54193
Description
Flashcards by Mark Arsenal, updated more than 1 year ago
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Created by Mark Arsenal
about 11 years ago
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| Question | Answer |
| What is the difference between Cell Mediated and Humoral Immunity? | Th0 is the undifferentiated form of cell and it can be differentiated dependent on required action. Th1 differentiation form T-cells which use cytotoxins to kill viruses (Cell Mediated Immunity) Th2 differentiation forms B-cells which use antibodies to kill Bacteria (Humoral). |
| Th1 differentiation is activated when: | We need T-cells to fight a virus. |
| Th1 differentiation is activated when: | We need T-cells to fight a virus. |
| Th2 differentiation is activated when: | We need B-cells to use antibodies to fight bacteria. |
| Why is Th0 differentiation known as a 'balance'? and how do we determine which is differentiated? | Because Th0 can only be differentiated into EITHER Th1 or Th2 NOT BOTH. Signalling proteins determine which is activated. The two pathways cross regulate each other and thus when 1 is active the other is suppressed. |
| How does exercise to fatigue effect differentiation to T and B cells? | Exercise to fatigue causes a decrease in the signalling proteins required to form Th1 (T-cells) but doesn't affect Th2 differentiation. |
| In terms of exercising to fatigue on Th0 differentiation what factor does Stress play? | Stress causes an increase in the signalling protein IL-10 which is significant in Th2 differentiation, thus B-cell numbers increase. |
| In terms of exercising to fatigue on Th0 differentiation what factor does Cortisol play? | Cortisol increases with exercise. Elevated cortisol levels causes a decrease in IL-12 which is a signalling protein in Th1 differentiation. Thus decreases Th1 differentiation. BUT high cortisol increases IL-10 which is key in Th2 differentiation, thus more B-cells are made. |
| In terms of exercising to fatigue on Th0 differentiation what factor does Catecholamines and Glucorticoids play? | Both suppress Th1 differentiation (decreased T-cells) and thus increased Th2 differentiation (increased B-cells). |
| What effect does diet have on Cortisol and thus Th0 differentiation? | A low CHO diet causes an increase in cortisol as we need to up-regulate Glucose production, thus this activates Gluconeogenesis but as we know causes Immunosupression. Soo if we ingest CHO during exercise our cortisol levels do not as greatly increase and thus less immunosuppression. |
| What happens to the Th0 differentiation signalling molecule IL-6 during exercise? | Usually exercise causes a decrease in Th0 signalling differentiation (immunosuppression) BUT IL-6 increases with exercise, which signifies that it is released from the skeletal muscle. IL-6 has been found to cause an increase in IL-10 which increases Th2 differentiation. Some beleive IL-6 is responsible for muscle damage BUT ITS NOT. Also been found that IL-6 increases much greater when glycogen levels are lower and thus it acts as a signal for energy crisis, thus IL-6 it is associated with increasing lipolysis for energy. |
| What is meant by T/B Cell Proliferation? | T or B cell proliferation is cell growth and division. This process occurs through the attachment of a specific immunogen to the specific surface antigen receptor on the T/B cell which then causes proliferation. |
| What happens to lymphocyte proliferation (T and B cells) following exercise? | Lymphocyte proliferation is temporarily reduces for approximately 3 hours after. |
| What effect does an increase in Blood Cortisol have on the Immune System and more specifically Cell Proliferation? | Both intense and prolonged exercise via different pathways increases Blood Cortisol which causes Immunosupression and Gluconeogenesis (G is turned on to deplete Glucose levels which are reduced during exercise). Additionally Cortisol decreases Cell Proliferation. |
| Do Trained or Un-trained have higher levels of circulating leukocytes? | Un-trained. This is due to regular training causing an increase in plasma volume which causes a decrease in leukocytes (WBC's) |
| Explain Neutrphil function (Phagosytosis) and explain how exercise effects Neutrophil number and function: | Process of Phagocytosis: Antigen attracts a neurtophil from the cell which engulfs the antigen, it then releases granules which degranulates the antigen, killing it. It has been found that exercise increase phagocytic capacity, but as we know un-trained have higher phagocytic capacity as they have a higher number of circulating neutrophils. Neutrophil amount circulating are increased immediately after exercise, but they are at there highest approximately 2.5hours after exercise. When circulating neutrophils are at there highest we also see a reduction in degranulation capacity, thus we may have more but they are less effective. |
| Explain Neutrphil function (Phagosytosis) and explain how exercise effects Neutrophil number and function: | Process of Phagocytosis: Antigen attracts a neurtophil from the cell which engulfs the antigen, it then releases granules which degranulates the antigen, killing it. It has been found that exercise increase phagocytic capacity, but as we know un-trained have higher phagocytic capacity as they have a higher number of circulating neutrophils. Neutrophil amount circulating are increased immediately after exercise, but they are at there highest approximately 2.5hours after exercise. When circulating neutrophils are at there highest we also see a reduction in degranulation capacity, thus we may have more but they are less effective. |
| What is the substance that forms the granules that Neutrophils release? | Elastase. |
| What are Natural Killer Cells? | Front line defence before a specific response from T or B cells. Can destroy cancerous cells. |
| What effect does exercise have on Natural Killer Cell Activity? | During exercise NKC activity trebles but in recovery it falls to lower than at rest, thus after exercise we are very vulnerable to infection. |
| How can we prevent the Natural Killer Cell Activity fall to lower than resting levels following exercise? | Through injection of Indomethacin, which is a prostaglandin inhibitor. BUT the immediate post exercise fall in NKC following exercise is not fixed by Indomethacin. |
