Types of fat & function of fat
Simple
- Triglycerides (most abundant
- Has glycerol back bone & methyl group
Compound
- Phospholipids
- Lipoproteins
Derived lipids
- Made up of both simple and compounds
- Cholesterols
Saturated
- Single bond
- Solid at room temperature
Unsaturated
- Double bond ( H on same side)
- Liquid at room temperature
Trans fat
- Not essential
- Double bond (H on opposite side)
Function of fat
- Energy provision
- Fat oxidation in aerobic metabolism
Fat vs CHO
- Fat stores are very large compared to CHO stores
- Fat contains about 50x more energy than CHO
Fat consumption in western societies
- Important to identify the type of fat
- Saturated fat levels below 10% of total energy intake
Fat sources
- Adipose tissue
- Muscle - intramuscular triglycerides
How do we get ATP from fat?
Fat Oxidation
1. Lipolysis 2. Removal of FAs from adipose tissue 3. Transport of fat into the blood stream 4. Transport of FAs into the muscle 5. Transport of FAs into the mitochondria 6. Oxidation of FAs in beta-oxidation and TCA cycle
What happens before oxidation can occur
Mobilised - triglycerides are split into glycerol and fatty acids so that FAs can be transported
Oxidation - then transported into the mitochondria
What is lipolysis
- The breakdown of triglycerides to fatty acids and glycerol
- For each triglycerides there are 3 fatty acids
What is the hormone sensitive lipase and what other hormones affect it
Responsible for splitting triglycerides into fatty acids and glycerol
HSL
- Epinephrine: Activates HSL and stimulates breakdown of triglycerides
- Insulin: Down regulates HSL and slows triglyceride breakdown
What happens to the fatty acid after triglyceride has been broken down
- Rest
- Exercise
During rest
- 70% of of the fatty acids stay in the adipose tissue
- Undergo Reesterification - reform triglycerides
During Exercise - Increased lipolysis - Increased catecholamine- epinephrine - Increased fatty acid availability Transported into the blood to be used by other tissues
What happens to the glycerol
- Glycerol is released from lipolysis into the blood stream to the liver (gluconeogenesis)
- Gluconeogenic substrate to form new glucose
What happens to the fatty acids after lipolysis & explain fat oxidation
Fatty acids need to be removed and transported into the blood
- The removal of fatty acids from adipose tissue required the transporter protein albumin. Fatty acid transport from adipocyte is dependent on:
- The amount of albumin in the blood
The available binding sites on the albumin protein itself
- As well as blood flow to the adipose tissue - Transport of fatty acids into muscle cells
- Intramuscular triglycerides - Transport of fatty acids into the mitochondria
- Transported into the mitochondria by the compound carnitine and eventually ends up as fatty acyl CoA - Beta-oxidation
- Series of reactions resulting in Acetyl CoA - TCA cycle
- Series of reactions occurring in the mitochondria that result in energy provision - Electron transport chain
- A process involving the transfer of electrons that drives the synthesis of ATP
What are the limitations of fatty acids being used in the muscle cell.
- Lipolysis
- Removal of FAs from adipose tissue (requires enough blood flow)
- Transport of fat into the blood stream (need transporter protein to be at the cell membrane to help fatty acids into the muscle)
- Transport of FAs into the muscle
- Transport of FAs into the mitochondria (complex process)
- Oxidation of FAs in beta-oxidation and TCA cycle
Fat oxidation in exercise
- Fat and CHO oxidation
CHO and fat oxidized (broken down) as a mixture relative contribution of either substrate dictated by a number of factors:
- Exercise intensity
- Exercise duration
- Diet
- Aerobic fitness levels
- CHO intake prior to exercise
Substrate use
- Relative proportion of each substrate - CHO & fat
- Expired gas fractions of oxygen and CO2 along with air volume to indirectly determine VO2 and VCO2 and ultimately energy expenditure
- RQ = 0.7 (predominantly fat oxidation)
- RQ = 1.0 (predominantly CHO oxidation)
Exercise duration
- Fat oxidation increases as exercise duration increases due to the reduction in muscle glycogen
Fat oxidation and exercise intensity
- Maximal rate of fat oxidation
- High intensities
- Why do fat oxidation rate drop during high intensity exercise
- Low intensity exercise: Fat oxidation predominate fuel source
- From LOW to MODERATE intensity exercise fat oxidation levels increase
- Around 60% exercise intensity there is a gradual decrease in fat oxidation
- Around 75% exercise intensity there is a dramatic decrease in fat oxidation
Maximal rate of fat oxidation
- 65% VO2 max
High intensities
- Fat oxidation is inhibited and the contribution of fat is negligible
- Low fat oxidation BUT lipolysis rate are still high
Why do fat oxidation rate drop during high intensity?
- Reduction in blood flow to adipose tissue = Decreased removal of FA from adipose tissue
- Lactate accumulation which ↑ Reesterification rates
exercise
Low plasma fatty acids level during high intensity exercise
- Only partially explains the low fat oxidation rate
Endurance Training Adaptation
- fat oxidation and aerobic capacity during endurance training influences
- BENEFITS of improved FA use?
Fat oxidation and aerobic capacity
Endurance training influences
- Substrate availability
* Greater use of fat
\+ Sparing glycogen stores
* Greater contribution of fat to overall energy expenditure
- Exercise capacity Endurance training adaptations
- Increased mitochondria
- Increased capillary density
- Increased transporter ability
What are some of the BENEFITS of improved FA use?
- Exercise capacity increases
- Muscle glycogen sparing
- Blood glucose sparing
- When using fat, less lactate produced
CHO and fat oxidation
- CHO 1 hr prior to exercise
Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise
CHO 1 hr prior to exercise - Increases insulin - reduction of fatty acid availabiliy (reduces lipolysis) - 30% less fat oxidation when compared to no CHO feeding
- Reduced lipolysis
- Reduced plasma fatty acid availability
- inhibitory effect on carnitine dependent fatty acid transport into mitochondria
Fat intake
- Fasting
- Short term high-fat diet
- Long term high-fat diet
Fasting
- Increases availability of lipids = increased oxidation
- Liver and muscle glycogen stores suffer - reduced performance and fatigue resistance
Short term high-fat diet
- 3-5 days
Increased availability of lipids - Reduced glycogen stores - reduced performance and fatigue resistance
Long term high-fat diet
- Increased fat oxidation?
- Don’t have enough evidence
- Effect on performance?
- Unclear
Fat intake recommendations
- Performance & Health
- Requires an accurate dietary assessment!!!
- 20 to 35% of energy intake
- <10% of exergy from saturated fats
- Remaining from mono-and polyunsaturated - Modify & tailor to individual
- Health risk profiles
- Blood lipid profiles
- Hypertension
