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Fat and CHO Oxidation During Exercise

Czean Holgado LIFE2097 - Muscle Physiology, Nutrition and Metabolism Year 2 English 10 cards

Cards in this deck (10)

  1. 1State the fuel sources of skeletal muscle1) Glucose
    2) Circulating FFAs
    3) Glycogen in cytosol
    4) Intramyocellular lipid droplets
  2. 2Outline Romjin et. al's (1993) study and its findings1) Fat and glucose labeled using stable isotopes
    2) Muscle substrate utilisation measured at different exercise intensities
    3) Found that plasma FFAs contributed the most to energy generation at low exercise intensities (i.e 25% VO2 max)
    4) Relative contribution of muscle triglycerides and glycogen increases significantly at 65% of VO2 max
    5) Muscle glycogen utilisaton predominant at 85% VO2 max
  3. 3State the 5 mechanisms used to explain the change in substrate utilisation with an increased exercise intensity1) The cellular ATP/ADP ratio
    2) An increased CHO flux and malonyl-CoA suppression of CPT1
    3) Increased CHO flux and reduced free carnitine availability
    4) Increased CHO flux and pH mediated CPT1 inhibition
    5) Increased fat flux and inhibition of PDC activation
  4. 4Explain how muscle substrate utilization changes using the cellular ADP/ATP ratio mechanism1) As exercise intensity increases - fat oxidation cannot meet the ATP demand - the rephosphorylation of ADP to ATP does not occur fast enough
    2) This causes a change in the ADP/ATP ratio - causing ADP and AMP to accumulate
    3) The accumulation of ADP and AMP stimulates glycogen breakdown and glycolysis, driving CHO oxidation and inhibting fat oxidation
  5. 5State the function of the enzyme AMP kinase1) Responsible for activating glucose uptake, glycolysis and fatty acid uptake at the onset of exercise
    2) Also inhibits glycogenesis
  6. 6Explain how muscle substrate utilization changes using the increased CHO flux and malonyl Co-A accumulation mechanism1) Increase in exercise intensity leads to a greater glucose flux - more pyruvate converted into Acetyl-CoA by PDC
    2) Excess Acetyl-CoA is formed which is shunted into acetylcarnitine by Acetyl transferase
    3) Acetylcarnitine is transported out of the mitochondria and is used to synthesis Malonyl-CoA - which inhibits CPT1 - which plays a role in the translocation of fatty acids into the mitochondria
    4) This leads to the decrease in the relative contribution of fatty acids in ATP generation
  7. 7Explain how muscle substrate utilisation changes using the increased CHO flux and reduced free carnitine availability mechanism1) Increase in exercise intensity increases CHO flux - producing excess Acetyl-CoA
    2) Acetyl-carnitine formation reduces the amount of free carnitine available in the cell
    3) This reduces the translocation of fat into the mitochondria, as fat can only get in through the formation of fatty acyl-carnitine, reducing fat oxidation
  8. 8Describe studies supporting this mechanismWall et al (2001)
    1) Ppts infused with free carnitine or CHOs
    2) Infusion of free carnitine led to a 50% reduction in muscle glycogen utilisation during 30 minutes of exercise - due to an increased fat translocation (through fatty acyl-carnitine formation) - increasing fat oxidation
    3) Results showed an accumulation of long-chain Acyl-CoA in the muscle in a high carnitine loaded state (Stephens et al, 2013)
  9. 9Explain how muscle substrate utilisation changes using the increased CHO flux and pH mediated CPT1 inhibition mechanism1) Increase in exercise intensity leads to an increase in CHO flux
    2) This causes the excess production of pyruvate, which is then shunted into lactate
    3) Lactate disassociates into a hydrogen and lactate ion, causing a change in the acid base balance
    4) Excess lactic acid production inhibits CPT1 - which is pH sensitive
    5) Change in pH causes a slow fatty acid entry into the mitochondria, reducing fat oxidation
  10. 10Explain how muscle substrate utilisation changes with an increase in fat flux and increased inhibition of PDC (i.e the Philip Randle/glucose-fatty acid cycle/lipid overflow mechanism)1) At low exercise intensities, there is an increase in lipid availability causing an increased lipid flux
    2) Excess lipid metabolites suppress the action of PDC, limiting CHO flux
    3) However, as exercise intensity increases, there is an increase in calcium ion secretion, which activates PDC
    4) The activation of PDC leads to the decreased suppression of the glycolytic flux, leading to a decrease in fatty acid oxidation

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Year 2 LIFE2097 - Muscle Physiology, Nutrition and Metabolism Flashcards on Fat and CHO Oxidation During Exercise, created by Czean Holgado on 22/05/2022.
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Czean Holgado
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