kin 321 notes test 1
kin 321 notes test 1 KIN 322
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Date Created: 02/02/16
KIN 321 Study guide Test 1 Lecture 1 thermodynamics study of energy exchange in physical science bioenergetics the study of the exchange of energy in the biological world mechanical system Chemical energy coal gasoline9heat9mechanical work Biological system Chemical energy food9 ATP and Heat cellular work as temperature increases the rate of the reaction also increases exponenUaHy 1st law of thermodynamics energy can neither be created nor destroyed but can be converted from one form to another 2nOI law of thermodynamics the exchange of energy is imperfect and some energy will escape in the form of heat ATP is used for many functions 1 chemical work driving reactions that are nonspontaneous 2 transport moving substances against their concentration gradients Na K pump 3 mechanical work cross bridge cycling ATP H209ADP Pi ATP changes very little even during intense exercise ATP is well buffered why if you deplete ATP the thick and thin laments can t dissociate If that occurred in the diaphragm muscles or in the heart you would die so the body is good at rebuilding ATP and fatiguing to assure you don t run out of ATP metabolism is the sum of all energy transformations within an organism It is hard to measure but it is the rate of heat production caorie the heat required to raise 1g of water by 1 degree C a kcal is 1000 calories caorimetry is a measurement of heat to determine metabolic rate direct calorimetry measure heat produced Ex Lavoisier s direct calorimeter measures 80kcal of heat to melt 1000g of ice Ex Use of bomb calorimeter indirect calorimetry measure oxygen consumption room calorimeter can use both direct and indirect measurements via direct and indirect calorimetry carbohydrates give 42kcalg and fats give 95kcalg via indirect calorimetry inside the body protein gives 42kcalg while outside the body bomb calorimetry values for protein are 57 bomb calorimeter can use nitrogen as a fuel source but the body cannot RQ C02 produced02 consumed RQ is 7 for fat and for a starving individual since they are relying only on fat 8 for protein 1 for carbohydrates and 82 for a mixed diet Lecture 2 functions of food 1 provision of energy 2 growth and development 3 regulation of metabolism dietary carbohydrates formula CHzO shows a ratio of 121 dietary carbohydrates are in the form of sugar starches and ber from plants cellulose caoric density of carbohydrates is 4kcag monosaccharides glucose fructose gaactose disaccharides sucrose glucose fructose lactose glucose gaactose and maltose glucose glucose oigosaccharides and polysaccharides starch complex CHO ber cellulose glycogen dietary lipids are insoluble in water and exist as liquids oils or solids fats dietary lipids structure carboxyl group COOH at one end and methyl group at other end separated by hydrocarbon chain that varies in length and degree of saturation dietary lipids caloric density is 9kcalg Simple dietary lipids are triglycerides fatty acids of dietary lipids vary in carbon chain length with the most common being 1424 carbons There is an even number of carbons because the carbons are lost in pairs of 2 short chain fatty acids have 6 carbons or less medium chain fatty acids have between 8 and 10 carbons long chain fatty acids have over 12 carbons saturated fatty acids no double bonds monounsaturated fatty acids one double bond poyunsaturated fatty acids more than one double bond most unsaturated fatty acids with double bonds are in the cis con guration processed foods often have trans unsaturated fatty acids H are on opposite sides of the double bond Termed partially hydrogenated trans fats have characteristics similar to saturated fatty acids but tend to be more solid at room temperature and have improved shelf life They raise LDL levels and lower HDL levels compound lipids include phospholipids and lipoproteins chylomicrons VLDLs LDLs and HDLs dietary proteins formed by the combo of up to 20 different amino acids via peptide bonds dietary proteins consist of CH amino group with nitrogen carboxylic acid group and a side chain caoric density of proteins is 4kcag acoho is a nonessential nutrient and has 7kcalg and moderate intake may increase HDL levels Gl function is important to exercise GI disturbances are not uncommon and may affect performance GI function is important to proper delivery of water minerals and macronutrients and can delay fatigue Dehydration hyperthermia and carbohydrate depletion are common sources of fatigue mechanica digestion begins in the mouth the liver secretes bile for lipid emulsi cation the gallbladder stores bile the duodenum digests food and absorbs nutrients water and electrolytes the stomach secretes HCL and proteases the pancreas secretes NaHC03 and digestive enzymes the ileum is responsible for the absorption of water and electrolytes spanchnic circulation the celiac artery is a branch of the abdominal aorta in the stomach The mesenteric artery feeds the intestines spleen and pancreas Both