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Musculoskeleton > Energy Metabolism Of Muscle > Flashcards

Energy Metabolism Of Muscle Flashcards

1
Q

ATP to ADP and vise versa mechanisms

A

When ATP is used by muscles, a hydrolysis cleaves the gamma (y) phosphate from ATP, generating energy and ADP

ADP is regenerated to ATP via phosphatases.

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2
Q

GLUT proteins

A

Glucose transporters that span membrane and conduct facilitated diffuse without ATP.

Has 5 different types for specific tissues

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3
Q

GLUT 1 is in what tissues?

A

Erythrocytes, blood barriers (brain, retinal, placental and testis)

-High affinity

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4
Q

GLUT 2 is in what tissues?

A

Liver, kidney, pancreatic (b)-cells,
Intestinal mucosa cells

High-capacity, low affinity

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5
Q

GLUT 3 is found in what tissues?

A

Brain and neurons.

  • main transporter of glucose in nervous system
  • High affinity
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6
Q

GLUT 4 is found in what tissues

A

Adipose tissues, heart muscle, skeletal muscle

  • insulin sensitive, high affinity transporters.
  • up-regulates in the prescience of insulin
  • high affinity
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7
Q

GLUT 5 is found in what tissues?

A

Intestinal epithelium & Sperm

  • technically a fructose transporter*
  • high affinity.
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8
Q

Type 2 diabetes

A

Developing insulin resistance causes GLUT 4 transporters to be deficient and not up-regulate in the presence of insulin.

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9
Q

Phosphofructokinase-1 characteristics

A

Irreversible reaction in glycolysis (glucose is stuck in glycolysis)

Rate-limiting and committed step

Inhibited by high concentration of ATP and citrate

Activated in muscle by high concentration of AMP

Activated in liver by high concentration of F 2,6 Bisphosphate

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10
Q

Hexokinase characteristics

A

Found in most tissues especially muscle (NOT liver)

Inhibited by high G6P concentrations

High affinity for glucose (low Km)

Low maximal Velocity (Vmax)

Very efficient enzyme

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11
Q

Normal Lactate production in muscle

A

Occurs via a build up of anaerobic glycolysis. (Specifically exercising skeletal muscle)

Usually transported to the liver and metabolized back to glucose via cori cycle (gluconeogenesis) to be used again in glycolysis

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12
Q

Why is glucose immediately transformed into glucose 6-P when entering cell?

A

glucose 6-P cannot escapes the cell. All can be used when needed

  • no transporters
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13
Q

examples of Abnormal lactate production in muscle

A

Hypoxia in muscles or extreme lactic acidosis

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14
Q

Types of lactic acidosis

A

Normal lactate (<2mmol)

Hyperlactermia (2-5mmol) w/ metabolic acidosis

Lactic acidosis (4-5mmol) without metabolic acidosis

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15
Q

Substrate level phosphorylation produces how much ATP?

A

2 ATP

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16
Q

Oxidative phosphorylation of one pyruvate produces how many ATP?

A

10 ATP

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17
Q

Pyruvate dehydrogenase complex (PDH)

A

Breaks down pyruvate into Acetyl CoA with 3 enzymes and 5 coenzymes

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18
Q

FAD coenzyme is produced by what?

A

Niacin (Vit B3)

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19
Q

NAD coenzyme is produced by what?

A

Riboflavin (Vit B2)

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20
Q

Coenzyme-A (CoA) is produced by what?

A

Pantothenic acid (Vit. B5)

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21
Q

Thiamine pyrophosphate (TPP) is formed by what?

A

Thiamine (Vit. B1)

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22
Q

Lipoamide is formed by what?

A

Naturally synthesized by human cells (does not need an essential vitamin)

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23
Q

Three enzymes of the PDH complex

A

E1 (pyruvate carboxylase)

E2 (dihydrolipoyl transacetylase)

E3 (dihydrolipoyl dehydrogenase)

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24
Q

Glucokinase

A

Similar to hexokinase except is found in liver.

