Unit 3 - Review Flashcards

1
Q

What is the purpose of training on low glycogen?

A
  • Low glycogen increases AMPK.
    • AMPK inhibits malonyl-CoA (which inhibits CPT 1).
      • Beta Oxidation - Fatty acids are able to enter into the mitochondria for fat oxidation.
        • Beta-HAD
      • Increase TCA Cycle
        • Citrate Synthase, Succinate Dehydrogenase
      • Increase ETC components
        • COX enzymes
    • AMPK increases PGC1-Alpha.
    • AMPK increases Nitric Oxide.

Manipulating glycogen activates AMPK and initiates processes that favor vasodilation and mitochondrial biogenesis.

  • Increasing FOX will come from adipose tissue.
    • Increase lipolysis.
      • Hormone-sensitive lipase.
    • Increase utilization of IMTG.
  • Athlete’s Paradox
    • Increase Fat Transporter (CD36)
      • Trained athletes have the capacity to take up more fat.
      • Greater machinery.
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2
Q

Methods of training with low glycogen

A
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3
Q

What are the methods for training with high glycogen?

A
  • Gatorade
  • Eating during exercise.
    • Increase insulin
      • Suppress fat oxidation (FOX).
        • Promote glucose uptake.
          • Insulin-dependent glucose uptake
          • Insulin-independent glucose uptake
        • Limit training adaptations around fat oxidation.
          • Blunt low glycogen adaptations (AMPK, PGC1-alpha, etc…)
            • So what?
              • This didn’t lead to greater performance.
  • Feeding
    • The critical window is 2 hours post exercise.
    • Post-Meal
      • 2-3:1 CHO: PRO
        • 1g/kg:0:33 g/kg CHO: PRO
      • Type of CHO: High GI
      • Type of Protein: Whey, Leucine Trigger (20-25g Whey; 3g Leucine, 8g EAA)
      • Don’t forget about smaller amounts of fats.
  • Big takeaway:
    • Eating for performance is different than eating for health.
      • Greater fat oxidation ≠ better time trial.
        • Randle Cycle
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4
Q

Peripheral Fatigue

A
  • Peripheral
    • Low Glycogen
      • Decrease ATP generation.
        • Decrease Ca2+ release
        • Decrease Na+/K+ ATPase
        • Decrease Myosin ATPase
    • Low Blood Glucose
      • Decrease ATP generation.
        • Decrease Ca2+ release
        • Decrease Na+/K+ ATPase
        • Decrease Myosin ATPase
    • High H+
      • Decrease Ca2+ release
      • Decrease Na+/K+ ATPase
      • Decrease Myosin ATPase
      • Decrease Ca2+ ATPase
        • All of this can affect myosin-actin cross-bridge cycling.
    • High Temperature
    • High Pi
    • Low PCR
      • Limit the ability to generate ATP.
    • Low O2
      • Hypoxia - Not common in humans.
        • Limit Mitochondria
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5
Q

Central Fatigue

A
  • Low Blood Glucose
    • GLUT1 Transporter
      • Low km, high affinity for glucose
  • High FFA
  • The rise in BCAA use
    • Central Fatigue Hypothesis
  • Low Glycogen
    • Increase Protein Oxidation
    • BCAAs are used; Decrease in blood.
      • Increase Tryptophan BCAA > Serotonin
        • Weak Evidence
      • FFA displaces Albumin Tryptophan = More Free Tryptophan
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6
Q

The vasculature is linked to metabolism. If you increase ______ _______, you increase ______ _______ of oxygen and nutrients

A
  • Blood flow; nutrient delivery
  • As oxygen demand increases, blood flow should match.
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7
Q

Fick Equation

A

VO2 = Q*A-VO2

Q = Stroke Volume * Heart Rate

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8
Q

Increasing cardiac output to working tissue increases vasodilation on three levels.

A
  1. Metabolic (Local level)
    1. Hypoxia, Adenosine, H+, Temperature
      1. Manipulate whether enzymes turn on or turn off.
      2. Signaling molecules to the local vasculature.
  2. Vasculature
    1. Nitric Oxide
  3. Myogenic
    1. The pressure of the contracting muscle moves blood/fluid forward throughout the vessel.
      1. Also, think about sex differences.
        1. Women have smaller muscles.
          1. Less impedance.
            1. Limits delivery of nutrients to tissues.
              1. Women are better at isometric contractions.
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9
Q

Nonworking tissue has a decreased O2 demand.

A
  1. Increase in Sympathetic Nervous System
    1. Typically promotes vasoconstriction.
      1. Norepinephrine
        1. Alpha Receptors
      2. Epinephrine
        1. Beta Receptors
  2. Chemicals - Local chemicals dominate over the sympathetic control.
    1. H+
      1. If a nonworking tissue doesn’t produce a lot of hydrogen, it signals that the tissue is not working hard; Wouldn’t see a change in vasodilation.
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10
Q

Training ______ capillary density.

A
  • Capillary Density
    • Increase AMPK
      • Increase VEGF
        • Vascular Endothelial Growth Factor
      • Increase NO
      • Increase PGC1-Alpha
    • Oxidative Capacity
      • B-HAD, CS, SDH, PFK, PDH
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11
Q

Feeding ______ insulin. Insulin ______ nitric oxide through ____ ____.

A
  • Increases, increases, shear stress.
  • Exercise decreases insulin.
    • Exercise increases shear stress.
    • Feeding increases insulin
      • Two different mechanisms.
  • Increased insulin occurs through endothelial Nitric Oxide Synthase (eNOS).
    • Insulin is effective from the large conduit artery to the microvasculature.
    • With feeding, insulin resistance people have limited blood flow and decreased glucose uptake.
    • Exercise increases blood flow through shear stress.
      • Nitric oxide mechanism.
      • Insulin-independent glucose uptake.
        • GLUT4 mechanism.
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12
Q

Exercise training increases eNOS activity.

A
  • Increased nitric oxide bioavailability.
  • Increased antioxidants.
    • Mitigates ROS accumulation and negative consequences.
  • Overfeeding leads to increased oxidative stress.
    • Exercise can mitigate the effect of energy balance.
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13
Q

Common Antioxidants

A
  1. Superoxide Dismutase (SOD)
  2. Glutathione Peroxidase (GPX)
  3. Catalase
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14
Q

Reactive Oxygen Species (ROS) locations:

A
  • Mitochondria
    • Resting-state.
  • Sarcoplasmic Reticulum, NAD(P)H, XO, Nitric Oxide, Cytosol
    • ROS paradox
      • ADP stimulating states (exercise).
    • Mitigate ROS.
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