arteries lead to the portal vein which goes to the liver monosaccharides and amino acids go through but not long chain fats Then comes the hepatic veins then vena cava then general circulation the stomach is a holding tank Only small amounts of alcohol and vitamin 812 are absorbed there The stomach is distensible 50mL fasting and expands to 10006000mL fed most absorption of water and solute occurs in the intestinal tract Therefore gastric emptying poses a limiting factor for absorption rapid rates of gastric emptying need to keep up with sweat rates as high as 24Lhr method of measurement for gastric emptying People ingest a uid with a dye and the dye will only disappear if it leaves the stomach gastric emptying is under neural and hormonal control Ensures delivery of water and solute at a rate slightly less than the intestine s absorptive capacity gastric emptying increases exponentially with increasing gastric vmume as volume increases gastric emptying rate increases as energy content increases gastric emptying rate decreases less than or equal to 68 68g CH20L is recommended as osmolality increases presence of glucose polymers the emptying rate decreases exercise greater than 7075 V02 max decreases gastric emptying rate dehydration decreases gastric emptying rate optima uidCHO replacement is 3060g CHOhr in 68 solution ingested at a rate of 6001200mlhr the purpose of digestion of carbohydrates is to reduce di and polysaccharides to monosaccharides the salivary glands secrete salivary amylase which goes to the mouth and stomach the pancreas secretes pancreatic amylase maltase sucrase and lactase which go to the small intestine Carbohydrate digestion of large starches to oligosaccharides maltoriose and maltose occurs primarily in the mouth and the stomach digestion of disaccharides to monosaccharides occurs primarily on brush border of the small intestine lumen the purpose of lipid digestion is to reduce triglycerides to fatty acids the mouth contains lingual lipase which comes from the salivary glands the stomach contains gastric lipase which comes from the stomach the small intestine contains bile which comes from the gallbladder the small intestine has pancreatic lipase which comes from the pancreas ipid digestion sequence large lipid droplet in the small intestine bile acids emulsify fat into smaller droplets lipase released from the pancreas breaks down fat into fatty acids diacylglycerols and monoacylgylcerols absorption through villi via micelles the purpose of protein digestion is to reduce proteins to tri and dipeptides and amino acids pepsin and HCI come from the stomach and are in the stomach the small intestine has trypsin chemotrypsin carboxypeptidase and elastase which come from the pancreas pathway for protein digestion protein is cleaved into tripeptides with pepsin from the stomach and then trypsin chemotrypsin carboxypeptidase from pancrease cleave tripeptide to dipeptide the small intestine is divided into three parts 1 duodenum rst 3m 2 Jejunum middle 12m 3 ileum last 1m surface area of the small intestine is increased up to 600 fold by 1 circular folds x3 2 villi x10 3 brush border x20 intestinal absorption of all solutes is driven by a concentration gradient from high lumen to low concentration epithelial cells water watersoluble particles monosaccharides amino acids and electrolytes enter hepatic portal vein water insoluble fatty acids enter lymph duct gucose and galactose are actively transported across the epithelium by sodium and glucose linked transporter molecule SGLT1 fructose moves by facilitated transport via GLUT5 It is faster than passive diffusion but slower than the active transport of glucose and galactose once inside epithelial cell glucose galactose and fructose exit basolateral membrane to portal circulation via GLUT 2 fatty acids digested from triglycerides are formed into micelles for absorption absorbed fatty acids reformed with cholesterol and phospholipids protein coat to form chylomicrons inside epithelial cells 85 T6 7 cholesterol 7 phospholipids 1 protein chyomicrons enter circulation through thoracic duct in the neck and deliver contents to a variety of tissues including liver adipose and skeletal muscle monosacchardies are absorbed via active transport and facilitated transport and their target is the liver fatty acids 410C long are absorbed via passive diffusion and their target is the liver fatty acids longer than 12C are absorbed via passive diffusion and their target is the lymph system amino acids are absorbed via active transport and their target is the liver water absorption is driven by an osmotic gradient from low to high osmolality the duodenum first 25cm of small intestine has a leaky epithelium and acts as an osmotic equilibrator hypotonic uid water entering the duodenum undergoes rapid absorption via osmosis hypertonic uid fruit juice entering the duodenum has secretions of uid into the lumen to lower osmolality diute uid is for later absorption water absorption can occur passively via osmosis or actively through SGLT1 SGLT1 mediated water absorption