Exercise Metabolism
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Exercise vs. Fed Fast Cycle
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fluctuation in activity levels
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difference in energy demand
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all energy derived from nutrients
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the energy demands of sports resemble the fed-fast cycle
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understanding of integration of metabolism required
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keep in mind the changes in level of hormones
Energy Metabolism in Exercise
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Energy systems at cellular level
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immediate, intermediate, long term​
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ultimately all provide ATP from substrate level oxidation (anaerobic, glycolysis) and/or oxidative phosphorylation (aerobic)
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ATP generated by oxidation o​f:
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CHO, fat and C-skeleton of AAs​
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source of substrates:
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food​
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body fuel stores
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![image.png](https://static.wixstatic.com/media/2ac116_c1d990a88686453ea2835e480c67db41~mv2.png/v1/fill/w_504,h_289,al_c,lg_1,q_85,enc_avif,quality_auto/2ac116_c1d990a88686453ea2835e480c67db41~mv2.png)
Energy Systems
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Immediate
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5-10 seconds
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ATP in muscle cells (minimal)
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we don't store it​
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creatine-P (phosphocreatine)
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5X the amount of energy as pre-formed ATP​
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very important in sprints and weight lifting
![Screenshot 2023-12-16 at 11.23.13 PM.png](https://static.wixstatic.com/media/2ac116_84ae42755f3f45d7b1099ae82c5cb4ab~mv2.png/v1/fill/w_545,h_278,al_c,q_85,enc_avif,quality_auto/2ac116_84ae42755f3f45d7b1099ae82c5cb4ab~mv2.png)
2. Intermediate​
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short term
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30 seconds - 2-4 mins
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anaerobic glycolysis
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quick but limited release of energy​
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high intensity (800m springtin, 100m swim)
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weight
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![image.png](https://static.wixstatic.com/media/2ac116_c980979ba48b4b1d9cde1303987a39c2~mv2.png/v1/fill/w_600,h_281,al_c,q_85,enc_avif,quality_auto/2ac116_c980979ba48b4b1d9cde1303987a39c2~mv2.png)
![image.png](https://static.wixstatic.com/media/2ac116_06594caba08f43d093087c5ef61ef500~mv2.png/v1/fill/w_434,h_213,al_c,q_85,usm_0.66_1.00_0.01,enc_avif,quality_auto/2ac116_06594caba08f43d093087c5ef61ef500~mv2.png)
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3. Long term (oxidative)
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aerobic metabolism
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takes longer to activate​
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lasts longer
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pyruvate from glucose
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directly from glycolysis or via the cori cycle​
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acetyl CoA via beta-oxidation of FA
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protein: C-skeletons from different AA can enter TCA at different location
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![image.png](https://static.wixstatic.com/media/2ac116_528ebfb87f8441b29fdebeed2f66904a~mv2.png/v1/fill/w_390,h_390,al_c,q_85,enc_avif,quality_auto/2ac116_528ebfb87f8441b29fdebeed2f66904a~mv2.png)
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blood is directly away from internal organs to:
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muscle (O2 delivery)​
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skin (heat removal)
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blood vessels dilate​
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release heat
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![image.png](https://static.wixstatic.com/media/2ac116_8bd599abfdf64a3da8d65546340b948e~mv2.png/v1/fill/w_276,h_231,al_c,q_85,usm_0.66_1.00_0.01,enc_avif,quality_auto/2ac116_8bd599abfdf64a3da8d65546340b948e~mv2.png)
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Limits to Exercise
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fuel limitations
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increased H+ and Lac-​
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probably not O2 delivery due to lungs
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probably is blood flow​
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deliver to O2 to muscle - in prolonged exercise, can lead to a return to anaerobic glycolysis​
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removal of heat
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most of us don't exercise that intensely
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Carbohydrate
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plasma glucose​
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muscle glycogen
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Fat
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free FA​
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TAG in lipoproteins
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IMTG (intramuscular triacylglycerols)
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Protein/Amino Acid
Muscle Fiber Types
Type I Slow Twitch - high oxidative, moderate glycolytic
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aerobic - lots of mitos
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fat is the primary fuel (never alone)
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"red muscle" due to hyoglobin (heme)
Type IIa - oxidative/glycolytic
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anaerobic and aerobic
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both glucose/glycolytic and fat/aerobic
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intermediate contractility
Type IIb - high glycolytic, low oxidative
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anaerobic glycolysis
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white fibers
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exercise can increase the size of muscle cells
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high intensity endurance --> increase in % of type I fiber
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strength/resistance --> increase in volume of both type I and type II
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the portion of each type of muscle fibers a person has is defined by genes
![image.png](https://static.wixstatic.com/media/2ac116_ddb07eaea3144e64b16dc655a759ac2c~mv2.png/v1/fill/w_528,h_420,al_c,q_85,enc_avif,quality_auto/2ac116_ddb07eaea3144e64b16dc655a759ac2c~mv2.png)
Muscle Fuel Use During Rest
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at rest, low demand, low expenditure
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skeletal muscle needs less energy than internal organs​
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use both CHO and fat
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glucose mainly from blood
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breakdown of muscle glycogen minimal at rest​
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fatty acids
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albumin bound FFA​
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hydrolysis of TAG in lipoproteins
