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Beckett, SPEX, 3rd Year > Nutrition Lecture Week 7 - Advanced Exercise Physiology, Metabolism and Inflammation > Flashcards

Nutrition Lecture Week 7 - Advanced Exercise Physiology, Metabolism and Inflammation Flashcards

1
Q

Cellular uptake of plasma CHO does not limit oxidation …

A

the major limiting step in oxidising ingestion CHO appears to be the transport across the intestinal mucosa

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2
Q

Role of insulin in glucose disposal …

A

Insulin stimulates a cascade of protein activity (phosphorylation) which causes GLUT-4 transport proteins to translocate to the plasma membrane

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3
Q

Muscle contraction can directly mediate cellular glucose disposal …

A
  • AMPK mediated
  • when both beta1 and beta2 subunits were genetically deleted, glucose uptake was reduced
  • PGC-1aplha activity was incereased in the beta1/beta2 knockout
  • Ca** mediated
  • tetanic calcium (Ca**) release (muscle contraction) also activates AMPK
  • Action of Ca2+/calmodulin dependant protein kinase
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4
Q

AMPK activity is reduced in AMPKalpha2 inactive mice when …

A

CaMKK is activated

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5
Q

Trained athletes use increased fat at same %VO2max …

A

at lower exercise intensity, fat oxidation increased further

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6
Q

Intramuscular triacylglycerol (IMTG) utilisation is …

A

fibre type dependant

- depletion of IMTG >60% in type 1 fibres

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7
Q

Increase in acetyl carnitine may inhibit CPT1 and down regulate FA entry into the mitochondria …

A
  • Free carnitine reduced as increased actyl groups from acetyl CoA during high intensity exercise binds to carnitine, inhibiting CPT1
  • free carnitine + acyl = acetylcarnitine = LCFA entry
  • lower free carnitine = low carnitine = lower CPT 1 activitiy
    =Effect of exercise intensity
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8
Q

Elevated plasma FA impairs…

A

impairs insulin signalling and intramuscular triacylglycerol oxidation

    • inhibits the insulin cascade for GLUT4 translocation - IRS1, Akt, AS160 inactivation
    • the metabolites PKC Ceramides and Fatty Acyl CoA impair the activation of insulin signalling intermediates
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9
Q

Why do people with obesity liberate IMTG at a lower rate …

A 
-- Insulin resistant = ↓ adipose
tissue FFA release
-- Therefore ↑ lpl activity and FFA
cellular availability
-- Greater FA oxidation by products
→ direct inhibition IMTG liberation
(adipose triglyceride lipase; agtl)
-- Exacerbated by inactivity as IMTG
turnover is reduced & FFA entry ↑
for energy storage (↑ FAT/CD36
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10
Q

Why do trained athletes have more IMTG ?

A
  • Due to regular depletion and enzymatic up regulation
  • CPT1 activity ↑
    • ↑ type 1 fibre expression
    with training
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11
Q

Niacin (vit b3)/ acipimox suppresses …

A

adipose tissue lipolysis

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12
Q

Acipimox increases IMTG utilisation during exercise and is associated with …

A

improved insulin sensitivity

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13
Q

Explain why Pdk 4 inhibitor reduces acetylcarnitine ?

A 
• PDK 4: an enzyme responsible for
converting pyruvate to acetyl-CoA
• Remember ↑ acetylcarnitine inhibits
CPT1 (and FA entry into mitochondria
• It stands if we ↓ acetylcarnitine we
can upregulate fat oxidation (and
liberate IMTG)
• Can this be achieved by dietary
manipulation?
• Increase fat oxidation and insulin
sensitivity
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14
Q

Can diet/exercise increase fat oxidation ?

A 
• ↓reliance on CHO
• ↑ fat oxidation
• ↑ circulatory ketone bodies
• ↑ ketone oxidation?
• Can fat provide enough energy
to sustain higher intensity (%
VO2max)?
• What about performance?
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15
Q

Inflammation is …

A

The first physiological response to harmful stimuli which is required for the healing of injured
tissue

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16
Q

What are causes of inflammation ?

