Exam 3 preparation EXSC401.txt

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Exam 3 preparation EXSC401.txt
2015-03-09 01:36:14
exsc metabolism ldh muscle contraction toxic end products
review from first exam
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  1. Steps involved in muscle contraction - detailed
    • 1. neurotransmitters, such as acetylcholine, are released from neurons
    • 2. acetylcholine binds to neurotransmitter (ACETYLCHOLINE gated) receptors on the membrane, ACTIVATING these CHANNELS allowing for an action potential to be generated
    • 3. This action potential helps ACTIVATE Ca IN THE SR to flow OUT OF THE SARCOPLASMIC RETICULUM and FLOOD the cell with Ca.
    • 4. In the muscle cell, 4 Ca molecules bind to troponin C, and it is only with this that binding that tropomyosin, located on the actin, is allowed to shift due to a conformational change that occurs with the binding of these positively charged Ca molecules to troponin C. This shift in tropomyosin exposes the myosin binding site on actin.
    • 5. ATP hydrolysis occurs on the myosin molecule, resulting in ADP + Pi bound to the myosin. This conformational shift due to a change in charge distribution allows for the myosin to now bind the actin at the myosin binding site.
    • 6. With myosin bound to actin, the phosphate is then released from the myosin, which causes another conformational change. This results in the cross bridge formation, which is essentially the power stroke step, resulting in the contractile motion of the muslce.
    • 7. Once the pulling force has completed, ADP is then released from the myosin (helped by ATPases) as well, and this causes another conformational change.
    • 8. It is only when ATP binds to myosin does this cause another change in charge distribution, allowing for the release of myosin to actin, RELEASING THE CONTRACTION and the cross-bridge formation.
  2. role of ATPases in muscle
    ATPases: Play a role in determining how fast ADP will be removed from myosin to allow for ATP to bind. This essentially controls the speed with which contraction can occur. If there are not many ATPases available, contraction will be slower. Also there are different types of ATPases, some which work faster than others.
  3. Ca role in muscle contraction
    • Ca LEAVES SR and floods the muscle cell in order to INITIATE CONTRACTION.
    • Ca leaves the CYTOSOL: allows for RELAXATION to occur
  4. Glucose pathways
    • Glucose, once it enters the body, goes through many different pathways, which play a role in many functions for the body.
    • Glucose first needs to be phosphorylated, into G-6-P. These series of steps, alterations and changing the molecule, allow it to ultimately be changed into a molecule that has less impact on the osmotic pressure.
    • 1. One pathway involves the Glucose converting to G-6-P, then ultimately to F-6-biP, where it can either undergo one set of reactions in a pathway which the end product is TRIGLYCERIDES, for storage of glucose.
    • 2. After F-6-biP…can enter another pathway (Glycolysis) which results in the conversion of glucose to pyruvate to use in the TCA and ETC in order to generate more ATP aerobically. Glycolysis itself generates some ATP as well as NADH
    • 3. Also, After Glucose is converted to G-6-P, it can then convert to GLUCOSE-1-Phosphate, where it is ultimately converted to GLYCOGEN, for storage of glucose.
    • 4. Along with Glycogen, Glucose can also undergo the PENTOSE PHOSPHATE pathway, which leads to the conversion of glucose into either ribose, used to make and build DNA. Another result of this pathway is the production of NADPH which is needed to synthesize many molecules in the body, and CO2, which can be breathed easily out of the body.
    • The purpose of storing glucose as a large molecule of glycogen is to get the molecule converted to a large single molecule versus a large amount of smaller molecules. This single molecule greatly DECREASEDS osmotic pressure OF THE CELL. Also, by storing glucose as fat-soluble triglyceride is a way to even further stop the osmotic pressure from occurring. This is inhibited bc TG is fat-soluble, so it does not dissolve in water, therefore having no impact on the osmotic pressure that
  5. First toxic end-product
    • 1. Heat!…heat generation occurs during metabolic activity, as there are many metabolic processes that are occurring, and their result is heat. During periods of exercise when muscle activity is increased, the need to generate more energy is increased, therefore generating more heat, which is a bi-product of energy production.
    • Heat: biproduct of CHEMICAL REACTIONS occurring during energy production. SINCE CHEM RXNS ARE NOT CONSERVED, HEAT FORMATION OCCURS
    • HEAT FLUIDIZES cell membranes, CHANGING the FLUIDITY of LIPIDS in cell membranes, allowing for leakiness to occur
    • With leakiness of membranes, EFFICIENCY of ATP SYNTHESIS DECREASES, therefore creating the need to undergo more metabolic processes to generate more ATP. This creates a cycle in which more metabolic processes need to occur due to the leakiness, and thus these reactions cause even more leakiness in the membranes.
    • When you have a lot of heat, and are not able to dissipate the heat out of the cell fast enough, the result is a leaky membrane.
    • Leaky membrane cause: The membrane leakiness can ultimately result in the loss in the membrane potential, which will Negatively impact the ability to generate an action potential. When action potentials aren’t able to be generated, in the diaphragm, for example, you lose the ability to be able to breath and death results.
    • Water has a high specific heat, so it is necessary that the body has enough water to allow for heat to be transferred from the cell to the surrounding water, in order to relieve the cell from any potential toxic end products caused by excess heat.
  6. Second toxic-end product
    • 2. Radical formation
    • Radicals are formed as a result of chemical reactions, which occur during the metabolic pathways
    • Oxygen Radicals: result from e-s not coupled to chemical reactions being picked up by OXYGEN in solution to become OXYGEN radicals
    • Hydroxyl radicals: these radicals can attack DOUBLE BONDS ANYWHERE, Resulting in DAMAGE and LOSS of FXN.
    • For EXAMPLE: unsaturated fatty acids which make up the phospholipid cell membranes can be attacked by hydroxyl radicals, creating leakiness in the membranes
  7. Leakiness in the mitochondrial membrane - how it affects a metabolic process (ETC)
    • Heat causes the membrane leakiness to occur, which can result in the Hydrogen molecules to leak out, which ultimately means less ATP generated (H pumped through into inner mit membrane, producing ATP).
    • By having leaky membranes: By allowing for H to leak out, it acts as a safety valve, trading efficiency of ATP synthesis for radical production and damage creation.
  8. LDH and pyruvate
    • Lactase dehydrogenase + pyruvate = LACTATE
    • LDH is located in the cytosol, and can bump into pyruvate to convert it to lactate.
    • Pyruvate + Mitochondrial Transporters = Acetyl-CoA in the Mit membrane
    • If there is less LDH available, or if there are MORE mitochondria, Pyruvate will be MORE likely to transfer to the mitochondria.
    • BOTTOM LINE: Lactate ALWAYS Being produced, NOT just during exercise
  9. Purpose of ETC
    • Helps to GET RID of E-s by attaching them to oxygen
    • Cytochrome c-oxidase: helps SAFELY ELIMINATE Radicals
  10. Effects of heat in terms of metabolism - in mitochondria
    • Heat, which causes leaky membranes: results in some TCA cycle molecules to leak out, specifically molecules like CITRATE and Acetyl-CoA
    • Anapleurotic RXNS: needed to help maintain the efficiency of TCA cycle
    • These reactions are Always occurring to generate energy, using amino acids and fatty acids via transamination and B-oxidation reactions, respectively