Nutrition Advice Flashcards

1
Q

Main function of ATP in muscle

A

Dissociation of actin-myosin complex

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2
Q

What does CK transfer?

A

a (P) from ATP –> Creatine

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3
Q

Type 1 muscle

A

Slow, Red, Fatigue resistant

High Mb and Mitochondria

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4
Q

Type 2a muscle

A

Intermediate

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5
Q

Type 2b Muscle

A

Fast, White, High glycogen and Low mitochondria

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6
Q

PFK2 difference in muscle? Why?

A

is NOT regulated by phosphorylation

It doesn’t have the SERINE target for phosphorylation by PKA

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7
Q

Glucagon effect on muscle

A

none… there are no glucagon receptors

Glycogenolysis isn’t stimulated by glucagon (only epi)

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8
Q

Fatty acid synthesis isoform in muscle

A

Acetyl-CoA Carboxylase II

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9
Q

FA metabolism is regulated by what in muscle?

A

Malonyl CoA (control CPT enzymes)

(AMP protein kinase is another important regulator)

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10
Q

In muscle, glycolysis is inhibited by

A

ATP and Citrate levels

*not PFK2

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11
Q

PFK2 in cardiac muslce regulation

A

Phosphorylated and activated by insulin-depenent kinase cascade

Phosphorylation increases PFK2 kinase activity and STOPS glycolysis

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12
Q

3 ways that glycogen phosphorylase is regulated (activated)

A
  1. by AMP in muscle
  2. Ca++ can activate via glycogen phosphorylase kinase
  3. Epi can activate Adenylate cyclase, which activates cAMP-dependent protein kinase.
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13
Q

AMP activation pathway (2 steps)

A
  1. Atp—> ADP + Pi (((this happens during contraction)))
  2. 2ADP —> ATP + AMP (((adenylate cyclase rxn)))
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14
Q

What is the “master metabolic regulator”?

A

AMP Protein Kinase (AMPPK)

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15
Q

Overall function of AMPPK

A

inhibits the processes that require ATP, stimulates the ones that produce ATP

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16
Q

4 important functions of AMPPK

A
  1. Induces GLUT4
  2. Inactivates AcetylCoA Carboxylase (and Increases Malonyl Decarboxylase)
  3. Inhibits HMG-CoA Reductase
  4. Activates PFK2 in cardiac muscle to increase glycolysis
17
Q

Metformin function

A

Activates AMPPK via LKB1 (kinase)

18
Q

How does is fatty acid entry into mitochondria affected by AMPPK?

A

It lowers AcetylCoA carboxylase 2 (isoform in muscle)

AND it increases Malonyl CoA carboxylase

**Both of these things mean there’s a lot less Malonyl CoA floating around to inhibit CPT, so fatty acids get metabolized since they get transported into the mitochondria more readily.

19
Q

Fatty acyl chains transported as…

A

Fatty acylcarnitine

20
Q

Dephosphorylation effect on AcetylCoa Carboxylase?

What else regulates it?

A

Activates!

It is inactivated by AMPPK and Palmitoyl CoA

21
Q

Most abundant immediate source of ATP

A

Creatine Phosphate

22
Q

Creatine synthesis pathway

A
  1. Glycine + Arginine –>> Guanidinoacetate + Ornithine
  2. Guanidinoacetate + SAM –>> Creatine + SAH
23
Q

Where is creatine synthesized

A

Starts in Kidney, ends in liver

24
Q

Creatinine synthesis pathway and properties

A

Creatine –>> CP –>> Creatinine –>> (Excreted in urine)

This is spontaneous, constant, and based on the amount of skeletal muscle mass.

Nonenzymatic cyclization in muscle and brain

25
Q

Lactate transport?

A

Converted to Alanine by muscle for transport

26
Q

What happens after lactate is taken up by other cells

A

it is converted to pyruvate by LDH

27
Q

Anaerobic exercise progression

A
  1. ATP generated from the formation of Lactate from glycogen
  2. Rise in AMP = increase in PFK1 and glycogen breakdown = More ATP
  3. Lactate goes on to be used by heart after conversion to pyruvate
28
Q

How much ATP from BCAAs?

A

20%

29
Q

Explain urine buffering in regards to BCAA

A

Release of NH<strong>3</strong> by the muscle buffers urine as H+ increases during exercise

30
Q
A