may account for 70 of total water absorption Lecture 3 ATP is in short supply and is enough for a few seconds of all out activity so we need to resynthesize ATP using 3 energy systems 1 Immediate located in the cytosol rate is very rapid fuel source is creatine phosphate 2 Glycolysis located in the cytosol rate is rapid fuel sources are glucose and muscle glycogen 3 Oxidative phosphorylation located in the mitochondria rate is slow fuel source is muscle glycogen glucose lactate and lipids resynthesis rates of ATP 1 creatine phosphate max ATP resynthesis rate is 9 and there is no time until max rate is reached 2 glycolysis max ATP resynthesis rate is 45 and time until max rate is reached is 510s 3 glycogen oxidation max ATP resynthesis rate is 28 and time until max rate is reached is several minutes 4 glucose oxidation max ATP resynthesis rate is land time until max rate is reached is greater than 45 minutes 5 fat oxidation max ATP resynthesis rate is 1 and time until max rate is reached is greater than 6090 mins creatine phosphate is 36x greater than ATP creatine kinase turns ADP CP ATP C together ATP and CP can sustain activities with a duration of no longer than 515 seconds creatine kinase is activated by a decrease in ATPADP ratio high intensity short duration bouts of exercise gycolysis is the breakdown of glucose and glycogen that does not require oxygen Louis Pasteur tested glycoysis in unicellular organisms yeast in asks with and without oxygen In the test tubes without oxygen lactate accumulated This shows that glycolysis occurs in many tissues even when oxygen is abundant The terms nonoxidative and oxidative glycolysis are out of date Slow glycolysis aerobic glycolysis provides a net of 3638 ATP There is little need to produce lactate at rest and low intensity exercise because the rate of pyruvate production is matched by the rate of pyruvate oxidation Also the rate of NAD regeneration via mitochondrial shuttles is adequate Rapid glycolysis anaerobic glycolysis provides a net of 2 ATP There is a great need to produce lactate during high intensity exercise because the rate of pyruvate production exceeds the rate of pyruvate oxidation Also the rate of NAD regeneration via mitochondrial shuttles is inadequate lactate accumulation results from conditions in which glycolytic production of pyruvate exceeds the rate of mitochondrial pyruvate oxidation not necessarily when oxygen is not available gycolysis is always occurring in red blood cells gycolysis occurs in type B bers across a wide range of exercise intensities gycolysis occurs in type bers only at max it is a RUMOR that lactate is a dead end metabolite that results from the lack of adequate oxygen supply lactate is produced under most conditions when pyruvate and NADH from the sarcoplasm enter the mitochondria to undergo oxidation in the Krebs Cycle and the Electron Transport chain respectively lactate is produced when the glycolytic rate is greater than the mitochondrial respiration rate NADH is oxidized while pyruvate is reduced to lactate in the sarcoplasm the net formation of lactate or pyruvate depends on the relative glycolytic and mitochondrial activities and not the presence of oxygen fates of lactate 1 oxidation at the site of production 2 oxidation at a distant site 3 used by the liver to make new glucose via gluconeogenesis the cori cycle skeletal muscle cannot release glucose into the bloodstream but it can release lactate and pyruvate that can be taken up by the liver and converted to glucose This provides a means for shuttling carbohydrate from skeletal muscle to tissues such as the brain that are reliant on glucose the cellcell lactate shuttle lacate produced in some sites may be oxidized in adjacent or distant sites Type B bers are mostly producers Type bers and the heart are mostly sites of oxidation Therefore glycogenolysis in one cell provides fuel supply for oxidation by another cell study looked at trained male cyclists for 90 mins at 65 55 and 55 with lactate clamp of V02 peak showed that lactate is the most ef cient form of carbohydrate for muscle to oxidize because it doesn t require the investment of energy unlike both glucose and glycogen NADH and NAD diffuse poorly across the inner mitochondrial membrane Therefore NADH is transferred into the mitochondria via 3 shuttles 1 malate aspartate uses NADH 2 glycerol phosphate uses FADH 3 intracellular lactate uses pyruvate lactate carrier MCT Lactate dehydrogenase is used to turn lactate to pyruvate while NAD becomes NADH all three carrier systems regenerate NAD and shuttle NADH to mitochondria for ATP production the intrcellular lactate shuttle is the only shuttle that shuttles the substrate into the mitochondria for ATP production it is a RUMOR that lactate causes fatigue by leading to lactate acidosis metaboic acidosis when glycolytic production of ATP glucose or glycogen turns to pyruvate leads to net H production The production of lactate consumes protons H as well as produces NAD Lecture 4 lipid mobilization depends on 1 rate of lipolysis 2 rate of reesteri cation 