Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Exercise Physiology
Bioenergetics and Muscle Metabolism
| Question | Answer |
|---|---|
| substrate | fuel source. carb fat protein |
| bioenergetics | conversion of substrates into energy at cellular level |
| metabolism | chemical rxns in body |
| how is E release measures? | from heat produced (raising 1g H2O from 14.5 to 15.5C =1 cal) |
| where is E from food stored | ATP bonds |
| resting fasted uses what % E from fat? | 50 |
| short, high intensity exercise uses what substrate? long and/or low mod intensity uses what subtrate? | more carb; carb&fat |
| why do we need to replenish glycogen stores? where is most glycogen stored? what makes carb the primary ATP source? | glycogen stores (110g/451 kcal liver, 500g/2050kcal muscle) are limited (2500kcal); primary ATP substrate for brain and muscles |
| what part of fat is used to make ATP | fatty acids |
| where is fat stored | 7800g/73,320 kcal in subcutaneuos and visceral fat. 161g/1513kcal in intramusclar. |
| kcal/gram fat, carb, protein | 9.4, 4.1, 4.1 |
| when is protein an energy substrate? what is it converted to and when? | for starvation converted into glucose (glucogenesis). for E storage and cellular E converted in FFA (lipogenesis) |
| Mass action effect. how does this relate to E releasred at controlled rate? | subtrate availbility affects metabolic rate. E release at controlled rate based on availbility of primary substrate/ More availble substrate=higher pathway activity. Excess of given substrate=cells rely on that more than others |
| two factors controlling rate of E production | substrate availbility and enzyme activity |
| how does enzyme activity control rate of E production | specific enzymes required for each step in biochemical apthway. more enz activity=more product. RATE LIMITING ENZYME influences activity by negative feedback to slow overall rxn and prevent runaway rxn. |
| how is ATP stored and used? | synthesis from by products (ADP+Pi+energy->ATP AKA phsphorylation) and can occur w/wo O2. ATP sotred in small amnts. Breakdown of ATP: ATP+H2O+ATPase ->ADP+Pi+E |
| since ATP storage is limited, how do we keep ATP availble? | constant synthesis of new ATP via anaerobic metabolism (ATP-PCr, glycolytic) and aerrobic metabolism (oxidative) |
| ATP-PCr-System. ana/aero? ATP yield? duration. | ana, substrate level metabolism. 1 mol ATP/1mol PCRr. 3-15s. |
| how does ATP-PCr system produce E? Role in body/exercise | Phsophocreatine (PCr)+creatine kinase -> Cr +Pi +E. E used to reassemble ATP but not for cellular work. replenishes ATP during rest. Recycles ATP during exercise until used up (3-15s max exercise) |
| what regulates ATP-PCr system? | Creatine kinase (CK) controls rate of ATP production via negative feedback. ATP hi-> CK decrease. ATP lo ADP hi CKactivity increase |
| Glycolytic System. ana/aero? ATP yield? duration. | ana. 2-3 mol ATP/1 mol substrate. 15s-2min |
| how does glycolytic system produce E? | glucose or glycogen as substrate. Uses 1ATP to convert glucose into glucose-6-phosphate. Uses 0 ATP for glycogen. 10-12 enzymatic rxns in cytoplams convert G6P to 2 pyruvic acid resulting in 2-3ATP |
| Role in body/exercise- glycolytic system. | allows muscles to contract when O2 is limited. premits shorter term, higher intensity exercise than what oxidative metabolism can sustain |
| Cons?- glycolytic system. | . -: low ATP yield (inefficient use of subtrate), converts Py acid to lactic acid when O2limited. Acidosis impairs glycolysis and muscle contraction |
| what regulates glycolytic system | Phoshofructokinase (PFK) rate limiting enzyme works same as CK regarding presence of ATP/ADP. glycolytic systme is also regulated by products of Krebs cycle. |
| Oxidative System. ana/aero? ATP yield? duration. | Aero, 32-33ATP/glucose and 100+ATP/1FFA. steady supply for hours |
| oxidatice ssytem occurs in the mitochondria. What determines the density of a mitochondria? Why is it important that mitochondria are spread out and not uniform in muscle cells? | density determined by demand. Location determined by oxygen diffusion to minimize excess O2 to prevent ROS (rective oxygen species). Distribution is nonuniform to maintain O2 delivery without toxicity to maintain high metabolic rates. |
| 3 stages of oxidative ssytem. where? | glycolysis, krebs, e- transport chain (cytosol, mitochondria, inner mitochondrial membrane) |
| Glycolysis (oxidation of carb) can occur with or without O2. What makes glycolysis different w/wo O2? How does this influence ATP yield? | General steps are same for ana andd aero glycolysis. In presence of O2, pyruvic acid -> acetly-CoA and enters Kreb. Wo O2, pyruvic acid-> lactic acid. ATP yield is same for both |
| steps of Krebs cycle (mention glucose, acetyl CoA, GTP, ATP, NADH, FADH H+) | 1mol glucos->2 acetly CoA for 2 cycles in Kreb. In Kreb, ACoA -> 2GTP->2ATP per cycle. NAD+ takes H+ to becomeNADH and takes H+ to ETC. FAD->2FADH2 & into ETC... |
| why is it important that NADH and FADH transport H+ to ETC? | too many H+ in cell causes acidosis |
| what regulates the krebs cycle | isocitrate dehydrogenase is rate limiting enzyme. Also regulates ETC |
| how does the Electron transport chain produce ATP? | H+ from NADH and FADH2 and e- travel down chain. H+ combines w O2 ->H2O. e- +O2 form ATP. |