A
  • Mechanical injury
  • chemical toxins
  • invasion by microorgnisms
  • hypersensitivity reactions
17
Q

Why do people with obesity liberate IMTG at a lower rate …

A 
-- Insulin resistant = ↓ adipose
tissue FFA release
-- Therefore ↑ lpl activity and FFA
cellular availability
-- Greater FA oxidation by products
→ direct inhibition IMTG liberation
(adipose triglyceride lipase; agtl)
-- Exacerbated by inactivity as IMTG
turnover is reduced & FFA entry ↑
for energy storage (↑ FAT/CD36
18
Q

Why do trained athletes have more IMTG ?

A
  • Due to regular depletion and enzymatic up regulation
  • CPT1 activity ↑
    • ↑ type 1 fibre expression
    with training
19
Q

Niacin (vit b3)/ acipimox suppresses …

A

adipose tissue lipolysis

20
Q

Acipimox increases IMTG utilisation during exercise and is associated with …

A

improved insulin sensitivity

21
Q

Explain why Pdk 4 inhibitor reduces acetylcarnitine ?

A 
• PDK 4: an enzyme responsible for
converting pyruvate to acetyl-CoA
• Remember ↑ acetylcarnitine inhibits
CPT1 (and FA entry into mitochondria
• It stands if we ↓ acetylcarnitine we
can upregulate fat oxidation (and
liberate IMTG)
• Can this be achieved by dietary
manipulation?
• Increase fat oxidation and insulin
sensitivity
22
Q

Can diet/exercise increase fat oxidation ?

A 
• ↓reliance on CHO
• ↑ fat oxidation
• ↑ circulatory ketone bodies
• ↑ ketone oxidation?
• Can fat provide enough energy
to sustain higher intensity (%
VO2max)?
• What about performance?
23
Q

How to attenuate inflammation ?

A
  • Disrupt the cytokine response
  • Prevent the inflammatory stimulus
  • ibuprofen, aspirin
  • n-3 & antioxidants
24
Q

What are causes of inflammation ?

A
  • Mechanical injury
  • chemical toxins
  • invasion by microorgnisms
  • hypersensitivity reactions
25
Q

What is the body’s reaction to causes of inflammation ?

A
  • Release of cytokines (signalling proteins)
  • ↑ blood supply to the affected area
  • capillary permeability is increased,
  • leucocytes migrate from the capillary
    vessels into the surrounding interstitial
    spaces to the site of inflammation or injury
    capillary permeability is increased
26
Q

Pro vs Anti inflammatory cytokines and proteins

A 
• Schenk 2009 - IKK-NkB
pathway increased in obese
and causes insulin resistance
• ↑ by FFA availability
• Reversed with training
- Training stimulus
- ↑ inflammation
- Temporary damage/disfunction to
the myofibrils (actin/mysiin
filaments)
- ↑ protein turnover →
repair
27
Q

Describe IL1 ( A key cytokine which activates the inflammatory response)

A

Produced by monocytes and many other cells

activate lymphocytes and many inflammatory cells

28
Q

Describe TNF ( A key cytokine which activates the inflammatory response)

A 
• Two forms:TNFa and TNFb.
• Produced by many cells including
monocytes (TNFa ) .
• Produced by T-cells (TNFb).
• Widespread activation of cells;
apoptosis, shock, cachexia
29
Q

Describe IL6 ( A key cytokine which activates the inflammatory response)

A

• Produced by T-cells but also
by many other cells too.
• Activates B & T-cells and
other cell types.

30
Q

Describe Interferons (IFNs) (A key cytokine which activates the inflammatory response)

A 
• 3 forms: a,b & g.
• Produced by monocytes (a),
fibroblasts (b) and T-cells (g).
• Antiviral, cell activating and
tumour suppressant effects.
31
Q

How to attenuate inflammation ?

A
  • Disrupt the cytokine response
  • Prevent the inflammatory stimulus
  • ibuprofen, aspirin
  • n-3 & antioxidants
32
Q

Name 4 anti-inflammatory foods / food types / minerals

A
  1. fibre
  2. B-Carotene
  3. Vitamin D
  4. Garlic
33
Q

Name 4 pro-inflammatory foods / food types / minerals

A
  1. saturated fat
  2. cholesterol
  3. Carbohydrate
  4. Protein

Beckett, SPEX, 3rd Year (8 decks)

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