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Midterm

4010-Midterm 1

12 Pages
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Department
Kinesiology & Health Science
Course Code
KINE 4010
Professor
David Hood

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Notes go along with the figures in the Lecture notes Lecture 1 Pg. 2  Primary factors are factors that itself will increase CHD  Secondary factors means it will increase the risk of CHD if one of the Primary factor is already there  ACSM says that risk of CHD is lower in people with more HDL-C high density lipoprotein cholesterol- negative risk factor when levels exceed 60mg/dl  Certain risk factors can be managed with exercise  Changing Physical inactivity the other risk factors will change with it o Ex. If you start exercising you will likely stop smoking, BP, cholesterol, weight will go down,  Suggested to have low fat diet, exercise regularly, and stress reduction Pg. 3  Total Cholesterol= VLDL + LDL + HDL Cholesterol o Density Lipoprotein o HDL is good cholesterol, the higher this is the lower the risk- the higher the total the greater the risk o Knowing the total is diagnostic o Should be lower than 5.2 mM/L of blood  150 minutes of exercise recommended a week  140/90- sys/dia- need to be lower than this  60-90 is a good resting HR  25 BMI o BMI= weight in Kg/ (height in meters)^2~~~ will be on exam Pg. 4  Lowest Physical inactivity levels in the country- BC- 43%  Marie times with highest levels of Physical inactivity- NFLD- >52%  Levels of inactivity for the Provinces increase from left to right  National average 48% is inactive Pg.5  Frog muscle contraction and measuring heat- metabolism generates heat- so this was used to measure metabolism  Fatigue is loss of force with continued contractions  Lactic acid was thought to be a poison Lecture 2 Pg.7  ATP- PCr covers the energy requirement for the first minute, the other two systems start to take into effect after this o All systems start at the same time, but the other pathways are slower  When you exercise ATP is used and broken down to ADP free+ P  ATP –(Myosin ATPase) ADP+ P o Phosphocreatine (donor molecule) donates a P so that ADP can become ATP  ADP +PCr –(CPK)Cr + ATP  PCr supply goes down and Cr goes up  CPK has a high activity  During recovery the reactions are reversed o We resynthesize PCr so it can be used for the next bout of exercise Pg. 8- Excitation- Contraction Coupling in Skeletal Muscle  Alpha neuron start in the spinal cord, receive input from motor cortex- spinal delivery, spinal neurons from motor cortex from spinal cord synapse w/ alpha motor neurons in spinal cord 1. Terminal end of Alpha motor neuron release Acetylcholine and binds to receptors 2. Action potential from this binding is spread down T tubules of muscle cells 3. AP in T tubules trigger Ca to be released from SR 4. Ca bind to Troponin on actin filaments and cause Tropomyosin to be moved which reveals binding sites on actin 5. Myosin cross bridges interact w/actin, pulling actin filaments toward center of sarcomere 6. Ca is actively taken up back to the SR when there is no longer AP 7. With Ca no longer around Tropomyosin moves back in place blocking the binding sites and contraction ends- relaxation Pg. 9 1. ATP and PCr are readily available high energy phosphagens 2. PCr is 3-4 times higher than ATP- good donor of phosphate groups 3. PCr is used rapidly, restored rapidly 4. PCr utilization depends on exercise intensity 5. PCr restoration depends on blood flow O2 delivery  aerobic ATP production from mitochondria during recovery from exercise  PCr does not continue to decrease and plateaus because we have 2 other systems that contribute to maintaining ATP  Blood flow is important to recovery o Mitochondria requires O2 to produce ATP through blood blow o To recover PCr we need high amounts of Cr which you have after exercise and high amounts of ATP from mitochondria o A study was done to stop blood flow externally- cuffed a leg and did a biopsy to check recovery- no PCr was recovered Pg. 10  ATP levels do not change at Rest, Mild, or Moderate intensities because we have really good regenerating systems, in Severe there is a tiny drop  ATP-PC system is important for all exercise types and intensities  Particularly important for events requiring a high power output  Rapidly available but does not last long Pg. 11  Important terms used in experiments  Knockout- genes taken out  Transgenic- more of same gene  In this experiment ATP-PC system was disabled by knocking out the CPK gene in mice  Muscle performance was decreased at the start of exercise and force plateaus after because the other systems start to take affect  Cr causes a large osmotic load- makes your muscles look bigger because water goes in  Cr coming in has to be turned into PCr to make it useful  Taking Cr supplements can increase PCr by 5-15% depending on the diet, if you normally eat meat then the effect of Cr will be less b/c you get Cr normally Pg. 12  Structure of Cr looks like an Amino Acid, but it is not a protein  It has been found that Cr works better when you take it with Glucose o When you eat Glucose, the Blood Glucose increases which stimulates pancreas to release Insulin to get rid of the Glucose from blood and goes to the muscle o Insulin also stimulates Amino Acid transport (AA Transporter) this will also carry Cr (b/c it looks like an AA) to the muscle; therefore, Cr gets into the muscle  PCr utilization and restoration improves with Cr ingestion because they start at a higher point and do not deplete as much- recovery rate is faster Lecture 3- Sept.16.2013 Pg. 13  High dose of 20g/day was initial assessment, now we learn that 3g/day will achieve same results  Research obtained from males  Most useful for patients with certain diseases (neuromuscular disease) Pg.15  Key regulating molecule is free ADP that turns on all 3 systems  ADPf is a substrate for CPK, and CPK is necessary for ATP-PC- simple system  Regulates Glycolysis regulating PFK- 13 steps  Rate limiting substrate for mitochondria- 13 steps plus organelle Pg. 16  Phosophofructo Kinase (PFK)- it is a rate limiting step (hwy example)  PFK has a very low Vmax and needs to be modified to go faster  To convert Fructose 6 P to Fructose 1,6,di P is limited by PFK  In the presence of ADP, Km goes down which means a higher affinity between F6P and PFK which will create more ATP, Lactic acid production also goes up  ATP-PC and Glycolysis take place in the cytoplasm Pg. 17  With Allosteric presence the reaction happens at a faster rate (number of enzymes remains the same)  Low and high affinity have the same Vmax, what has changed is the Higher affinity moves left on the graph  Km- strength of affinity o Definition: It is the substrate concentration that gives you 50% of the maximum velocity of the reaction o The higher the Km the lower the affinity  To increase Vmax is to have more enzymes  Vmax doubles if enzymes are doubled (ex. Adaptations to training and increasing mitochondria enzyme in cell) Pg. 18  Substrates come to the Active site of enzyme (reaction takes place)  Allosteric site- other molecules come and can change the confirmation/ shape of enzyme  Affinity- strength of reaction  Road widens with ADPf changing the shape of PFK to have a high affinity with F6P Pg. 19  Energy substrates are fuels  Fatty Acids have 16-24 carbon chains and come from Triglycerides  Glucose breaks off into two 3 carbon molecules Pyruvate dehydrogenase converts it into 2C Acetyl CoA and enters Kreb cycle, 4C OAA adds on the Acetyl CoA and becomes 6C Citric Acid and then you lose 2 carbons to CO2- in the process of this cycle NADH2 and FADH2 are produced and sent to the ETC to produce a lot of ATP Pg. 20  ADPf comes into the Mitochondria through Adenine Nucleotide Translocase and exchanges it for newly made ATP, one to one exchange  ETC consist of series of proteins called Cytochromes and at the end of the chain is COX (Cytochrome Oxidase)- oxygen is converted to H2O here  ATP Synthase makes the ATP by combining ADP with a P Lecture 4 Pg. 19  When we talk about aerobic metabolism we are talking about the metabolism of fat and carbohydrates  Carb supply in body is low and Fat content is really high, even in the leanest of people  What limits us during exercise is the limited availability of Carbs Pg. 20  FFA- Free Fatty Acids  ETC is a series of proteins called Cytochromes and they have a Heme group inside o Heme is red- found in Cytochromes- the more mitochondria you have in a muscle will mean more Cytochromes and more Hemes so the muscle will be redder  Cytochromes- electron transfer proteins  NADH dehydrogenase- is a protein at the start of ETC- it oxidizes NADH2 to NAD o Splits atom into H+ and e-  2H is then split off with the Electron and goes through the ATP synthase which is opened when ADPf passes by- this action of going through gives it energy to make ATP, then 2H goes to end of ETC to form H2O  Proton gradient- is source of potential energy in the cell- H+ going from inside to outside  Electrons move from one protein to the next until COX, then takes the Electron with an Oxygen atom and combines it with 2H to make H2O- oxygen is consumed to make this (Oxygen Consumption at Mitochondria level)  COX deficiency or Cyanide poisoning doesn’t allow the 2e to go anywhere, so ATP can’t be produced and you die  Deficiency reduces COX to 10% efficiency (ex. Mitochondria myopathy) caused by mutations or hereditary- harder to make ATP from ETC  Oxidize one NADH2 you create 3 ATPs  With no O2 = no electron flow no ATP syntheses  Under normal exercise situations, there is always O2, never limited by O2  Never produce Lactic acid because you are Hypoxic- unless you do it purposely Pg. 21  Lactic acid production depends on intensity  At Resting state we have 1mM of lactic acid in our blood  45-75 seconds have the highest production of HLa, 25-30mM Pg. 22  Anaerobic- ATP-PC and Glycolysis don’t use O2 in reactions o They still have O2 but just don’t use it  Aerobic system uses O2 Lecture 5 Pg. 21  If interested in short term high intensity exercise then the Anaerobic systems will be used a lot  Depending on the intervals chosen, high quality exercise can be done without invoking Acidosis that comes along with HLa production  Acidosis- increase of acid in the blood, pH goes down  Acidosis in muscle is associated with fatigue  Want to avoid any changes in pH  Keeping exercise high intensity and short you can do high quality work without the acidosis  You can get aerobic/cardiovascular benefits by doing repeated intervals Pg. 23  10 sec work, 20sec rest- PCr went down dramatically and 20 secs was not enough to resynthesize- ATP is well maintained  Not invoking Acidosis with 10/20, but a lot with 60/120 same in Blood HLa  Blood and Muscle Lactate graphs mirror each other b/c Blood enters Muscle  Does it have an Aerobic benefit? Yes  Ex. Swimming intervals- not enough time for HR to go back down so it is kept up Pg. 24  O2 Deficit- Anaerobic contributions here and no O2 is being used in reactions  O2 Debt- when you stop exercising oxygen consumption does not shut off, your still breathing and there is an excess of O2 o Two other names: Recovery O2, Excess Post exercise O2 Consumption EPOC  In moderate exercise HLa goes down because we are using aerobic system and HLa is being metabolised  In severe, Aerobic system tries to match it but can’t- you reach maximum Aerobic capacity (Max VO2)- so there is always an Anaerobic system being used thus HLa keeps increasing and only comes back down when exercise stops  Fast component of O2 debt is responsible for resynthesizes of O2 consumption during recovery without this excess O2 consumption you would not make ATP and wouldn’t be resynthesizing PCr during recovery  Slow component- people think it is related to body temperature, higher temperatures result in faster reactions- during exercise your body is hot  Endurance training- Aerobic system improves and Max VO2 increases o Muscle O2 extraction increases o With increase on Aerobic system, less reliant on Anaerobic which cause less HLa Pg. 25  Before and after training if you do the same exercise- if it is a submaximal exercise at the same workload there will be no change in
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