3 rate of fatty acid export via circulation the proportion of fatty acids reesteri ed is high during rest and high intensity exercise the transition from rest to exercise results in a decrease in the proportion of fatty acids reesteri ed 5070 is reesteri ed at rest and 2035 during exercise fatty acids are transported in the plasma in association with the protein albumin There are three high af nity fatty acid binding sites fatty acid export from adipose tissue is dependent on fatty acidalbumin ratio since albumin has a decreasing affinity as more fatty acids bind It is also dependent on adipose tissue blood ow if the increase in fatty acids via lipolysis is greater than the increase in adipose blood ow there is an increase in the fatty acid albumin ratio and this an increase in reesteri cation fatty acids are taken up by skeletal and cardiac muscle which originate from plasma free fatty acid pool and fatty acids are bound to albumin There is likely also some uptake from lipoproteins with lipoprotein lipase acting upon them is the uptake of fatty acids by skeletal muscle correlated with plasma concentration through passive diffusion No saturation kinetics show that lipid uptake is likely facilitated transport across the sarcolemma there are three key fatty acid transporters 1 Sarcolemmal FABP membrane bound 2 FATCD36 translocated from sarcoplasm Translocation is initiated by insulin and muscle contraction 3 Cytosolic FABP the abundance of fatty acid transporters increases with endurance training and high fatlow carb diets fatty acids in the sarcoplasm have two potential fate they can be esteri ed into intramuscular triglycerides IMTG or transported into the mitochondria for oxidation pior to either esteri cation or mitochondrial transport fatty acids are activated ATP is required and results in the formation of fatty acylcoA This occurs in the outer mitochondrial membrane fatty acids must enter the mitochondrial matrix to undergo oxidation Short and medium chain fatty acyl coA enter via speci c carrier proteins and are under little to no regulation Long chain fattyacyl coA enters via carnitine and carnitine acyl transferase enzymes mitochondria transport of fatty acids is likely the most important rate limiting step of lipid oxidation with CATI being the rate limiting enzyme carnitine de cient patients have a reduced capacity to oxidize lipids at rest and during exercise once inside the mitochondria fatty acyl coA undergoes BOxidation beta oxidation cleaves two carbons from fatty acids per cycle end products of beta oxidation are acetyl coA and reducing equivalents such as NADH and FADH acety coA enters the kreb s cycle while the reducing equivalents enter the electron transport chain compete oxidation of a typical fatty acid palmitate results in a net production of 129 ATP promoters of fatty acid oxidation Low acetyl CoA low NADHNAD low intensity exercise CHO depletion nhibitors of fatty acid oxidation High acetyl CoA high NADHNAD high intensity exercise CHO supplementation ntramuscuar triglyceride use during exercise may be limited during normal exercise conditions 6090 minutes of moderate intensity exercise in the fed state with carbohydrate supplementation another condition in which IMTG use may be important is during exercise recovery MTG use during recovery was tested with well trained males consuming a high carbohydrate diet before and after exhaustive exercise bouts up to 20 minutes at 75 of V02 max then alternating 2 minute bouts at 90 and 50 V02 max until exhaustion at about 90 minutes ooked at metabolism during recovery in healthy moderately active men and women Were told to exercise 89 min at 45 V02 peak and 60 min at 65 V02 peak They were matched on energy expenditure and time matched control Recovery consists of 3 hours with no food intake with wheelchair transport as needed showed low RER values during recovery from exercise which means heavy reliance on fat as a fuel source although Carbohydrate is the primary energy source during moderate to high intensity exercise SO80 of energy expenditure lipid oxidation is substantial during recovery 6585 of energy expenditure lipid oxidation is the same during recovery from 4565 V02 peak as long as exercise energy expenditure is the same Lecture 5 all amino acids contain both amino NH3 and carboxyl COO groups use of amino acids as fuel sources is limited to fasting and prolonged exercise must remove N containing amino group in order to use remaining carbon skeletons as fuel source nitrogen can be removed from amino acids by 1 Oxidative deamination occurs only in the mitochondria of the liver and involves NAD as an oxidizing agent 2 Transamination occurs in many tissues including skeletal muscle and involves the transfer of nitrogen urea cycle is a means of nitrogen excretion The NH4 is a product of oxidative deamination and it combines with C02 to form carbamyl phosphate Laspartate is a product of transamination Urea goes to the kidneys for excretion in urine most amino acid carbon skeletons are converted to either 1 pyruvate 2 acetylcoA 3 TCA cycle