on CHO oxidation?
- ↑intensity → ↓fat, ↑CHO utilisation
- At high intensities → ↓FFA availability, ↑glycolytic flux which inhibits CPT activity and mitochondrial FA uptake
- Due to ↓Carnitine availability
- CHO oxidation → ↑power & require less O2 for ATP prod
- Med Chain FA oxidation does not change at high intensity (not limited by mitochondrial transport system)
What is the effect of training on lipid metabolism?
- ↑FA uptake & Fat oxidation (greater) – uses more muscle triglyceride
- Uses both blood & Muscle FA
- ↑Muscle CPT levels
- ↑FA transport