metabolism

1. Definebasal metabolic rate. Name some cellular functions that require ATP as a fuel source. Name some heat producing cellular functions.

Amount of energy it takes to keep you alive BMR is the lowest metabolic rate an individual can have. Heat can be produced by metabolism and shivering (muscle movement) Activity, caffeine, eating, body temp, and epinephrine are factors that will increase metabolism

1. Explain what a Respiratory Exchange Ratio (also called a respiratory quotient) is. How is it measured? What is a normal resting value? What does the RER increase during exercise? Why can it go above 1?

Tells you about the kind of substrate you are consuming to produce ATP VCO2 (producing) / VO2 (consuming) RER = 0.7 = burning fat RER = 1.0 = burning glucose Increase during exercise because of lactic acid (once anaerobic threshold is reached), raises above 1 when VCO2 increase, H+ from lactic acid causes an increase in CO2

1. Explain how the immediate increase in ventilation at the onset of exercise is a feed forward mechanism.

At the onset of exercise, there is no immediate change in PO2, PCO2, or pH. Rather, the movement of muscles acts as a feed forward mechanism for the body to prepare for exercise by prematurely increasing ventilation. Activates proprioceptors which detect change in muscle length, tension, and joint angle

1. Compare and contrast direct (heat) and indirect (oxygen) calorimetrymethods for measuring the BMR. Which method is used in the exercise lab and why?

Direct calorimetry is where the food is burned in a bomb calorimeter and the heat released is trapped and measured. One kilocalorie is the amount of heat needed to raise the temperature of one liter of water by 1 degree Celsius. Indirect calorimetry is the measurement of oxygen consumption, which is the rate at which the body consumes oxygen as it metabolizes nutrients. Indirect/oxygen calorimetry is used in this experiment

Compare and contrast the internal work and heat production as measured by VO2and the external work performed on the bicycle ergometer. This is basically the efficiency calculation we perform in the exercise lab.

Efficiency = work output / work input (Minimum amount of energy to bike at 100 w if 100% efficient) / (work we put into the system - this includes the BMR) The internal work was empirically determined to be 1.4kcal/min = 100 watts (output) based on the amount of heat required to raise a liter of water by 1 degree centigrade (kcal) over a certain period of time. At 100 watts, our subject had a VO2 of 1.68 L/min. At rest, VO2 was .37 L/min. To find subject's input, (VO2 Exercise- VO2 Rest) x 4.8 kcal/L O2. Then take output / input to find efficiency. 1.4 / (1.68 - 0.37) x 4.8 = 1.4/6.288 x 100 = 22.3% efficiency

1. Explain the relationship between increased fat breakdown (lipolysis and beta oxidation) and the production of ketones(by product of excess acetyl CoA production).

Fatty acids in the liver are converted to acetyl CoA, but the lover has a very low concentration of the enzyme oxaloacetate that allows fatty acids to be made into ATP, therefore the lover converts fatty acids into ketone bodies which the brain can use to make ATP in prolonged starvation lipolysis breaks a TGL into glycerol and 3 FA. The 3 FA are oxidizied into acetyl-CoA, however sometimes acetyl-CoA is made faster than the krebs cycle can burn it so the accumulation of it creates a ketone. Ketone can be sent out to the body to be used for E

1. Identify the direction of glucose flow between the liver cells and the blood and the channel through which the glucose is moving. Describe the concentration gradient that exists between the liver cells and the blood.

