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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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