| What is the effect of prolonged training/competition on Natural Killer Cell Activity? | Intense prolonged training causes a decrease in Natural Killer Cells is lower after intense exercise, which suppresses the bodies immunity ability. Although it has been found that moderate training is good. |
| Explain Niemann's J-shaped model? | This model explains that after exhaustive or high intensity exercise we have a high chance of URTI but Moderate exercise decreases the chance of URTI. Low intensity exercise is slightly higher risk than Moderate, but much lower than High intensity. |
| What are the 2 branches of the bodies Immune System (Defense against pathogens)? | Innate Immunity and Acquired/Specific Immunity. |
| Explain what forms the Innate Immune System: | The Innate Immune system is the bodies natural defense and thus fast in response to pathogens. It is formed by Anatomical/Chemicsl Barriers, Phagocytes, Natural Killer Cells, Complement Proteins and Interferons. |
| Explain what forms the Acquired/Specific Immunity System: | This Immunity requires time. Requires previous exposure to pathogen, which forms a clone of antigen specific T-cells (which can respond to the antigen when exposed henceforth, this is Cell Mediated Immunity). Antigen specific T-cells are formed in relation to Cell Mediated Immunity and B-Lymphocytes are formed in relation to Humoral (Liquid) Immunity. (SAME PROCESS FOR B-LYMPHOCYTE ANTIGEN SPECIFIC IMMUNITY) |
| What are the 2 types of cell which form the Immune System? | Granulocytes and Agranulocytes. |
| What cells are Granulocytes and what are there individual functions? | Neutrophils- Use Phagocytosis (engulfs antigen) the most common cell. Eosinophil- Destroy parasites. Basophil cause Inflammation. |
| What cells are Agranulocytes and what are there function? | Lymphocytes and Monocytes. Lymphocytes directly attack cells and Monocytes use Phagocytosis (engulfs antigen). |
| What is the broad name given to the cells of the Immune System? | Leukocytes (White Blood Cells) All Granulocytes and Agranulocytes are Leukocytes. |
| What effect does brief intense exercise have on circulating Leukocyte concentrations? | Biphasic Leukocytosis. (Immediately rise, then fall, then gradually rise once more) Broken into to phases, 1st phase ( immediate rise) is caused by increased Lymphocytes and Neutrophils. The second phase (gradual rise) is caused by increased Neutrophils only (lymphocytes do not increase). |
| What effect does prolonged high intensity exercise on circulating Leukocytes? | Prolonged high intensity exercise causes a prolonged sustained Leukocytosis. |
| What causes the increase in circulating Leukocyte counts? | Exercise causes shear stress which causes an increase in catecholamines which decreases the adherence of the leukocytes on vessel walls- this causing increased circulating leukocyte counts. |
| How can we explain the Biphasic Leukocyte response after brief intense exercise? | Exercise causes the initial immediate increase in circulating leukocytes through the reduced adherence of leukocytes on the vessel walls. Stress can explain the secondary rise as it is a delayed response through a psychological neural pathway which mobilizes neutrophils from the bone marrow into the blood. |
| What is Oxidative Stress? | Oxidative Stress is an imbalance between our defensive anti-oxidants and the attacking pro-oxidants which are formed of Free Radicals and Reactive Oxygen Nitrogen Species. Oxidative stress causes the oxidation of molecules such as proteins, lipids, DNA and oxidation of these is associated with human diseases. |
| How are Free Radicals formed? and give 3 examples of Free Radicals: | Free Radicals are formed of a molecule with a single unpaired electron in the outer ring. Superoxide, Hydroxyl Radical. Nitric Oxide. |
| What are RONS? and give 3 examples of RONS: | RONS are reactive species which arise from Nitrogen or Oxygen. Hydrogen Peroxide, Hypochlorous Acid, Ozone. |
| What effect does exhaustive exercise have on Oxidative Stress? | Exhaustive exercise causes damage which increases the oxidation of proteins, fats and DNA which can cause such consequences as changes to cell structure and function, atheroscelrosis and cell death. |
| What effect does Moderate exercise have on Oxidative Stress? | Moderate exercise decreases RONS which in turn causes adaptation, which in turn causes cell up-regulation and gene up-regulation which increases the number of protective anti-oxidants and enzymes for exercise adaptation, these in turn reduce Oxidative stress and cause vasodilation and thus improve blood flow. |
| How can we measure Oxidative Stress directly? | Electron Spin Trapping- Micro-dialysis isolates the distinctive unpaired electron structure that Free Radicals have and then use a probe to show them. Flow Cytometry- Method by which we measure oxidative stress on the RBC's by measuring the generation of Reactive Oxygen Species and then the oxidation of membrane lipids (fats) as an indication of the membrane damage caused by Oxidative stress. |
| How can we measure Oxidative Stress In-directly? | Using Markers of Oxidative Stress- Molecules form on the tissues when they have been exposed to Free Radicals (lipid peroxides form on lipids) thus we can measure these molecules to indirectly measure oxidation and thus oxidative stress. Using the Assessment of Anti-oxidant Status. This works by measuring anti-oxidant capacity through injecting known substance of anti-oxidant and meauring the effect it has on ROS and FR, this therefore indicates the bodies anti-oxidant capacity (Lower anti-oxidant capacity the higher the oxidative stress) |
| How do the Mitochondria play a large role in Oxidative Stress at rest? | During exercise when muscular demand for oxygen is high the oxygen in the muscle is consumed for energy production through the ETC (the electrons remain in the ETC to produce ATP) HOWEVER at rest when oxygen demand is low (and ATP levels are high) electrons leak from Complexes 1,2 and 3. These singular unpaired electrons form to molecules forming a ROS. Thus ROS formation at rest is much higher at rest than during exercise. |
