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30 Cards in this Set
- Front
- Back
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What are the fuels for muscle? |
1. Liver Glycogen 2. Muscle Glycogen 3. Adipose TG 4. Intermuscular TG (cyotsol) |
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3 things that help regulate oxidative metabolism |
1. O2 2. Acetyl-coA 3. ADP conc |
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5 sights of energy regulation in the muscle |
1. FA-albumin into cytosol (requires FA transporter) 2. Glucose uptake into cytosol (GLUT1&4) 3. Pyruvate uptake into mito (PDH) 4. Fatty Acetyl-CoA into mito (CPT+ carnitine) 5. Phosphorylation cytosol (glycogen -> G-1-P...G-1-P -> G-6-P into glycolysis) |
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How are enzymes regulated ? (types of reactions) |
1. Near- Equilibrium Reaction 2. Non- Equilibrium Reaction 3. Covalent Reaction |
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What is a near equilibrium reaction? |
-determined by gradient -increase substrate = increase product -lactate dehydrogenase |
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What is a Non- equilibrium reaction? |
-highly regulated -ADP is an example of this...high ADP indication you are low on energy -increase activity phosphorylation (enzyme) -"modifier" ....allosteric regulation -dimmer light switch |
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ADP is known as a ____________ and that is categorized as ______________regulation. |
Modifier Allosteric |
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What is a covalent modification? |
KEY: door fully open -major changes in demand -light switch on or off -major surge of calcium with intense exercise |
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What does glycogen phosphorylate do? |
strips 6 carbons off glycogen (phosphorylation) to be turned into glucose ---> pyruvate |
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Glycogen Phosphorylate and PDH have two states, and active and an inactive form. True or false. |
True |
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What serves to activate glycogen phosphorylate? |
-ADP -Ca |
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What serves to activate PDH? |
Ca |
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What serves to inactivate PDH? |
ADP |
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With progressive increases in exercise intensity (%VO2 max) why does fat utilization go down as CHO utilization increase? |
-ADP + Ca stimulation of glycogen phosphorylate -Ca stimulation of PDH |
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What methods are available to determine what limits substrate utilization during exercise? |
1. Blood Samples (artery/vein) 2. Infusions (stable isotopes) 3. Pulmonary gas exchange 4. Muscle biopsies |
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How can we determine fuel utilization through pulmonary gas exchange? |
-observe RER -RER=0.7 indicates most energy provided by mobilizing fat (FA) -RER=1 indicates mainly CHO breakdown providing energy |
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How can we determine fuel utilization through blood samples? |
-could measure blood lactate...issue is la taken out of blood regularly -more accurate if you take lactate conc before muscle (artery) and after muscle (vein) to determine how much of specific fuel burned...must know blood flow rate |
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In Van Loon paper on "effects of increasing exercise intensity on muscle fuel utilization" how did they measure total rate of energy ? |
Measured VO2 |
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n Van Loon paper on "effects of increasing exercise intensity on muscle fuel utilization" how did they determine %CHO and %FAT? |
RER |
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In Van Loon paper on "effects of increasing exercise intensity on muscle fuel utilization" how did they measure contribution of specific substrates? |
Biopsy Isotope tracers |
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How do infusions of stable isotopes show fuel utilization? |
For example: FA* infusion -use a FA (palmitate) with slightly different mass...some FA* will be taken up by adipose tissue (TG)... RA (rate of appearance) in the blood will determine how much FA in blood derived from adipose tissue...observe rate at which FA* taken up into muscle and oxidized for energy ROX...when FA* combusted in mito...labelled carbon will show up in breath |
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Therefore...able to compare RA and ROX. |
... |
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Why might someone think that fat utilization with increasing workloads is a delivery issue rather combustible issue? |
-Ra goes up then goes down at higher intensity levels ***** BF to adipose does decrease with increased intensities therefor somewhat of delivery problem***** |
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What was the key finding n Van Loon paper that solidified fat utilization is mainly limited by ability to oxidize it in the mito? |
-%Ra that is oxidized decreased at highest workload intensities -THEREFORE....issue is with oxidation of fat at high workloads |
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What is responsible for the limitation in our ability to oxidize fat at high relative workloads? |
-very slight changes in pH can inherently reduce activity of CPT (through moderate and intense exercise) -THEREFORE at high intensities La build up = change in pH = reduce CPT activity = less efficient fat oxidation |
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4 components of VO2 paradigm (UIHL) |
1. Upper limit to oxygen uptake 2. Individual differences in VO2 max 3. High VO2 max prerequisite for endurance success 4. Limited by cardiorespiratory system |
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Potential limiting factors for VO2 max (PCOS) |
-Pulmonary diffusing capacity -Cardiac output -O2 carrying capacity -Skeletal muscles |
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What is the fick eqn |
VO2 = CO x A-V O2 diff |
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How can Pulmonary diffusion capacity be limiting factor for VO2 max? |
-elite athletes have decreased TT of RBC in pulmonary capillary=less time to fully absorb oxygen in blood *overcome with supplemented O2 |
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Why don't we see fall in O2 saturation with non-elite athletes? |
Likely Q is not high enough to cause reduction in arterial desaturation |