GLUT2 transporters are always present in the plasma membrane of the liver to transport glucose, just depends on the gradient for the way glucose moves In the absorptive/fed state, plasma glucose levels are high, so glucose moves into the liver cell and is phosphorylated by hexokinase (which is activated by insulin binding) In the postabsorptive/fasted state, plasma glucose levels are low so the liver produces glucose and it moves out into the blood to be used by the brain

1. Describe the actions of glucagonon the liver and the regulation of glucagon secretion.

Glucagon targets the liver forgluconeogenesis - stimulates reactions and some triglyceride and glycogen breakdown Secretion due to: - Decrease in glucose and or insulin - Increase plasma amino acids

1. Describe the journey that glucose, amino acids take from their site of absorption in the GI tract to the peripheral cells where they are used and stored. Remember for our discussions of the GI tract that amino acids and sugars are absorbed into the venous blood and carried by the hepatic portal veinto the liver.

Glucose from GI tract travels into the blood via secondary active transport and facilitated diffusion - It can reach the liver via the hepatic portal vein and can be combined with fatty acids and synthesize triglycerides (fat) - It can go to most tissues and be used to make ATP (oxidation) - Goes to skeletal muscle and liver for glycogen storage Amino acids from GI tract enter blood by secondary active transport - Amino acid from the blood undergo deamination to form keto acids in the liver - Small amount can be oxidized to make ATP in liver (from the keto acids) - Amino acids in liver can be used for protein synthesis - Keto acids can be converted into triglycerides (from excess) - Keto acids can also be made into glucose which can also be made in triglycerides Glucose is absorbed in the GI tract into the hepatic portal system and brought to the liver to be metabolized. the liver turns most of the glucose into glycogen. If there is extra glucose, it is turned into fat! Glucose also goes to adipose tissue to be used as an energy source. excess glucose is then stored as triglyceride in adipose tissue. glucose goes to muscle and is stored as glycogen. Glucose is used as an energy source in almost all cells in the body.Amino Acids are absorbed in the GI tract and put into the hepatic portal system to be sent to the liver. some are deaminated and turned into urea. Carbon remaining can be used as energy, and the extra is stored as fatty acid. AA goes to muscle to be turned into protein.

1. Describeglucose sparingand explain how it supports the energy needs of the body during the postabsorptive state; in other words, explain how the body uses TGLs for energy so that glucose is spared for the brain.

Glucose sparing limits the tissues use of sugar so that the brain can have access to it In the absence of insulin, glucose transporters are removed from the plasma membrane and sit in vesicles so that adipose tissue and muscle do not have access to glucose All other tissues (except for the brain and liver) can use fatty acids / triglycerides to make ATP

1. Explain how glygcogenesis(synthesis of glycogen) and lipogenesis(synthesis of fat) in the liver prevent large spikes of plasma glucose after a meal.

Glycogenesis occurs when there is an excess of glucose and the extra is turned into glycogen. After the maximum amount of glycogen is created, excess glucose is turned into fat via lipogenesis. This transformation keeps there from being major spikes in blood glucose levels after eating.

1. Explain how insulin promotes the reactions of the absorptive state. Insulin effects the liver differently than the skeletal muscle and fat tissue. Explain the effects of insulin on liver, muscle and fat.

In the absorptive/fed state, insulin activates hexo-kinase, which phosphorylates glucose into glucose-6-phosphate. This keeps free intracellular glucose low relative to free plasma concentration. Now glucose diffuses into hepatocytes on the GLUT2 transporter operating in the reverse direction.Insulin enhances cellular utilization and storage of glucose by activating and inhibiting different enzymes.Insulin enhances utilization of amino acids by activating enzymes used in protein synthesis.Insulin promotes fat synthesis and inhibits B-oxidation of fatty acids. Insulin causes the liver to take up glucose and other cells to increase glucose transport

1. During the post absorptive state, explain how the absence of insulin prevent the skeletal muscle and fat tissue from having access to the glucose in the blood.

In the post absorptive state there is no insulin since plasma glucose levels are low No insulin = no binding and translocation of transporters So, transporter move back into their vesicles and wait for the next insulin stimulation Since there are no glucose transporter on the membrane anymore, they have no access to glucose

1. Explain how the glycogenolysis(breakdown of glycogen) and gluconeogenesis(synthesis of new glucose from non-carbohydrate sources) by the liver maintains plasma glucose level; remember that glucose is the most important substrate for brain function during the postabsorptive state.