| How in relation to Oxygen muscle flow can we generate ROS through the breakdown of Purine to Uric Acid (forms a electron)? | When oxygen is high in the muscle (rest) Xanthine Dehydrogenase is active which breaks down Purine to Uric acid and the formed electron is donated to NAD+ to form NADH. When oxygen in the muscle is low (during isometric contraction) Xanthine Dehydrogenase is converted to Xanthine Oxidase. When oxygen is again increased (immediately after isometric contraction) the Xanthine Oxidase is still active which transfers the formed electron from the breakdown of Purine to Uric Acid on to Oxygen forming a ROS. |
| How long have studies found that lipid peroxidation was elevated for following a marathon? (OXIDATIVE STRESS) | Lipid peroxidation was elevated for 2 weeks, there was also found to be damage to the DNA which was recovered after 3 days. |
| What effect do different intensities and types of exercise have on Oxidative Stress? | A study of untrained males (running at 70-75%) for 45mins. Results found that Total Anti-oxidant capacity was increased following exercise, but not enough to buffer the exercise associated ROS increase. |
| What is the difference between Short term exercise and Long term training on ROS formation and thus Oxidative Stress? | Short term exercise increases ROS which causes damage, BUT the formed ROS can cause adaptation in Long term exercise regimes, this is due to the structural and bio-mechanical changes which cause an increase in enzymatic anti-oxidants which thus decreases Oxidative Stress. Thus ST exercise increases ROS and thus OS but LT causes an increase in anti-oxidant capacity through adaptation. |
| What training type is most associated with Oxidative Stress adaptation rather than damage? | Long term Moderate Aerobic exercise up-regulates NFkB which is associated with the increased enzymatic activity associated with forming anti-oxidants. But the whole process is underpinned by Xanthine Oxidase/Dehyrogenase activity. |
| What is the relationship between Exercise and Infections? | There is both anecdotal evidence and study evidence of increased levels of Upper Respiratory Tract Infections following exercise. But this could be due to other factors such as having higher levels of body awareness or respiratory muscle fatigue) |
| What is the effect of exhaustive exercise and pathogens? | Exhaustive exercise increased replication levels of the pathogens Coxsackie and Ifluenza ans thus mortality is mice. |
| What happens to T-cells (fight infection) response following exhaustive exercise? | They decrease following exhaustive exercise, thus it suppresses the immune system. |
| How does Insulin Resistance affect Blood Viscosity? | Fibrinolysis is the process by which we remove blood clots. This process is controlled by Fibrin. PAI prevents the breakdown of Plasminogen --> Plasmin --> Fibrin. Thus PAI prevents the clot removal leading to more viscous blood. Insulin resistance causes an increase in PAI, but we can use drugs to decrease PAI levels. |
| How does diet effect Insulin Resistance? | A high fat diet causes an in Increase in Insulin resistance, additionally a high fructose diet increases levels of TAG. |
| Explain the relationship between Insulin Resistance and Cholesterol: | People who are obese have higher levels of Triglyceride in the blood, this greatly affects Lipoproteins. TAG rich VLDL's unload TAG on to LDL's and HDL's subsequently TAG rich HDL's are catabolized leading to decreased HDL's (bad as they are anti-atherogenic) and additionally the TAG rich LDL's are hydrolysed to form smaller and denser LDL's (bad as they are more atherogenic when smaller and denser). |
| How can we treat Insulin Resistance? | Thiazolidinediones. T's increase Insulin Sensitivity by decreasing TAG and FFA levels in the blood. They also increase HDL's. |
| What is the relationship between Insulin Resistance and Hypertension (High Blood Pressure)? | If you are Insulin Resistant you have a greater chance of Hypertension. |
| What causes Hypertension when you are Insulin Resistant? | Hyperinsulinaemia causes a decrease in sodium excretion which causes an increase in water retention which increases Blood Pressure. Insulin acts as a Vaso-dilator (through NO) and thus if you are more resistant then the vasodilation effect is decreased which thus increases Blood Pressure. These effects are exaggerated in obese people as the adipose releases increase levels of TNF-alpha which inhibits the Insulin cascade which in turn inhibits eNOS (enzyme that produces Nitric Oxide) thus no Vaso-dilation effect. |
| What is the Metabolic Syndrome? | It is the circular relationship between Obesity and Insulin Resistance which are effected and effect each other and how these linked factors cause an increased risk of developing CVD. |
| How are Obesity and Insulin connected in terms of increased CVD risk? | Obesity is effected by and effects Insulin Resistance through factors associated with Insulin Resistance which increase the risk of CVD. These factors Decreased HDL's, Decreased LDL size (dense and more atherogenic), Increased TAG, Increased Blood Pressure and increased PAI-1 (PAI-1 prevents process which breaks down blood clots) |
| What effect does Diabetes have on Insulin Resistance? | Diabetes causes Insulin resistance and the data shows that this factor greatly increases the chance of mortality. |
| What can be used to overcome Insulin Resistance? | Hyperinsulinaemia. This is the process by which we produce more Insulin to overcome the resistance. However both Insulin resistance and Hyperinsulinaemia cause an increase risk in developing CVD. |
| How do Age and Obesity effect the risk of Metabolic Syndrome? | They both increase the risk of Metabolic Syndrome. |
| Does being Insulin Resistant cause Obesity? | in normal people Ghrelin naturally slightly increases over time (throughout the day), but when being injected with Insulin (appetite suppressant) this decreases in normal people. But people with T2 Diabetes (thus Insulin Resistant) the effect of Insulin on Ghrelin is much less effective thus they eat more. Additionally Insulin triggers LPL (clears fat from the blood) but LPL is activity is inhibited by prolonged Insulin in the blood, in people who have T2 Diabetes or those with Insulin Resistance (thus Hyperinsulinaemia) Insulin remains elevated thus LPL cannot clear blood and therefore more fat is stored as adipose, thus contributing to obesity. |