intermediates branch chain amino acids Ieucine isoleucine and valine are preferentially oxidized by skeletal muscle compared to other amino acids the use of BCAA as a fuel source begins with transamination to glutamate guconeogenesis is essentially the reverse of glycolysis with the following enzymes that differ 1 Pyruvate oxaloacetate via pyruvate carboxylase 2 oxaloacetate phosphoenolpyruvate via phosphoenolpyruvate carboxykinase 3 fructose 16 bisphosphate fructose 6 phosphate via fructose 16 bisphosphatase 4 glucose 6 phosphate glucose phosphate via glucose 6 phosphatase amino acids undergo removal of nitrogen and then go to the urea cycle where urea is excreted in urine the carbon skeleton of the amino acid becomes acetyl coA or a TCA cycle intermediate or Pyruvate which all go into the TCA cycle Pyruvate can also become alanine and go through gluconeogenesis iver glycogen turns into glucose 6p when there is high epinephrine and glucagon and low insulin muscle glycogen turns to glucose 6P when there is high epinephrine AMP Ca and low ATPADP ratio gucose 6P turns to pyruvate when there is a low ATPADP ratio high ADP AMP and pi This would be inhibited by high ATPADP and H pyruvate can either turn to lactate or to acetyl coA adipose triglycerides turn to free fatty acids when epinephrine glucagon cortisol and caffeine are high This is inhibited by insulin and lactate IMTG turn to fatty acids when epinephrine cortisol and caffeine are high lnsulin inhibits this pathway fatty acids go to the mitochondria for beta oxidation when there is a low glycolytic rate A high glycolytic rate inhibits this endogenous fuel stores are mainly in the form of adipose lipid 90000120000kca IMTG 2000 kcal muscle glycogen 1600 1800kca and liver glycogen 400600 kcal fat is a very efficient form of energy storage 9kcalg for fat vs 4kcalg for carboydrates Each gram of carbohydrate is stored with 3g of water which shows storage inefficiency carbohydrate is a more efficient source of energy during exercise greater kcalL 02 consumed than fat higher rates of ATP resynthesis are possible with carbohydrate than fat exercise across a wide range of intensities derives most ATP re synthesis from oxidation of acetylcoA and other TCA cycle intermediates the ability of macronutrients to meet acetyl coA demand during exercise in large part determines their relative use and substrate partitioning factors in uencing fuel use during exercise include 1 intensityenergy ux 2 duration 3 fuel availability diet and exercise duration 4gender 5 ambient temperature exercise intensity is a primary factor and all others are secondary the crossover point to using more carbs than fat is near 55 v02 max why does relative contribution of lipids to energy expenditure decrease with increasing intensity Higher necessary ATP resynthesis rates Carbohydrate metabolism regulates lipid metabolism and increased glycolytic ux likely decreases long chain fatty acid transport into mitochondria Increased recruitment of fast twitch bers Decreased FFA availability epinephrine induced lipolysis is counteracted by reduced adipose blood ow and lactate during lowmoderate exercise 2035 of fats are reesterified during high intensity exercise 7090 of fats are reesterified due to reduced adipose tissue blood ow as exercise intensity increases there is an increase in liver and muscle glycogenolysis and an increase in lipolysis that is counterbalanced by reduced ATBF increasing exercise duration results in increased reliance on plasma sources of fuel glucose and free fatty acids and decreased reliance on intramuscular fuel sources glycogen IMTG and increased reliance on lipids and decreased reliance on carbs approximate depletion times of carbohydrate fuel sources during moderate intensity exercise Muscle glycogen in about 6090 mins and liver glycogen in about 80120 mins the longer the duration of exercise the more you rely of fat for ATP resynthesis carbohydrates are the preferred fuel source during moderate intensity exercise carbohydrate supplementation leads to increased reliance on carbohydrates during exercise hepatic glucose production is reduced which spares liver glycogen Muscle glycogen use is likely not affected endurance training adaptations favor greater reliance on lipids at the same absolute intensity training adaptations include increased capillary density increased expression of sarcolemmal fatty acid transporters increased mitochondrial density higher activities of beta oxidative enzymes and higher activities of TCA cycle enzymes pattern of fuel use at the same relative intensity is unaltered for the most part by endurance training Still tied to relative exercise intensity likely by catecholamine and hormonal response Carbohydrate needs are not reduced by endurance training and are instead likely increased due to improved ability to sustain higher exercise intensities and longer exercise durations Lecture 6 hormones are chemical messengers that act either locally acetylcholine norepinepherine or generally epinephrine norepinepherine insulin glucagon etc hormones interact