Week 4 - Fat Metabolism Flashcards
What is the main fuel source during high intensity exercise?
Why?
CHO, not lipids. Specifically muscle glycogen.
You are working at 70/80%+ of VO2max.
Not enough oxygen can get into the body to metabolise the fat.
When are fats used for energy?
At lower intensities.
In rests/recovery between bouts.
Ultramarathons.
Fatty acids provide the energy and are found in adipose tissue/within muscle as triacylglycerols.
What is the anaerobic threshold?
When does it occur?
The switch from aerobic to anaerobic metabolism.
Around 60% VO2max.
How is insulin involved in fat oxidation?
Insulin inhibits fatty acid availability. When insulin is low the inhibition is removed.
Insulin is suppressed during exercise - fatty acid availability increases.
What is lipolysis?
The breakdown of triglycerides into glycerol and fatty acids.
Outline the process of lipolysis
How is it affected by training?
Triacylglycerol is broken down into diacylglycerol and a fatty acid by ATGL - adipose triglyceride lipase.
This process happens twice more via HSL - hormone sensitive lipase and MGL - monoglycerol lipase.
Training increases the activity of these enzymes.
How is lipolysis affected by diet?
The first 1-2 hours after eating, lipolysis won’t take place especially if the meal was high in carbohydrates because the body burns what is available to it.
How is RER calculated?
Describe the different values of RER.
VCO2/VO2.
RER reduces as fat metabolism increases.
Working harder produces more CO2 so RER increases as we are burning more CHOs.
Fasted state = fats burning RER = 0.7/0.8
Non-fasted fed state RER = 0.8/0.9 - increase in CHO metabolism
End of VO2 RER = 1.1/1.15
What is Fat max?
When does it occur?
The exercise intensity that elicits maximal fat oxidation.
Around 50-70% if VO2max - similar to anaerobic threshold.
It is usually around 0.5-0.6g/min.
How does fat oxidation change with endurance training?
The contribution of fat to endurance exercise increases.
This is mainly from muscle-derived fat sources (intra-muscular triglycerides and very-low density lipids).
The oxidation of fat in the blood does not change - no benefit of a high fat diet pre-competition.
Lowers reliance of CHO which spares muscle glycogen.
Fat oxidation with low-intensity endurance training.
Lipid synthesis goes down (ACC2 gene), lipid hydrolysis/breakdown increases (LPL). This promotes the breakdown stage - better catabolic state.
Training generally increases fat usage and decreases fat storage.
Exercise fasted or fed?
Breakfast before exercise increases glucose utilisation.
Exercise when fasted almost doubles fat oxidation.
Depends on goal.
One off session not performance setting.
What is the role of carnitine?
12 weeks supplementation can increase muscle carnitine through co-ingestion of CHO - an insulin response is needed to push carnitine into the muscle.
Prevents an increase in fat mass with overfeeding of 160g CHO per day - not necessarily a fat loss supplement.
Testing the fat concentration in muscles
Need a muscle biopsy to properly test - taken from the vastus lateralis (less major blood vessels in the thigh).
Biopsy ‘snap freezed’ in liquid nitrogen immediately to maintain gene expression.
Muscle is sliced using a cryostat to produce really thin layers of muscle.
Sample stained to show the fat droplets.
Oil Red O often used as the chosen stain (pink stain) but LipidTOX is better as greater spatial resolution - you can see the individual lipid droplets). Important as location influences insulin resistance. LipidTOX stains green.
How does location of fat droplets influence insulin resistance?
Intermyofibrillar - Within the muscle fibres - endurance adaptation - this is good. Around the mitochondria so can be oxidised.
Subsarcolemmal - around the muscle fibre - causes insulin resistance.