| Describe how levels of Intramuscular Triglyceride (IMTG) are used differently in lean people as opposed to those who are obese, inactive or suffer from T2 Diabetes: | Inactive, Obese and T2 Diabetics have higher levels of IMTG and thus higher amounts of Lipid Derivatives which in turn inhibit the insulin cascade. However in trained individuals because training increases the number of Mitochondria (through Mitochondrial Biogenesis) more of the IMTG is used for energy, thus there are lower levels of Lipid Derivatives, thus no interference to the Insulin cascade. |
| What effect does Exercise have on the number of GLUT4 transporters in the muscle? | Exercise in both young and old individuals causes an increase in the number in GLUT4, however some of the increase is solely due to increased AMPK. |
| What effect does exercise have on Glucose Storage? | Exercise causes an increase in Glycogen Synthase which results in an increase in glycogen synthesis (Glycogenesis) thus increased Glucose storage. |
| Does the ability to uptake fat into the cell for energy supply (Beta Oxidation in the Mitochondria) change between those who are healthy and those who are Obese or suffer from T2 Diabetes? | Those who suffer from T2 Diabetes or are Obese have greater Fat transporters (CD36) on the cell membrane but similar amounts in the whole muscle. The more receptors on the cell membrane which means more FFA enters the cell and thus more is stored as TAG in the cell. |
| What effect does Diabetes have on the Mitochondria and can exercise training help this? | Diabetes causes Mitochondrial dysfunction (Reduced Mitochondrial density and activity). Yes exercise training helps to restore Mitochondrial function through causing Mitochondrial Biogenesis. This occurs through exercise increasing gene expression of PGC-1a (in nucelus of the cell) which is key in Mitochondrial Biogenesis. |
| What is the relationship between exercise and AMPK induced fat oxidation: | Normally AMPK phosphoryllates Acetyl-CoA (through ACC) to Malonyl-CoA which inhibits fat oxidation through the inhibition of the fat transport mechanism (CPT-1) moves fat from cytoplasm into the Mitochondria for Beta Oxidation. When we exercise we inhibit the enzyme ACC thus Malonyl-CoA is not formed and therefore there is no inhibition of CPT-1 allowing for more fat transport into the Mitochondria for Oxiodation. |
| How does regular physical activity effect change Glycaemic control in people who have T2 Diabetes? | In people who have T2 Diabetes increase Glycaemic Control by making them more Insulin sensitive- thus increased Glucose uptake into the cell from the cell. |
| How Effective is a Healthy Lifestyle and Exercise in prevention in developing T2 Diabetes? | It is very effective, even more effective than the most effective drug. |
| Does Insulin act as slight Vasodilator or Vasoconstrictor? | Insulin acts as a slight Vasodilator through Nitric Oxide thus Insulin causes slight vaso-dilation during the Insulin cascade. But with increasing fat levels this increases TNFalpha's which decrease tyrosine phosphoryllation and increase serin phosphoryllation thus this inhibits the Insulin cascade, thus Insulin does not act as a slight vasodilator and therefore explains why those who are Insulin resistant have higher blood pressure. |
| What effect does Aerobic Training have on Capillary Density? | 8 weeks of aerobic training at 80% VO2 Max caused an increase in Cappilirisation of the muscle which thus allows for greater Glucose and Insulin delivery to the muscle. |
| Does training cause an increase in Insulin Receptors (allow Insulin to enter the cell)? | No, it does not increase the number of Insulin receptors but it does increase autophosphoryllation of tyrosine at the start of the Insulin cascade and thus speeds up GLUT4 translocation and thus Glucose entry. Additonally it has been found that exercise increases the activity of P13 Kinase (key enzyme in Insulin cascade). |
| Why does Obesity cause Insulin Resistance? | People with high adiposity have higher levels of Fatty Acyl-CoA, Diacylglycerol and Ceramides from FFA inside the cell which activate PKC which along with TNF alpha which cause a decrease in tyrosine phosphoryllation and an increase in serine phosphoryllation thus preventing the Insulin cascade, which thus in turn causes Insulin (need more Insulin to overcome issue). |
| What effect does training have on Adipocytokines such as TNFalpha, Leptin and Adiponectin? | Training causes a decrease in the detrimental to health TNF alpha (decreases tyrosine phosphoryllation and increases serine phosphoryllation, thus more Insulin is required to overcome this effect= Insulin Resistance) and Leptin (detrimental as it causes Insulin Resistance) and increases the beneficial adipocytokine Adiponectin (increases fat oxidation) |
| Explain the relationship between obesity, T2 Diabetes and Intra-Muscular Lipid Content and its effect: | Obese people and those with T2 Diabetes have higher Intra-muscular Lipid Content and this causes a decrease in Insulin sensitivity (Insulin Resistance). |
| How does acute exercise effect Glucose uptake in skeletal muscle? | Single bout transiently increases Glucose uptake into the muscle through, Increased GLUT4 translocation, Increased No. of GLUT4 transporters, Increased muscle profusion, increased Glycogen Synthase activity. |
| How does regular physical activity effect change Glycaemic control? | We know a single bout of exercise transiently increases Glycaemic Control (increased Glucose uptake) but regular PA has been found to cause a baseline adaptation. |
| What effect does Nitric Oxide have on Exercise Induced GLUT4 Trans-location? And what effect does exercise have on GLUT4 protein production? | Nitric Oxide is required in exercise induced GLUT4 trans-location. When it is blocked through L-NAME GLUT4 trans-location fell to below the control group. Exercise causes a production in GLUT4 within several hours of finishing exercise. |
| What is the primary role of Insulin? | Insulin's primary role is in Glucose Homeostasis. As blood Glucose levels increase (following a meal) the Pancreas releases Insulin which reduces blood Glucose levels through GLUT4 trans-location in the cell allowing Glucose to enter the cell from the blood. Aside from this Insulin has many many functions. |
| What is Diabetes and how is it caused? Additionally what are the differences between T1 and T2? | Diabetes is caused by a CHO metabolism disorder which is characterized by high blood glucose levels (hyperglycaemia). Develops when Insulin production or Insulin use is inadequate. Type 1 is Insulin dependant (body cant produce I) and T2 is Non-Insulin dependant (body can produce Insulin but tissues cannot respond to it). |