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LPL in skeletal muscle increases when fasted
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hydrolysis of IMTG (low because HSL is at rest)
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Postprandial to Fasted
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Postprandial: HIGH INSULIN
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increased GLUT4 --> increased glucose uptake by muscle --> increased glycolysis --> increased levels of pyruvate and acetyl-CoA --> high malonyl CoA --> decreased CPT-1 --> decreased beta-oxidation​
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When transitioning to fasted state
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decreased insulin --> decreased GLUT4 --> decreased glucose uptake --> decreased glycolysis​ --> decreased pyruvate and acetyl CoA --> decreased malonyl CoA --> decreased inhibition on CPT-1 --> increased beta-oxidation of FA
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decreased insulin --> decreased inhibition of HSL in adipose tissue --> increased FFA from lipolysis --> increased FFA in plasma
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![image.png](https://static.wixstatic.com/media/2ac116_e4e05faea07547008ada7592663df9b7~mv2.png/v1/fill/w_476,h_347,al_c,q_85,usm_0.66_1.00_0.01,enc_avif,quality_auto/2ac116_e4e05faea07547008ada7592663df9b7~mv2.png)
Randall Cycle​​ (glucose-fatty acid cycle)
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inhibition of glucose utilization when fatty acids are available as an alternative fuel and vice versa
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proposed that increased beta-oxidation --> increased acetyl-CoA --> increased inhibition of PDH + increased citrate --> inhibition of glycolysis and oxidation of pyruvate from glucose in mito
When fasted
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in skeletal muscle, LPL activity increases
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in adipose tissue, LPL activity decreases
When re-fed
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in skeletal muscle, LPL activity remains elevated
Therefore
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when fed, FA in chylomicrons and VLDL directed to adipose
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when fasted, FA in VLDL directed to muscle for oxidation
Fuel Utilization in Working Muscle
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A person's max aerobic capacity is VO2 max
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the point when further increase in exercise intensity no longer leads to increase in oxygen uptake​
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low intensity: 25% VO2 max​
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moderate intensity: 60% VO2 max
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high intensity: 80% VO2 max
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athletic training increases VO2 max
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via cardiovascular fitness​
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slows heart rate​​
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increased volume pumped
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![image.png](https://static.wixstatic.com/media/2ac116_7291d1b9aeb64f9da4ed9ed6859a5d01~mv2.png/v1/fill/w_425,h_483,al_c,q_85,usm_0.66_1.00_0.01,enc_avif,quality_auto/2ac116_7291d1b9aeb64f9da4ed9ed6859a5d01~mv2.png)
Exercise increases FA availability to muscle
Net effects: increased FFA in muscle for beta-oxidation
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exercise also increases beta-oxidation capacity​​
![image.png](https://static.wixstatic.com/media/2ac116_058b1c5943f841559b394b4becff8a2d~mv2.png/v1/fill/w_600,h_152,al_c,q_85,enc_avif,quality_auto/2ac116_058b1c5943f841559b394b4becff8a2d~mv2.png)
Utilization of CHO in Working Muscle
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increased glucose uptake by muscle: exercise increases GLUT4 via insulin-dependent pathway
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plasma glucose comes from
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hepatic glyceogenolysis​
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dietary CHO
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muscle glycogenolysis
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glycogen depleted muscle can oxidize FA more efficiently​
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low acetyl CoA (and malonyl CoA​​
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low PDH activity
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high free carnitine
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Utilization of a Mixture of Fuels
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muscle always uses a mixture of substrates as fuel
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each source of fuel contributes a different proportion to the total energy expenditure in muscle
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at rest, fat plays an important role
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fat burns most at moderate intensity
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as intensity increases, CHO (especially glycogen) becomes more important
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Adaptation to Exercise
Cardiovascular
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increased cardiac output
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increased gas exchange in lungs
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increased capillary density in skeletal muscle
increased mito in skeletal muscle
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5X increase
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seasonal variation: during season vs off season
increased activity of enzymes involved in oxidation
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decreased lactate production
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aerobic oxidation is more efficient in producing ATP
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same amount of glycogen can last longer
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lower H+ --> less exercise stress and fatigue
Reduced reliance on CHO, early mobilization of fat
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in athletes, IMTG is higher
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exercise inhibits acetyl-CoA carboxylase --> less malonyl CoA -> more FA oxidized
Initial Muscle Glycogen
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Exercise uses fatty acids as a major fuel
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we know (from fasting states) that our cells need CHO to burn fat because OAA is needed to bring acetyl-CoA from fatty acid oxidation into the TCA cycle
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therefore, no matter how much, how fast our bodies can mobilize fat, we need to have enough CHO in the system
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in addition, as intensity increases, CHO contributes more to fuel
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glycogen depletion is the single most consistently observed factor that contributes to fatigue
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high initial muscle glycogen level correlates to longer time to exhaustion in submaximal workload
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does not apply in low intensity exercise becaues glycogen is not a limiting factor
Carbohydrate Loading
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used to maximize muscle glycogen contents
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common practice for endurance athletes
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start about one week before event
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general strategy: CHO depletion followed by CHO reloading
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desired results: higher muscle glycogen level than before start
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specific regimens vary
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