Also has a higher Km and higher maximal Vmax

not as efficient however in excess glucose, is better than hexokinase

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25
Q

PDH complex regulation

A

Activated by increased concentrations of
- Pyruvate, NAD+, ADP, Calcium, CoA

Inhibited by increased concentrations of
-Acetyl CoA, NADH, ATP

Can be allosterically inhibited by phosphorylation and activated by dephosphorylation

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26
Q

Irreversible steps of Citric acid cycle (TCA)

A

Citrate synthase

Isocitrate dehydrogenase

(A)-ketoglutarate dehydrogenase complex

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27
Q

Citrate synthase activation and inhibition

A

High OAA concentrations =. Activates

High Citrate concentrations = inhibits

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28
Q

Isocitrate dehydrogenase activators and inhibitors

A

Inhibited by: high concentrations of ATP and NADH

Activated by: high concentrations of ADP and calcium

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29
Q

(A)-ketoglutarate dehydrogenase complex activators and inhibitors

A

Inhibited by: High succ-CoA concentrations

Activated by: High calcium concentrations in muscles

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30
Q

Adenylate kinase (Myokinase) function in Fatty acid oxidation

A

Takes 2 ADP molecules and generates 1 ATP and 1 AMP molecules

  • quick way to generate ATP and signal the muscle cells to produce Malonyl-COA de carboxylase and allow FAs to enter muscle cells.
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31
Q

Overall fatty acid oxidation steps in muscle cells

A

Albumin or other carriers carry FAs into cytosol.

FAs are activated into fatty-CoA which is transported to outer mitochondrial membrane via conversion into fatty acylcarnitine by carnitine.

Fatty acylcarnitine is transported into the inner mitochondrial membrane and converted back into fatty-CoA

Fatty CoA is oxidized in inner mitochondrial membrane into multiple Acetyl-CoA

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32
Q

Regulations of fatty acid oxidation in skeletal muscles

A

Occurs via disabling transferring of fatty acid into mitochondria

  • excess citrate from Citric Acid cycle can leave and produce Malonyl-CoA via ACC-2 enzyme which inhibits fatty acid transferring into the mitochondria
  • occurs when high ATP
  • Malonyl-CoA decarboxylase activates when ATP is Low (high AMP) and reverses the above reaction.
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33
Q

Mobile components of ETC

A

Coenzyme Q

Cytochrome C

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34
Q

Cardiolipin

A

Two glycerol molecules esterfied through phosphate bonds

Exclusive to the inner mitochondrial membrane

Maintains the structure and function of the ETC complexes 1-4

35
Q

Coupling in normal mitochondria

A

ATP synthesis is coupled to the electron transportation through the complexes.

  • every 4 protons generates 1 ATP
36
Q

Uncoupling in normal mitochondria

A

Back flow of electrons down the complexes without ATP generation

-importaint for thermogenesis
Can be natural or synthetic

37
Q

Natural uncoupling

A

Uses uncoupling proteins localized in inner mitochondrial membrane

UCP 1 = found in brown adipose tissue

UCP 2-5 = found in every other tissue

38
Q

Synthetic uncoupling

A

Uses synthetic uncouplers that are chemical that increase the permeability of the inner mitochondrial membrane to electrons

  • aspirin is the mot well known
39
Q

Inhibitors of complex 1 in ETC

A

Amytal and Roterone

40
Q

Inhibitor of complex 3 in ETC

A

Antimycin C

41
Q

Inhibitors of complex 4 in ETC

A

Carbon monoxide (at the end of complex 4 to oxygen)

Cyanide and sodium azide (at the beginning of complex 4)

42
Q

Glycogen storage in both the liver and muscle respectively

A

100g and 400g respectively

Muscle has more glycogen however liver is more concentrated

43
Q

Products of glycogenlysis in both liver and muscle

A

Blood glucose in liver (transported to muscles to be used)

ATO, lactate and CO2 in muscle cells (glucose is actually broken down all the way)

44
Q

What two bonds are present in glycogen?

A

(A) 1,4 and (a) 1,6 glycosidic bonds.