| What is happening to Diabetes levels in the UK? | They are increasing. Diabetes has increased by 82% between 1995-2005. There is a similar pattern in the USA. |
| Does Adiposity have an effect on Diabetes levels? | Yes, with increased Adiposity there is an increased chance of developing Diabetes and with Diabetes comes a much higher chance of Mortality- equal to the increased risk of death as CHD. |
| How can we measure Insulin Sensitivity/Resistance? | Hyperinsulinaemic Euglycaemia Clamp, Oral Glucose Glucose Test and through the Homeostatic Model Assesment. |
| What is the procedure for the Hyperinsulinaemic Euglycaemia Clamp method of measuring Insulin Sensitivity/Resistance? | Inject the subject with Insulin which through the Insulin cascade causes GLUT4 translocation to the cell membrane, which thus decreases blood (plasma) glucose. You then inject Glucose gradually until Insulin matches level of Glucose being taken up by the tissues, thus we can determine the relationship through calculations to determine Insulin Sensitivity. |
| What is the procedure for the Oral Glucose Tolerance Test method of measuring Insulin Sensitivity/Resistance? | This is where you give the participant a 75g glucose tablet/drink and then measure blood Glucose levels after 2 hours, by this point Glucose levels should be normal. |
| What is the procedure for the Homeostatic Model Assessment method of measuring Insulin Sensitivity/Resistance? | This is essentially the Diabetes equivalent of BMI. Using a calculation R=[Glucose]x[Insulin]/22.5 we can determine whether the participant is diabetic or not. |
| What happens with Glucose uptake into the cell during Exercise? | Glucose uptake increases with increasing intensity exercise. When exercising Glucose is not dependant on the Insulin cascade as exercise causes GLUT4 Translocation to the cell membrane, but the combination of glucose and Insulin causes the greatest Glucose uptake due to increased GLUT4 trans-location. We also know that exercise causes an increase in GLUT4 trans-location through a process independent of the Insulin cascade, as when P13-kinase (key enzyme in I cascade) was blocked using Wartmannin GLUT4 trans-location was still increased. Additionally exercise deactivates the Insulin cascade by decreasing the activity of the enzyme P13 Kinase. |
| What causes Exercise Induced GLUT4 trans-location? | Both the increase in intracellular Ca and the increased ratio of AMP:ATP caused by exercise cause the activation of AMPK (fuel sensor) which causes increased Glucose uptake through causing GLUT4 trans-location. |
| How is GLUT4 physically trans-located? | Through the conversion of Rab GDP to Rab GTP. Either PKB (Protein Kinase B) from Insulin cascade or AMPK from exercise induced trans-location activates TBC1D4 which convertes Rab GDP to Rab GTP thus causing GLUT4 trans-location. |
| What happens to our weight as we age? | As we age our weight increases, in fact between the ages of 20 and 55 we on average put on 11kg. This effect is exaggerated by sedentary lifestyles, the more sedentary the more weight gain as we age. |
| What is the relatioship diet, exercise, weight loss and subsequent weight gain? | It has been found that people who solely diet found dramatic short term weight loss but often put weight back on whereas those who both dieted and exercised put less weight back on following the regime, thus rebound weight gain is decreased with a combination of exercise and diet induced weight loss. |
| What causes a Negative or Positive Energy Balance? | A Positive energy balance is whereby we eat more calories than we burn and thus causes weight gain. A Negative energy balance is whereby we burn more calories than we eat thus causes weight loss. |
| Approximately what % of daily calorie expenditure is due to Basal Metabolic Rate (BMR)? And are people effective at matching calorie intake with calorie burn? | Approximately 60-75%. No, people are bad at matching calorie intake and burn, they often eat more than they burn (belief that they burn more than they do). |
| What is Compensation? and what effect does it have on energy balance? | Compensation is whereby people do less NEAT when they follow an exercise program, which then acts to restore energy balance. A study found that approximately people compensate for 30% of additional calorie burn through exercise by decreasing NEAT. Also the more intense exercise causes greater levels of compensation. Additionally a low fat diet has been linked with a decreased energy expenditure and thus more compensation. |
| What is Compensation? and what effect does it have on energy balance? | Compensation is whereby people do less NEAT when they follow an exercise program, which then acts to restore energy balance. A study found that approximately people compensate for 30% of additional calorie burn through exercise by decreasing NEAT. Also the more intense exercise causes greater levels of compensation. Additionally a low fat diet has been linked with a decreased energy expenditure and thus more compensation. |
| What role does Glycogen play in Weight Loss? | When we exercise we deplete Glycogen stores (approximately 70%) as we lose Glycogen we also lose weight through water loss. Exercise training increases glycogen stores whereas diet decreases glycogen stores. Both diet and exercise decrease levels of fat, but the increases weight loss in solely diet comparative to solely exercise is associated with the increased loss of weight through the loss of Glycogen and thus water. Additionally it has been found that trained athletes replenish glycogen levels quicker than untrained. |
| What effects does diet and exercise have on body composition? | An un-desired effect of solely diet regimes is a reduction in weight through muscle loss, exercise helps to protect us against this. A loss in muscle mass is soo un-desirable due to its significant contribution to BMR (due to its large size). Per 2.35kg of muscle we burn an additional 30.5 kcals daily. |
| What effect does diet and exercise have on the Appetite regulating hormones? | Diet increases levels of Ghrelin (on-switch) as does exercise. Additionally Ghrelin increases with Weight Loss. Diet also decreases levels of Leptin which is beneficial as Leptin plays a role in causing Insulin Resistance (although negative in terms of less suppressant of hunger). |
