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| Question | Answer |
| When you increase CHO what happens to muscle glycogen throughout exercise? | It is better maintained |
| What is the difference between trained athletes and untrained athletes with regards to glycogen. | Trained athletes can replenish glycogen quicker than untrained individuals |
| How do trained individuals replenish glycogen quicker? | They have more GLUT-4 so more glucose is taken to the muscles from the bloodstream. They then build more glycogen from this glucose |
| What is GLUT-4? | A transporter protein |
| How does pre exercise muscle glycogen content and exercise intensity effect fuel metabolism? Describe the testing. | 6 males completed 4x60min rides at 45% or 70% Vo2max in glycogen loaded or depleted states. |
| How does pre exercise muscle glycogen content and exercise intensity effect fuel metabolism? What were the findings? | When RER is low = fat oxidation When RER is high = CHO oxidation Glycogen contribution increases as muscle glycogen availability increases |
| What are the potential underlying mechanisms? | 1) Regulation of glycogen phosphorylase 2) Low CHO diet |
| How does the regulation of glycogen phosphorylation work? | The quantity of glycogen that is available is a limiting factor for how quickly glycogen can be synthesised. Adrenaline starts this process |
| How does maintaining a low CHO diet work? | Increases resting PDH kinase PSH kinase regulates PSH, therefore PSH activity decreases. |
| What is exercise induced activation of PSH attenuated with? | Reduced pre-exercise muscle glycogen content even when fed pre-exercise CHO. |
| What effect does glycemic index have? | High GI decreases glycolysis in adipose tissue Low GI increases fat oxidation |
| Why does high GI have that effect? | High GI inceases insulin - this decreases free FA concentrations which decreases glycolysis in adipose tissue |
| Why does low GI have that effect? | Insulin response is lower from low GI foods This is a better response during exercise |
| What do reduced plasma FFA and glycerol suggest is happening to lipolysis? | HSL is the rate limiting enzyme in lipolysis HSL increases when fasted so lipolysis increases When fed there is no difference for HSL throughout exericse. |
| Lipolytic suppression following CHO ingestion limits fat oxidation during exercise. What happens when we increase suppression of lipolysis | fat oxidation increases |
| Lipolytic suppression following CHO ingestion limits fat oxidation during exercise. What are happens to levels of glucose and fructose? | They are equal |
| Lipolytic suppression following CHO ingestion limits fat oxidation during exercise. When fasted what happened? When fed what happened? | High rate of fat oxidation Muscle glycogen is the primary fuelsource, fat oxidation decreases |
| Lipolytic suppression following CHO ingestion limits fat oxidation during exercise. When fed and lipids are infused what happens? In the fructose trial what happened? | Fat oxidation is increased but not as much as in the fasted trial Muscle glycogen is used the same amount as in the glucose trial but fat oxidation is increased. |
| If lipid infusion does not restore fat oxidation rates to those that occur in the fasted state, where else can that attenuation occur? | LCFA entry into the mitochondria. An increase in glucose equals an increase in flux. This decreases carnitine availability. |
| What does reduced carnitine availability, caused by high PDH flux, limit? | It limits the capacity for LCFA uptake into the mitochondria which CHO is ingested before/during exercise. |
| What does an increase in acetyl-carnitine lead to? | An increase in PDH activity |
| What does a decrease in free carnitine lead to? | A decrease in CPT-1 activity. |
| What happens when the body is subjected to a constant high fat diet? | It adapts |
| When a time trial was completed, what was the difference between the fat adapted trial and the high CHO conditions. | There was no difference |
| During 2 hour exercise, what happens to fat oxidation compared to CHO or fat adapted conditions? | There is high fat oxidation regardless of which condition |
| What does increasing CHO do to the flux of PDH? | By increasing CHO there is an increase in flux of PDH. PDH is higher during a 1 min sprint. |
| What is endogenous carbohydrate availability referring to? | Muscle glycogen |
| What is exogenous carbohydrate availability referring to? | Blood glucose |
| Can the interaction of endogenous & exogenous CHO availability affect training-induced skeletal muscle adaptations to exercise? | Low CHO leads to a greater increase in mitochondrial mass in the muscle |
| Is breakfast before training really a good thing? What is citrate synthase? | A marker of mitochondrial mass |
| Is breakfast before training really a good thing? What did measuring citrate synthase and beta-HAD show? | Exercising in a fasted state increases the capacity of oxidation and increases mitochondria |
| What does training low allow us to do? | Increase adaptation |
| What does competing high allow us to do? | Increase performance and recovery |
| Does exercise increase p53 phosphorylation? | Matched work high intensity interval training (HIIT) & continuous running induces similar increases in phosphorylation of p53 in the mitochondria. |
| Does reduced CHO availability affect the exercise-induced increase in p53 phosphorylation? How? | Yes ACC increases the regulation of LCFA Increase in Malonyl is driven by the increase of ACC activity for regulation of CPT-1 There is a greater capacity to oxidate FFA's |
| What does upstream AMPK signalling lead to? | downstream and temporal signalling of p53 to coordinate up-regulation of both nuclear and mitochondrial genomes. |
| CHO availability can modulate fatigue. What can deliberate training in conditions of reduced CHO availability allow? | Increased lipid oxidation this sparing glycogen utilisation. |
| What does strategically periodising out training and nutrition allow us to do? | Develop the muscle's capacity to utilise CHO thus preserving the capacity to exercise at high intensities. |
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