45
Q

Why are glycogen branches important?

A

(A) 1,6 creates branches on glycogen which are used for two reasons.

1) to increase the solubility of glycogen molecules
2) increase number of non reducing ends and allow for fast synthesis and degradation

46
Q

Phosphoglucomutase

A

enzyme used to generate G1P from G6P in glycogenesis

47
Q

Glycogen synthase

A

Generate UDP-glucose form G1P in glycogenesis

rate-limiting step of glycogenesis

48
Q

Transferase (branching enzyme)

A

Binds glucose-UDP molecules to the chain of glycogen making it longer

49
Q

Glycogenin

A

Primer for glycogen synthesis.

Is the starting molecule for creating a new glycogen strand.

Tyrosine is the attachment point on glycogen for UDP glucose

50
Q

Glycogen phosphorylase

A

Enzyme for glycogenolysis which breaks (a) 1,4 bonds

Rate limiting regulatory step found only in muscle and liver tissues

51
Q

Debranching enzyme

A

Same activity as glycogen phosphorylase except targets (a) 1,6 bonds.

52
Q

Glycogen phosphorylase activation and inhibition in muscles

A

Activated by high concentrations of

  • AMP
  • Ca2
  • Epinephrine

Inhibited by high concentrations of

  • Insulin
  • Glucose 6-P
  • ATP
53
Q

Glycogen synthase activation and inhibition in muscles

A

Active by large contractions of

  • Glucose 6-P
  • Insulin

Inhibited by large concentrations
- Epinephrine

54
Q

Glycogen synthase inhibition and activation in liver

A

Active by large concentrations of

  • G6P
  • Insulin

Inhibited by large concentrations of

  • Glucagon
  • Epinephrine
55
Q

Glycogen phosphorylase activation and inhibition in liver

A

Activation occurs in high concentrations of

  • Epinephrine
  • Glucagon

Inhibition occurs in high concentrations of

  • G6P
  • Glucose
  • ATP
  • Insulin
56
Q

Lysosomal (a) 1,4-glucosidase

A

Product of a housekeeping gene

Degrades Glycogen at optimal pH of 4.5

Deficiency causes Type 2 Pompe disease

57
Q

Type 2 Pompe disease

A

Lysosomal disease caused by deficiency of (a) 1,4 glucosidase in muscle cells

  • causes excessive glycogen build up in lysosomes and leads to muscle weakness and cardiomegaly
  • appear large inclusion bodies in lysosomes in histology slides
  • fatal in infantile form and treated by replacement therapies
58
Q

Type 5 McArdle syndrome

A

Deficiency of muscle glycogen phosphorylase enzyme in skeletal muscle only

Myoglobinuria and mygolbinemia can be present

Causes accumulation of glycogen in skeletal muscle fibers (can be seen in staining)

Relatively benign and chronic condition.

59
Q

Type 6 Hers disease

A

Liver glycogen phosphorylase deficiency

  • causes mild hypoglycemia since glycogen can’t be broken down, however gluconeogensis is still conducted.
  • also causes hepatomegaly and cirrhosis of the liver if untreated.
60
Q

Type 3 cori disease

A

Deficiency in debranching enzyme

Can’t break down (1) 1,6 glycogen bonds

  • causes hypoglycemia and abnormal glycogen structures
  • left uncheck produces hepatomegaly and myopathy
61
Q

Inhibitors of Complex 5

A

Oligomycin

62
Q

Cytochrome C

A

Acts on caspase to initate apoptosis.

63
Q

CPT - 2 deficiency

A

Mutation in the carnitine transporter that disables fatty acid COA from entering the mitochondria preventing oxidation.

Autosomal recessive

3 forms

Leather neonatal

Severe infantile

Mild myopathic

64
Q

Insulin affects on muscle

A

Turns on AkT and inhibits glycogen degradation as well as turns on glycogen synthesis

65
Q

Epinephrine affects on muscle regulation

A

Turns on adenylate Cyclase which initiates the following signal cascade

1) produces cAMP
2) cAMP turns on protein kinase A
3) protein kinase A both turns off glycogen synthase and activates phosphatase A
* Reciprocal regulation*

4) generates G1P and G6P which turns into lactate and ATP

66
Q

Allosteric regulation of calcium in muscle

A

Free calcium in muscles bind to calmodulin.