| Why are the Mitochondria so important in metabolism? | Because many energy producing pathways occur in the Mitochondria- TCA, ETC, Beta-Oxidation. |
| How does Mitochondrial Biogenesis occur? | An increase in Mitochondria is caused by the gene PGC-1alpha. |
| What happens to PGC-1alpha (gene that expresses Mitochondrial Biogenesis) with exercise and diet? | Exercise induces a dramatic, yet transient increase in PCG-1alpha transcription and thus Mitochondria in muscle. Diet has also been found to increase the number of Mitochondria, through increasing levels of the hormones TFAM and PPARGC1A which switch on Mitochondrial Biogenesis. BUT dieting decreases the respiratory capacity of the Mitocondria, thus we have more M but they are less effective. |
| What is Triiodothyronine (T3) and how is effected by exercise and diet? | T3 increases BMR. It has been found that dieting decreases levels of T3 whereas exercise increases levels of T3, and the combination of diet and exercise still decreases T3 but a-lot less than solely dieting. |
| What happens to hunger during and following exercise? | Hunger decreases when exercising, it is also lower in the early recovery period of exercise but hunger does recover in the period following exercise. |
| What is Cholecystokinin (CCK)? | CCK is a turn off switch to eat which is produced in the GI Tract (Duodenum and Jejunum) which acts upon are the Arcuate Nucleus. It decreases food intake and increases satiety. It increases after eat, especially after eating fats. |
| What is Leptin? | Leptin is an off switch hormone which is produced in the Adipose tissue which acts upon the Arcuate Nucleus. It causes a decrease in food intake. It slightly decreases after eating and has a tonic action to regulate adiposity. Additionally it has been found that Obese become Leptin deficient. Leptin additionally plays a part in Insulin resistance. Interestingly in obese people who have high Leptin levels (partial cause of Insulin Resistance) the beneficial action of hunger suppressant is lost due to desensitization, but the negative factor (insulin resistance) remains in tact. |
| What is PYY? | PYY is hunger suppressant hormone produced from the GI Tract (Ileum and Colon) which acts upon to the Arcuate Nucleus. It causes a decrease in food intake and increased levels of fullness. Levels increase after eating. Only the activated form (PYY 3-36) can cross the Blood Brain Barrier. |
| What effect does PYY (3-36) have on the body and are there any differences in its effect between lean and obese? | PYY decreases feeding thus helps in weight loss. Both Obese and Lean people ate less when they were infused with PYY. PYY levels increase with increasing calories intake. Naturally PYY levels are lower in obese people and thus require a higher amount of calories to reach the same levels of PYY as lean people. |
| What controls the release of PYY? | The Vagus Nerve. In a rat study it was found that when the Vagus Nerve was removed levels of PYY decreased, thus showing some neural control from the Vagus Nerve. |
| What is Glucagon Like Peptide-1 (GLP-1)? | GLP-1 is a hormone which decreases desire to eat. It is produced in the GI tract (by the Ileum and Colon) and acts to decrease food intake and increase fullness ratings. Additionally it spikes after eating. |
| What controls the release of Ghrelin? | The Vagus Nerve and Stomach Distension (stomach emptying seems to stimulate release of Ghrelin) In rat studies it has been found that when the Vagus Nerve was removed Ghrelin levels did not spike. |
| What effect does eating pattern have on the activity of Ghrelin? | Eating 3 square meals causes spikes of Ghrelin whereas snacking throughout the day causes more continual constant elevation of Ghrelin levels. |
| Does the effect of Ghrelin on Obese people and Lean people differ? | Yes. Obese people are much more sensitive to Ghrelin than lean people. People, both lean and obese eat more when they are infused with Ghrelin. Mal-nourished people ate more when they were infused with Ghrelin. |
| How does Insulin modulate Glucose (G) entry into the cell? | Insulin translocates GLUT4 which allows Glucose (G) entry into the cell. This is achieved through the following process: Insulin (I) enters the cell which allows the IRS-1 to dock to the intracellular I receptor through the phosphoryllation of tyrosine. The IRS-1 is then phosphoryllated which activates PDK-1 which in turn activates PKB and PKC which then translocate GLUT4 to the cell membrane for G entry. |
| What effect does exercise have on Glucose entry into the cell? | Exercise translocates GLUT4 to the cell membrane without the need for the Insulin cascade. |
| What effects does being Obese have on the Insulin cascade and therefor Glucose entry into the cell? | Obesity causes Insulin Resistance. This means that the Insulin cascade is inhibited in obese people and a study found that because of this obese people have upto 53% less Glucose uptake than normal people. This is due to the inhibition of both tyrosine and IRS-1 phosphoryllation, both integral in the Insulin cascade. |
| What causes Insulin Resistance? | Insulin Resistance is caused by increased Serine Molecules. Serine increases with increasing levels of fat. Serine molecules cause a decrease in the phosphoryllation of tyrosine (key in I cascade thus it is inhibited). This is due to fat releasingh TNF-alpha which is the cause of the increased serine. Additionally fat releases Resistin which inhibits the effect that Insulin has on G entry. |
| What is Resistin and what role does it play in I resistance and thus glucose entry? | Resistin is released by fat, and it significantly inhibits the effect of I on G entry. Additionally location of stored fats has an effect on how much Resistin is released, abdominal fat releases the most Resistin and thus high levels of abdominal fat causes an increase in the chance of developing Coronary Heart Disease. |
| What is Adiponectin and what role does it play in Muscle fat oxidation? | Adiponectin is a protein which increases fat oxidation in the skeletal muscle. Malonyl-CoA is a co-enzyme which suppresses fat oxidation, Adiponectin increases fat oxidation through the inhibition of Malonyl-CoA. |
