47543
Description
Flashcards by Mark Arsenal, updated more than 1 year ago
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Created by Mark Arsenal
over 11 years ago
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| Question | Answer |
| What effect does Malonyl-CoA have on Fatty Acid Oxidation? And what can causes a build up on Malonyl-CoA? | Malonyl-CoA inhibits CPT-1 which prevents Fatty Acid uptake into the cell. Malonyl-CoA is caused through the carboxyilation of Acetyl-CoA which builds up with Glucose Metabolism (Pyruvate-->Acetyl-CoA)- thus also explains why fat and glucose metabolism are reciprocal. Hyperinsulinaemia and Hyperglycemia also cause an increase in Malonyl CoA, thus decreasing Fatty Acid uptake. |
| Is Carnitine a limiting Factor in Fat Metabolism? | Yes. Carnitine is crucial in CPT1 fatty acid entry into the cell. Free Carnitine decreases with increase CHO metabolism, thus less Fatty acid oxidation. Additionally with high intensity exercise we form lactate which is acidic causing acidosis which has been found to drastically reduce CPT1 activity. |
| How can we increase Fatty Acid Availability? | We can increase Fatty Acid availability is increased by Heparin. Heparin breaks down TAG through expression of Lipoprotein Lipase. So with increased Heparin we increase TAG breakdown thus increasing Fatty Acid availability. |
| How do Fatty Acid's enter the cell? | The Transported CD36 brings Fatty Acids into the cell. AMPK causes the translocation to the cell membrane. Both Fatty Acid and CD36 increase with exercise thus we increase Fatty Acid Cell Uptake. |
| So now Fatty Acid is in the cell how is it broken down for energy? | CPT-1 brings the FA from the Cell's Cytoplasm into the Mitochondria for Beta Oxidation. CPT-1 is usually is normally inhibited, but AMPK removes this inhibition. Malonyl CoA causes this inhibition. Intense Exercise causes an increase in Malonyl CoA, thus suppresses CPT-1 which helps explain why CHO metabolism increases and fat metabolism decreases with increased intensity. |
| So what effects does increase FA availability have? | As expected, increased FA availability decreases CHO metabolism and increases Fat metabolism (Beta Oxidation). Beta Oxidation causes an accumulation of Acetyl CoA (Acyl-CoA--->Acetly CoA) which causes a decrease in the breakdown of Pyruvate to Acetyl CoA which in turn decreases the TCA cycle so the substrate Citrate accumulates which inhibits the enzyme PFK (in Glycolysis) thus Glycolysis is inhibited, which explains why CHO breakdown decreases. |
| What is Fat Max and at what workload is it at its max? | Fat Max is the zone of optimal fat burning which is at 55-65% Heart Rate Max |
| Describe the relationship of CHO and Fat Metabolism: | CHO and Fat metabolism are reciprocal, this means as intensity increases CHO metabolism increases and Fat metabolism decreases. The point whereby CHO and Fat contribution is equal is called the Cross-Over Point |
| How do we regulate Glycolysis (CHO metabolism)? | The energy charge of a cell regulates Glycolysis. A high AMP:ADP:ATP ratio (High levels of AMP) and a decreased pH (more acidic) activate the enzyme Phosphofructokinase which increases Glycogenolysis (CHO breakdown) Additionally Glycogenolysis requires Pi from ATP breakdown so as intensity (ATP breakdown) increases as does Glycogenolysis. |
| Why does CHO breakdown (glycogenolysis) increase with increased intensity? | As we increase intensity we breakdown ATP to AMP at a faster rate, additionally we increase levels of Adrenaline. Both activate Glycogen Phosphoryllase which causes Glycogenolysis. Furthermore AMPK (fuel sensor- increases as energy availibility decreases) increases GLUT4 translocation which thus increases Glucose uptake. |
| Why is Fat metabolism higher at moderate exercise but lower at higher intensity? | This is due to decreased Fatty Acid availability at higher intensities, this decreases Fatty Acid uptake into the cell for Beta Oxidation in the Mitochondria of the cell. |
| What determines Fatty Acid Availability? | Hormone Sensitive Lipase- HSL is stimulated by AMPK and increased Plasma Adrenaline. HSL draws Fatty Acid from Adipose Tissue into the blood. Worth noting that AMPK is stimulated by Exercise, but inhibited by Insulin (when Glucose is high). It is also dependent on Fatty Acid Concentration in blood which is directly affected by the level of blood flow to the adipose tissue. |
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