Calmodulin activates phosphorylase kinase B

phosphorylase kinase B stimulates glycogen degradation.

67
Q

Type 4 Andersen disease

A

Branching enzyme deficiency in muscle

Causes infantile hypotonia, cirrhosis and death

Glycogen having few branches is the pathological confirmation

68
Q

CPK/CK 1

A

Creatinine kinase founds only in the Brain

69
Q

CPK/CK 2

A

Creatinine found only in the Heart

presence in blood/urine signals a myocardial infarction

70
Q

CPK/CK 3

A

Creatinine kinase found in both skeletal and cardiac muscle

71
Q

Type 2 oxidative muscle fibers

A

Fast-twitch red fibers

High myoglobin content and use oxidation to generate energy

Average resistance to fatigue

Large fiber diameter (2nd fastest movement)

72
Q

Type 2 glycolytic muscle fibers

A

Fast-twitch white fibers

Low myoglobin concentration appears white.

Fast-glycolytic fibers

Easily fatigued and not energy efficient

Used for sprinting/ quick explosive movements

Very large fiber diameter (fastest movement)

73
Q

Type 1 muscle fibers

A

Slow-twitch red fibers

High myoglobin concentration appears red

Slow-oxidative fibers

Very high resistance to fatigue

Used for prolonged aerobic activities

Small fiber diameter (slow speed)

74
Q

Myoglobin

A

Similar structure to hemoglobin however can only bind 1 oxygen molecule (heme molecule).

Found in skeletal and heart muscle

High affinity than hemoglobin and becomes saturated quicker.

75
Q

AMP activates what in muscles?

A

GLUT 4 transporters

FA transporters

Glycogenolysis and glycolysis

76
Q

Ca2+ activates what?

A

Glycogenolysis

PDH complex activation

CTC cycle

77
Q

Timing of both creating phosphate and ATP in exercise

A

creatine phosphate =. 5-20 sec

Glycolysis = 20 sec - 2 min

-creatine phosphate is only used for the first minute or so until storages run out. At this point ATP (muscle muscle glycogen) becomes fuel source until exhaustion

78
Q

Carbs and FA usage in exercise

A

Carbs: used in vigorous contractions and explosive forces

Fatty acids: used in low intensity exercises

79
Q

Aerobic vs anaerobic exercise

A

Aerobic:
- increases aerobic capacity by increasing mitochondria in fast fibers

  • utilizes Fatty acids
  • uses nutrients from blood
  • primary protein in mechanisms is PGC-1a

Anaerobic:
- increases muscle size and number

  • utilizes carbs, creatine kinase and glycogen
  • does not require external fuels from bloods
  • myostatin is a special hormone protein that inhibits protein synthesis up to a certain point (prevents over hypertrophy)
80
Q

The athlete paradox

A

Lipid droplet accumulation in muscle cells that are used as energy actually cause increased insulin sensitivity in athletes rather than insulin resistance.

81
Q

Sarcopenia

A

Age-related skeletal and muscle mass decline/function

Affects nearly 50% of all 70+ people.

Idiopathic etiology and is multifactorial

82
Q

Cachexia

A

Wasting of muscle in cancer patients

Caused by protein wasting of muscles and not being rebuilt via satellite cells

Malabsorption

Immune dysfunction

Increased glucose turnover and increased energy expenditure via tumor activity.

83
Q

Cardiac muscle cells characteristics

A

CANNOT store energy

Always aerobic and rich in myoglobin

Utilizes primarily Fatty acids

Also uses glucose and ketone bodies produced by liver.

Lactate is more damaging to cardiac cells than skeletal cells

84
Q

Why does blood flow increase in aerobic exercise?

A

Lactate relaxes blood vessels

Musculoskeleton (36 decks)

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