| Describe the relationship between Adiponectin and BMI: | As BMI increases levels of Adiponectin decrease thus lean people have higher levels of Adiponectin. |
| What are Adipocytokines? | They are proteins which are released by fat which has an effect on metabolic function through effect on metabolic regulators such as Adiponectin, Leptin and Resistin and TNF-alpha. They are detrimental to body health. |
| How does training effect Adipocytokines? | Exercise training has been found to help decrease TNF-alpha and Leptin levels (suppresses hunger) and increase Adiponectin (increases Fat Oxidation) in Obese people. |
| What effects do drug treatments such as Orlistat and Sibutramine have on Metabolic Regulators such as Leptin, Resistin and Adiponectin | Both S and O found to increase Weight Loss thus causing a decrease in Waist Circumference. Additionally they decreased Leptin (suppresses hunger) and Resistin (inhibits I effect on G entry) and increased Adiponectin (Incraeses fat oxidation in the muscle). |
| Define Hunger: | Discomfort caused by a lack of food (a craving for food). |
| Define Satiation: | Process that leads to the termination of eating, accompanied by a feeling of satisfaction. |
| Define Satiety: | Feeling of fullness that persists after eating, which potentially suppresses further energy intake until hunger returns. |
| What system controls Hunger and how does it work? | Cortico-Limbic System. It controls hunger through input from the Hypothalamus. 3 regions of the Hypothalamus play a role in Hunger, the Paraventricular System is 'turned on' to burn calories (stop eating), the Lateral Hypothalamic Area is 'turned on' to eat and the Arcuate Nucleus which is controlled by peripheral signals such as change in hunger hormones tells the body to eat (mainly influenced by Ghrelin). The Nucleus of the Solitary Tract sends impulses through neurons to determine which areas of the Hypothalamus are 'turned on'. |
| What hormones act to increase appetite? | Ghrehlin which is produced in the stomach. |
| What hormones act to decrease Appetite? | Peptide YY (3-36), Glucagon-like Peptide-1, Cholecystokinin, Pancreatic Polypeptide, Oxyntomodulin- all of which are produced by different sites in the GI Tract. |
| What is Ghrelin and how does it work? | Ghrelin acts to increase hunger. It is a 28 chain Amino Acid and must be modified before it becomes active (can cross the blood brain barrier). It is modified by Ser3 by n-octanoic acid (3rd AA in the chain). It acts upon the Arcuate Nucleus |
| How does Ghrelin affect the body? | Ghrelin acts to increase hunger. It has been found that G spikes in anticipation of food and then decreases after feeding due to increased Glucose levels which increases Insulin levels which reduces Ghrelin due to insulin acting as the off-switch for Ghrelin, thus Insulin is the mirror image of Ghrelin in terms of spikes and decreases. |
| Is Postprandial Lipaemia a Transient or Continual state? and what determines this? | Transient, Postprandial Lipaemia only lasts while Lipoprotein Lipase activity is elevated. |
| What happens to Intramuscular TAG following exercise? | It decreases due to exercise stimulating LPL activity thus we see greater TAG clearance. |
| What happens to Blood Flow when we exercise in the Postprandial Lipaemic State? and what effect does this have? | Blood flow increases to the skeletal muscle and the liver (2 key tissues in TAG clearance) thus TAG clearance is increased (TAG decrease). |
| What effect does regular exercise have with regard to Lipoproteins and TAG clearance? | Increases LPL activity, Increased FFA delivery to the skeletal muscle, Increased TAG clearance, When TAG is cleared via LDL we also see the transfer of cholesterol from VLDL to HDL's. |
| What effect does Insulin have with regard to Lipoproteins and TAG clearance? | If you are more Insulin resistant then you are more LPL resistant and thus TAG clearance is decreased and FFA release is increased, this means that with increased I resistance causes an increase in VLDL production (more atherogenic). |
| What is LCAT and what effect does it have on cholesterol? | LCAT is a key enzyme in cholesterol reversal, thus Macrophage become HDL's rather than LDL's and VLDL's. Exercise increases LCAT. |
| What is CETP and what effect does it have on cholesterol? | CETP causes cholesterol storage and deposit. Its activity is reduced with exercise training and thus with training increases cholesterol reversal which causes Macrophages to become HDL's. |
| What effect does increased levels of TAG rich VLDL's have on the other Lipoproteins and thus the body in general? | TAG rich VLDL's unload there TAG onto HDL's and LDL's which causes catabolization of the anti-atherogenic HDL's. Additionally the TAG unloaded on to LDL's causes them to become smaller and denser which makes them more atherogenic. This process causes increased cholesterol delivery to the artery walls, decreased levels of HDL's (additionally some HDL's become VLDL's through heavy deposit of cholesterol) |
| What is Postprandial Lipaemia? | High blood lipid content following a high fat meal. |
| What is the study protocol in inducing and thus studying the effects of Postprandial Lipaemia? | Either Exercise or Rest --> Normal Evening Meal--> High Fat meal in the morning --> Blood tests every hour for 6 hours (measure blood TAG content). |
| How does exercise effect the Lipaemic Response (Postprandial Lipaemia)? | It has been found that simply walking decreases the lipeamic response following a high fat meal (decreased TAG in the blood through increased TAG clearance). Additionally it has been found that Moderate Exercise improved TAG clearance greater than Low Intensity. Duration of exercise also has an effect on TAG clearance with increasing duration increasing TAG clearance (also the same amount of time exercise performed intermittently throughout the day improved TAG clearance greater than continual exercise). |
| Does Fat distribution on the body have an effect on health? | Yes, it has been found that a higher percentage of body fat distribution on the upper body increases the chance of developing Coronary Heart Disease. |
| What effect does exercise have on Cholesterol, LDL, TAG and HDL levels? | Exercise causes a decrease in total cholesterol amounts, decrease in LDL and TAG and an increase in the anti-atherogenic HDL's. |
