Theme 3 How does the muscle cell regulate whether we predominantly use CHO or fat?
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Created by V B
over 8 years ago
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Close
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Created by V B
over 8 years ago
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How much is plasma FFA from adipose tissue or plasma glucose from the liver utilised as a fuel at these exercise intensities?
40% Vo2 max
55% Vo2 max
75% vo2 max
What happens to the contribution of fat sources as exercise duration increases?
Does the glucose fatty acid cycle regulate fuel selection during exercise?
What does the Randle cycle suggest?
Does the glucose FA cycle regulate fuel selection during high intensity exercise?
How can we assess this?
What was the effect of increasing the concentration of FAs in the blood in normal conditions?
What was the effect of increasing the concentration of FAs in the blood in experimental conditions?
What does increasing the concentration of FAs in the bloodstream do to the rate of glycogenolysis?
What do we expect this to be due to according to the Randle cycle?
What would increased AMP & ADP do to glycogen phosphorylase activity?
Does the glucose FA cycle regulate fuel selection during high intensity exercise?
Name the 5 key sites of lipid metabolism during exercise.
During exercise at 65% vo2max what happens to FFA concentration and for how long?
During exercise at 80% Vo2max what happens to FFA concentration for how long of exercise?
Is oxidation significantly higher at 65% or 80% of Vo2 max?
What happens if we artificially raise plasma FA levels?
Does lipolysis meet energy demands?
What are the three key enzymes/substrates for FA entry into the mitochondria?
How is CPT-1 regulated?
What does CPT-1 drive?
What does this reaction produce?
What happens to acyl-carnitine?
What is the expected reason that long chain fatty acid (LCFA) uptake into the mitochondria is reduced during high intensity exercise?
When this was tested, what was shown?
Is Malonyl CoA affected by pre-exercise muscle glycogen?
Why does acetyl-CoA increase?
What effect does this have?
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How can Acetyl CoA increase without decreasing exercise capacity?
What does this explain?
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What does reduced carnitine availability do?
What happens to carnitine levels when exercise intensity decreases?
What happens to carnitine levels when exercise intensity increases?
Can we increase muscle carnitine?
Why is the rate of lipid oxidation increased and CHO oxidation decreased during prolonged exercise?
What does PDH do?
How do we increase PDH?
What do these two studies suggest that reduced CHO oxidation is due to?
So how do we oxidise fat?
