7 - Metabolic Regulation During Endurance Exercise

Flashcards by V B, updated more than 1 year ago
Created by V B over 5 years ago


Theme 3 How does the muscle cell regulate whether we predominantly use CHO or fat?

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Question Answer
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 40% - equally 55% - more muscle glycogen than plasma FFA's 75% mainly muscle glycogen, FFA contribution is smaller
What happens to the contribution of fat sources as exercise duration increases? Lipolysis increases leading to an increase in the contribution of fat sources
Does the glucose fatty acid cycle regulate fuel selection during exercise? What does the Randle cycle suggest? Increasing acetyl CoA from FA's leads to the inhibition of PDH Increasing citrate inhibits PFK which will inhibit glycolysis, this means glucose-1-phosphate increases but glucose-6-phosphate can not be produced
Does the glucose FA cycle regulate fuel selection during high intensity exercise? How can we assess this? Increase the concentration of FA's in the blood.
What was the effect of increasing the concentration of FAs in the blood in normal conditions? In normal conditions FA concentration stayed low.
What was the effect of increasing the concentration of FAs in the blood in experimental conditions? In experimental conditions FFA concentration increased after 20 minutes to double the control.
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? Decreases the rate by 45% The increase of aceltyl CoA & citrate. (however this isn't true)
What would increased AMP & ADP do to glycogen phosphorylase activity? Increased FFA availability reduced glycogen breakdowndue to reduced glycogen phosphorylase activity, via decreased ADP and AMP allosteric activation
Does the glucose FA cycle regulate fuel selection during high intensity exercise? No
Name the 5 key sites of lipid metabolism during exercise. 1) TAG lipolysis (adipose tissue) 2) FA uptake into the muscle 3) IMTG lipolysis 4) FA entry into the mitochondria 5) Beta-oxidation
During exercise at 65% vo2max what happens to FFA concentration and for how long? FFA concentration increases for 120m of exercise.
During exercise at 80% Vo2max what happens to FFA concentration for how long of exercise? FFA concentration was 2/3 fold less for 30 minutes of exercise
Is oxidation significantly higher at 65% or 80% of Vo2 max? 65%
What happens if we artificially raise plasma FA levels? Infusing FA increased concentration at 85% of Vo2max. Significantly more FFA were oxidised however, it is still low.
Does lipolysis meet energy demands? No Oxidation rates still aren't restored to that observed at 65% Vo2max.
What are the three key enzymes/substrates for FA entry into the mitochondria? 1) Carnitine 2) CPT-1 3) CPT-2
How is CPT-1 regulated? Malonyl CoA increases which inhibits CPT-1 The increase in Malonyl CoA is caused by eating food, this increases insulin which increases acetyl-CoA-carboxylate.
What does CPT-1 drive? What does this reaction produce? Carnitine & fatty acyl-CoA being combined Acyl-carnitine
What happens to acyl-carnitine? It is translocated into the mitochondria by CPT-2
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? We expect because malonyl CoA is increased which may drive a decrease in CPT-1 activity reducing the uptake rate. Across exercise intensities malonyl CoA remains constant.
Is Malonyl CoA affected by pre-exercise muscle glycogen? No - despite increased lipid oxidation.
Why does acetyl-CoA increase? What effect does this have? LEARN FOR EXAM The TCA cycle cant kep up so acetyl CoA is increased to assist. However this down regulates PDH-decreasing exercise capacity.
How can Acetyl CoA increase without decreasing exercise capacity? What does this explain? LEARN FOR EXAM If the acetyl CoA levels increase too much, they buffer by binding acetyl with carnitine generating acetyl-carnitine. This decreases carnitine so decreases CPT-1. Less fatty acids can then be transported into the mitochondria. This explains why lipolysis is used less during high intensity exercise.
What does reduced carnitine availability do? Reduced carnitine availability, due to high PDH flux, limits the capacity for LCFA uptake into the mitochondria during high intensity sub maximal exercise.
What happens to carnitine levels when exercise intensity decreases? What happens to carnitine levels when exercise intensity increases? There is lots of free carnitine to react with CPT-1 Free carnitine decreases
Can we increase muscle carnitine? Yes but we need high insulin levles. Is it pointless to take carnitine when you also need a very high CHO diet?
Why is the rate of lipid oxidation increased and CHO oxidation decreased during prolonged exercise? As exercise duration increases free plasma FA concentration increases resulting in the switch from CHO to lipid. PDH also decreases and PDK increases as duration increases.
What does PDH do? inhibits fat oxidation
How do we increase PDH? With PDh phosphatase.
What do these two studies suggest that reduced CHO oxidation is due to? Reduced substrate, decreased PDH activity and increased PDH kinase.
So how do we oxidise fat? Run/cycle long, at a moderate intensity, fasted and glycogen depleted.
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