hormones interact with binding sites of target tissues Poypeptide hormones interact with receptors on cell surfaces sterioid hormones move through cell membranes and interact with the cell nucleus hormones generally have 3 effects 1 alter permeability of cell membrane to metabolites or ions 2 activate an enzyme or second messenger cAMP 3 activate genetic apparatus to manufacture intracellular proteins epinepherine stimulates adenyl cyclase which turns ATP into cAMP which thus turns Inactive PK to active PK and this turns inactive HSL to active HSL and the physiological responses are 1 glycogenolysis 2 triglyceride hydrolysis 3 hormone release if insulin is present it binds to the insulin receptor on the adipocyte and phosphodiesterase is turned on which turns cAMP to AMP which presents the PK cascade from occurring hormones are secreted from endocrine glands hypothamus tells the anterior pituitary gland to release Growth Hormone the adrenal medulla releases epinephrine and norepinepherine the adrenal cortex releases cortisol the pancreas releases insulin and glucagon the ovaries release estrogen and progesterone hormones interact with tissues via receptors potency is a function of 1 concentration 2 receptor density 3 durabilityhalf life the hypothalamus controls the activity of the anterior and posterior pituitary glands the hypothalamus receives neural input and is sensitive to blood metabolite concentrations growth hormone is essential for normal growth it stimulates protein synthesis and bone growth growth hormone increases during exercise it mobilizes fatty acids from adipose tissue and aids in the maintenance of blood glucose by increasing gluconeogenesis and reducing glucose uptake by adipose Ussue the adrenal medulla secretes epinephrine and norepinepherine and promotes ipoysis as well as liver and muscle glycogenolysis the adrenal cortex secretes 1 Aldosterone maintain plasma Na and K and regulate blood pressure 2 cortisol promotes lipolysis protein catabolism and gluconeogenesis the adrenal medulla s release of catecholamines is heavily in uenced by neural input from the sympathetic nervous system This explains why catecholamines are so closely tied to relative exercise intensity pancreas secretes digestive enzymes and bicarbonate into the small intestine It also releases hormones such as insulin and glucagon which are critical to maintaining blood glucose insuin promotes the storage of glucose amino acids and fats gucagon promotes the mobilization of fatty acids and glucose from the liver the ovaries release estrogen and progesterone which establish and maintain reproductive function Levels of estrogen and progesterone vary throughout the menstrual cycle estrogen may promote lipolysis although progesterone may have anti estrogen effects on metabolism during the beginning of the follicular phase estrogen and progesterone levels are low but nearing the end of the follicular phase estrogen levels peak during the luteal phase estrogen and progesterone rise but progesterone levels are highest hormone effects are on 1 metabolism supply or mobilization and use 2 uid balance 3 blood pressure 4 muscle repair and hypertrophy insuin promotes glucose uptake and free fatty acid storage gucagon causes glucose release and free fatty acid release epinepherine causes glucose release muscle glycogen use and free fatty acid release cortisol growth hormone estrogen and testosterone all cause free fatty acid release ooked at endurance training with cyclists that were untrained and trained effects on insulin for acute exercise reduction in insulin from rest to exercise due to increasing time since last meal epinephrine induced inhibition of insulin secretion and increased importance of contraction for glucose uptake effects on insulin for chronic exercise reduction in insulin at rest following training due to training induced increase in insulin sensitivity No change in insulin during exercise following training effects on glucagon for acute exercise increase in glucagon from rest to exercise due to increasing time since last meal and increase blood glucose availability to counterbalance increase in blood glucose uptake effects on glucagon for chronic exercise No change in glucagon at rest or during exercise following training Glucagon is secondary to epinephrine in regulating hepatic glucose production during exercise effects on epinepherine for acute exercise increase in epinephrine from rest to exercise sympathetic stimulation of the adrenal medulla that is proportional to the intensity of exercise effects on epinepherine for chronic exercise lower epinephrine during at the same absolute intensity but similar epinephrine at the same relative intensity following training Catecholamine release scales to relative exercise intensity whether the subject is untrained or trained acute and chronic changes in hormone response to endurance exercise aid in matching fuel supply with fuel use Hormone response to endurance exercise is scaled to relative exercise intensity
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