In the postabsorptive state, plasma glucose levels are low The liver is responsible for making glucose for the brain The liver breaks down its glycogen stores through glycogenolysis to produce glucose Amino acids coming from protein break down are deaminated into keto acid which can be converted to glucose or used to make ATP

1. Describe negative feedback regulation of insulinby blood glucose levels.

Insulin is produced by beta cells in the pancreas and it helps to decrease the plasma glucose levels - Cause glucose to move down its concentration gradient into cells since it is high in the plasma - Increases glucose transport - Enhances cellular utilization and storage of glucose - Enhances utilization of amino acids - Promotes fat synthesis Insulin is produced in the pancreas by islets of Langerhans cells (specifically the beta cells). In the fed state, insulin dominates over glucagon and the body undergoes net anabolism (making larger molecules from smaller ones). Its release is triggered by increased plasma glucose, Increased plasma amino acids, feedforward effects of GI hormones, and autonomic nervous system (parasympathetic) activity.Because insulin activity is triggered by plasma glucose levels and acts to decrease plasma glucose by allowing it to enter into cells, it has a negative feedback mechanism.Insulin causes GLUT receptors to insert on the basolateral side of cells, increasing its absorption, when blood glucose levels are above 100 mg/dL

1. Discuss the storage of absorbed triglyceridefrom a meal and triglycerides synthesized by the liver. Remember that a TGL is three fatty acids covalently bound to a glycerol backbone. This the most abundant energy storage molecule in the body.

Triglycerides from a meal (dieatary triglycerides) from the intestinal cells into the blood as chylomicrons - these are broken down into a monoglyceride and 2 fatty acids so they can be transported into adipose tissue where they are reassembled into triglycerides and stored Remnants from the broken-down chylomicron are sent to the liver, combined with other synthesized fats and sent back to the blood as VLDLs Triglycerides from a meal are sent to the lymph and to the adipose tissue. It travels as a fatty acid and monoglyceride because a triglyceride is too large to pass through the membrane and reassembled as triglycerides to be stored in the adipose tissue. triglycerides synthesized in the liver from glucose and AA are also sent to the adipose tissue for storage.

1. Describe the relationship between diabetes mellitus and hyperglycemia. Basically if insulin helps the cells of the body use glucose, then DM (an inability to make or respond to insulin) will cause high levels of blood glucose (hyperglycemia).

Type 1 - insulin deficiency Type 2 - insulin resistant Causes elevated plasma glucose concentration = hyperglycemia Diabetes causes hyperglycemia because insulin cannot work to reduce plasma glucose People with diabetes either do not produce insulin or are resistant to the affects of insulin. Because of this, their body does not receive the signals to put GLUT channels into their cells, cannot take glucose into their cells, and end up with high levels of blood glucose.

1. Describe how the cardiovascular and pulmonary systems change to support exercise function and draw conclusions about which system is best suited to support high levels of exercise.

Ventilation and heart rate increase Ventilation is best suited to support high levels of exercise because it is not limited Pulmonary system: arterial Po2, arterial Pco2, and venous Po2 don't change hardly at all with increased exercise, what does increase is the ventilation, Cardiovascular: Cardiac output increases with exercise due to increased venous return and sympathetic stimulation of HR and contractility, blood flow also increases dramatically when skeletal muscle arterioles dilate. Arterioles in other tissues constrict. Decreased tissue O2 and glucose or increased muscle temp, CO2, and acid act as paracrine signals and cause local vasodilation, Mean arterial BP increases slightly as exercise intensity increases. The pulmonary system is better suited for supporting exercise. Cardiac output is a limiting factor for the cardiovascular system because when stroke volume and heart rate increase, there comes a point when the heart is pumping faster than the it can fill up all the way before it pumps again.