| What happens to circulating TAG levels after eating? | Circulating TAG increases following a meal which in turn increases TAG which is transported as VLDL. The TAG is released from the Gut which enters the Thoracic Duct which then enters the blood which from there enters the Liver (at the liver some of the TAG is broken down into FFA, some passes straight through, but the FFA is repackaged into VLDL by APO B100) from the liver the TAG and VLDL enters the blood once again before through Lipoprotein Lipase in stored in the muscle. |
| How can asses Body Composition? | MRI, DEXA, Underwater Weighing, Skin Folds, Waist:Hip Ratio, BMI, Bio-electric Impedence. BMI is used as the standard industry measure, due to being cheap and can be used in studies with a large sample size. |
| What is the BMI equation? | Weight(kg)/Height2(M). It is the industry standard measure but it is bad as it does not reflect adiposity. |
| Explain the relationship between Obesity and chance of mortality and explain study findings in relation to this? | Higher levels of fat the higher chance of mortality (an increase of 5kg/m2 BMI increases chance of mortality by 30%). Throughout history the amount of physical labor has decreased and calorie intake has increased thus this plays a large part in the increase in Obesity levels. Although there are contradictory studies in regard to whether calorie intake has increased or decreased since 1971. Additionally a study has found that amounts of saturated fats eaten has decreased. Another study additionally found that on average men were 7.9kg heavier in 2000 than in 1986, and women were 5.1kg heavier in the same time period. |
| Been found in recent studies that calorie intake is decreasing, so what is causing the increase in obesity levels? | A decrease in Physical Activity. Studies have found that increasing numbers are not getting the Government recommended amount of weekly exercise- factors such as a decrease in walking/biking and an increase in use of cars have been found to be a major cause of this. This is directly related to Non Exercise Activity Time (NEAT) as found in a study on the Amish who have higher levels of NEAT, lower time spent on computers and lower Obesity levels. Thus we can assume that a decrease in NEAT is the major cause in increasing obesity levels. |
| What are the associated health risks of being Overweight or Obese? | Increased chance of mortality, increased disease risk, CVD, increased Blood Pressure, Increased chance of Strokes, Cancer, Diabetes, Increased chance of becoming Insulin resistant (less fat clearance from the blood). We also see an increase in plasma Triacyglycerol in Overweight and Obese people. Additionally we see higher levels of circulating TAG and FFA which are packaged in the atherogenic lipoproteins VLDL which thus increase cholesterol (Good HDL's are also decreased) thus there is an increased chance of Atherosclerosis. |
| What effect on Medical Prescriptions has the increase in commonality of Circulatory Diseases caused? | The increased prescription of statins. |
| What is the most common source of death? | Heart Disease, although rates are decreasing. |
| Give some examples of changeable and unchangeable causes of Cardiovascular Disease (CVD). | Changeable- Smoking, Exercise, Weight. Unchangeable- Gender, Age, Race. |
| What is the relationship between Obesity, Physical Activity and chance of CVD? | Obesity (BMI>30+) causes an increased chance of CVD whereas Physical Activity causes a decrease in the chance of CVD. Additionally it has been found that the higher the VO2 the lower chance of CVD. |
| What is Atherosclerosis? | Atherosclerosis (A) is the build up of fat on coronary walls (arteries). Arteries have 3 layers which are formed of Endothelial Cells (Adventitia, Media, Intima) and it is damage to these Endothelial Cells that causes A. |
| State and explain the 3 stages of Atherosclerosis: | 1) Plaque Initiation: This is whereby there is damage to the Endothelial cells of the artery walls. This damage causes Inflammatory Cytokines to recruit White Blood Cells to the damaged area. The WBC's attach to adhesion molecules and through a process called Diapedesis go through the wall. 2) Plaque Progression: Platelets, Endothelial Cells and Macrophages release growth factors and cytokines which promote smooth muscle cells to migrate from the Media into the Intima which causes a narrowing in the artery. This narrowing causes an increase in the deposit of blood lipid (oxidized LDL cholesterol). This additional cholesterol causes the Monocyte to mature to Macrophage and then to become Foam Cells. 3) Plaque Erosion: Macrophage/Foam Cells release Matrix Metalloproteinases (MMP's) and Reactive Oxygen Species (ROS) which cause cellular cytoxicity which causes Necrotic Core Formation. |
| What role does Nitric Oxide play in Atherosclerosis? | NO is synthesized by the enzyme Endothelial Nitric Oxide Synthase (ENOS) and it flows in normal arteries. Its role is to decrease White Blood Cell Adhesion to the Endothelial Cell walls. Thus preventing Diapedesis. The branch points in arteries are areas of high risk due to the decreased amount of ENOS and thus NO that flows there. |
| Roughly how much Cholesterol do we have in the body? | Approximately 140g in the body, additionally we eat approx 1g per day and excrete 1g per day thus maintaining amounts. |
| What are the 3 types of Lipoproteins and give a brief explanation: | VLDL's are rich in Triacylglyceride and are large in size (>30nm). They are very bad and are atherogenic (cause Atherosclerosis- formed of Apoliprotein B) and because of this increase the risk of CVD. LDL's are packed with Cholesterol and are 20-22nm in size, again these are atherogenic and cause CVD. HDL's are packed with Protein and Phospholipid and are small in size (9-15nm) and are anti-atherogenic (Apoliprotein A) and thus fights against CVD. |
| What happens to LDL's and HDL's in relation to Atherosclerosis? | LDL's when oxidised form Oxidised LDL which speeds up the process of Monocyte changing to a Macrophage and finally a Foam Cell. Whereas HDL's inhibit A by inhibiting adhesion molecule formation, inhibiting LDL oxidation and by promoting cholesterol leaving Foam Cells. |
| What effect does exercise have on LDL's and HDL's? | Exercise increases HDL's and decreases amounts of both LDL's and Triacylglyceride. |
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