| What is yeild of ATP per NADH and FADH2 | 2.5 per N, 1.5 per F |
| Breakdown of net totals of ATP in Oxidation (glycolysis, GTP, NADH, FADH2) | 1 glucose=32, glycogen=33 ATP :. glycolysis=2-3ATP, GTP from krebs=2ATP. 10NADH=25 ATP. 2 FADH2=3ATP. |
| Where do NADH and FADH produce ATP in glcolysis and oxidation? How much ATP is produced at substrate level phophorylation of glucose and phophorylation in KRebs? | 2NADH=5 ATP in glucose->Pyruvate. 2NADH=5 in pyr->ACoA. 6NADH=15 and 2FADH=3 in oxidative phosphoylation/ETC (H+transport). 2 ATP; GTP=2 ATP from substrate level phosphorulation. |
| Oxidation of fat. ana/aero? ATP yield? what regulates rate. | lipolysis carried out by lipases: triglercerides broken down to 1 glycerol and 3 free fatty acids. slower than glucose oxidation- rate of FFA entry into muscle is dependent on concentration gradient. ATP yield 3-4x that of glycolysis. |
| oxidation of fat steps | b-oxidation of fat (FFA-> ACoA)-> Krebs/ETC |
| b oxidation of fat process purpose, ATP yield, what varies. | process of converting FFA->ACoA for KRebs (requires 2 ATP). Number of ACoA depends on C# of FFA. 16C FFA (palmitic acid)=8ACoA. |
| substrate levvel oxidation/direct oxidation of fat ATP yield ...palmitic acid | FFA activation: 0. b-oxid (occurs 7 times): 0 Krebs (occurs 8 times): 8 subtotal 8 |
| oxidative phsphorylation of fat ATP yield...palmitic acid | FFA activation: -2 b-oxid (occurs 7 times): 28 Krebs (occurs 8 times): 72 subtotal 98 |
| total ATP from oxidatizaion palmitic acid (fat) | 106 |
| oxidation of fat Krebs cycle and ETC | ACoA enters Kreb and follows same path as glucose but may take more cycles bc varying #of C. |
| roles of white fat vs brown fat | WF: lipid storage and lipolysis. BF: transfer E from food directly into hear. contains many small lipid droplets, mitochondria, and blood vessels |
| Oxidation of fat. ana/aero? ATP yield? what regulates rate. | lipolysis carried out by lipases: triglercerides broken down to 1 glycerol and 3 free fatty acids. slower than glucose oxidation- rate of FFA entry into muscle is dependent on concentration gradient. ATP yield 3-4x that of glycolysis. |
| oxidation of fat steps | b-oxidation of fat (FFA-> ACoA)-> Krebs/ETC |
| b oxidation of fat process purpose, ATP yield, what varies. | process of converting FFA->ACoA for KRebs (requires 2 ATP). Number of ACoA depends on C# of FFA. 16C FFA (palmitic acid)=8ACoA. |
| substrate levvel oxidation/direct oxidation of fat ATP yield ...palmitic acid | FFA activation: 0. b-oxid (occurs 7 times): 0 Krebs (occurs 8 times): 8 subtotal 8 |
| oxidative phsphorylation of fat ATP yield...palmitic acid | FFA activation: -2 b-oxid (occurs 7 times): 28 Krebs (occurs 8 times): 72 subtotal 98 |
| total ATP from oxidatizaion palmitic acid (fat) | 106 |
| oxidation of fat Krebs cycle and ETC | ACoA enters Kreb and follows same path as glucose but may take more cycles bc varying #of C. |
| roles of white fat vs brown fat | WF: lipid storage and lipolysis. BF: transfer E from food directly into hear. contains many small lipid droplets, mitochondria, and blood vessels |
| how is protein oxidized as a substrate? | only when stravation. converted into glucose (glucogenesis) and/or converted into ACoA |
| why is ATP yield from protein noto easy to determien? | nitrogen presence is unique per protein and nitrogen excretion requires ATP expenditure. Since its so minimal, estimates ignore protein metabolism. |
| how is lactate used as a fuel in exercise? | 1. lactate produced in cytoplam taken up by mitocondria of same fiver and oxidized. 2. lactate transported via MCP transporters to another cell and oxidized there (lactate shuttle). 3. can recirculate back to liver->pyruvate->glucose (glucogensis) |
| what are products of oxidative system of fat and glucose other than ATP? | CO2 and H2O |
| what is the cross over concept? | when working below 60% VO2 max (rest/lt exercise), lipids are primary substrate. When above 75%, carbs are primary. Crossover point is the intersection, which is the point of optimal fat oxidation. |
| example of crossover concept | note that crossover pt is related to VO2 max, which is affected by training. intensity 20%=85%fat, 15% c- 100kcal=85 from fat. VS 75% intensity=60% CHO, 40% fat- kcal 350/hr=140kcal of fat. Total amt of fat burned more at mod-high intensity |
| what determines a muscle's oxidative capacity? | enzyme activity, fiber type composition, edurance training, O2 availability vs O2 need. |
| how does enduarance training enhance oxidative capacity? | enhances oxidative capcity of type II fibers by developing more and larger mitochondria, develoing more oxidative enzymes (succinate dehydrogenase and citrate synthase) per mitrochondrian, |
| why do type I fibers have greater oxidative capacity than type II? | Type I have more mitochondria, high oxidative ensyme (succinate dehydrogenase, citrate synthase). However, Type II have ebetter glycolytic E production |
| why does intensity of exercise cause more O2 needed? | intensity increase= ATP demand increase= more oxidative ATP production :. more O2 intake and delivery. |
| how can we measure O2 needs of a muscle? | O2 levels entering and leaving can bee measured to estimate O2 needed in muscle. |
Created by:
kellyyrosse
Popular Physiology sets