Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Musculoskeleton > Energy Metabolism Of Muscle > Flashcards

Energy Metabolism Of Muscle Flashcards

(84 cards)

Start Studying
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

GLUT proteins

A

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

Has 5 different types for specific tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

GLUT 1 is in what tissues?

A

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

-High affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

GLUT 2 is in what tissues?

A

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

High-capacity, low affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

GLUT 3 is found in what tissues?

A

Brain and neurons.

  • main transporter of glucose in nervous system
  • High affinity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GLUT 5 is found in what tissues?

A

Intestinal epithelium & Sperm

  • technically a fructose transporter*
  • high affinity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

examples of Abnormal lactate production in muscle

A

Hypoxia in muscles or extreme lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Types of lactic acidosis

A

Normal lactate (<2mmol)

Hyperlactermia (2-5mmol) w/ metabolic acidosis

Lactic acidosis (4-5mmol) without metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Substrate level phosphorylation produces how much ATP?

A

2 ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Oxidative phosphorylation of one pyruvate produces how many ATP?

A

10 ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pyruvate dehydrogenase complex (PDH)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

FAD coenzyme is produced by what?

A

Niacin (Vit B3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

NAD coenzyme is produced by what?

A

Riboflavin (Vit B2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Coenzyme-A (CoA) is produced by what?

A

Pantothenic acid (Vit. B5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Thiamine pyrophosphate (TPP) is formed by what?

A

Thiamine (Vit. B1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Lipoamide is formed by what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Three enzymes of the PDH complex

A

E1 (pyruvate carboxylase)

E2 (dihydrolipoyl transacetylase)

E3 (dihydrolipoyl dehydrogenase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
PDH complex regulation
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
26
Irreversible steps of Citric acid cycle (TCA)
Citrate synthase Isocitrate dehydrogenase (A)-ketoglutarate dehydrogenase complex
27
Citrate synthase activation and inhibition
High OAA concentrations =. Activates High Citrate concentrations = inhibits
28
Isocitrate dehydrogenase activators and inhibitors
Inhibited by: high concentrations of ATP and NADH Activated by: high concentrations of ADP and calcium
29
(A)-ketoglutarate dehydrogenase complex activators and inhibitors
Inhibited by: High succ-CoA concentrations Activated by: High calcium concentrations in muscles
30
Adenylate kinase (Myokinase) function in Fatty acid oxidation
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.
31
Overall fatty acid oxidation steps in muscle cells
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
32
Regulations of fatty acid oxidation in skeletal muscles
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.
33
Mobile components of ETC
Coenzyme Q Cytochrome C
34
Cardiolipin
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
Coupling in normal mitochondria
ATP synthesis is coupled to the electron transportation through the complexes. - every 4 protons generates 1 ATP
36
Uncoupling in normal mitochondria
Back flow of electrons down the complexes without ATP generation -importaint for thermogenesis Can be natural or synthetic
37
Natural uncoupling
Uses uncoupling proteins localized in inner mitochondrial membrane UCP 1 = found in brown adipose tissue UCP 2-5 = found in every other tissue
38
Synthetic uncoupling
Uses synthetic uncouplers that are chemical that increase the permeability of the inner mitochondrial membrane to electrons - aspirin is the mot well known
39
Inhibitors of complex 1 in ETC
Amytal and Roterone
40
Inhibitor of complex 3 in ETC
Antimycin C
41
Inhibitors of complex 4 in ETC
Carbon monoxide (at the end of complex 4 to oxygen) Cyanide and sodium azide (at the beginning of complex 4)
42
Glycogen storage in both the liver and muscle respectively
100g and 400g respectively Muscle has more glycogen however liver is more concentrated
43
Products of glycogenlysis in both liver and muscle
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
What two bonds are present in glycogen?
(A) 1,4 and (a) 1,6 glycosidic bonds.
45
Why are glycogen branches important?
(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
Phosphoglucomutase
enzyme used to generate G1P from G6P in glycogenesis
47
Glycogen synthase
Generate UDP-glucose form G1P in glycogenesis rate-limiting step of glycogenesis
48
Transferase (branching enzyme)
Binds glucose-UDP molecules to the chain of glycogen making it longer
49
Glycogenin
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
Glycogen phosphorylase
Enzyme for glycogenolysis which breaks (a) 1,4 bonds Rate limiting regulatory step found only in muscle and liver tissues
51
Debranching enzyme
Same activity as glycogen phosphorylase except targets (a) 1,6 bonds.
52
Glycogen phosphorylase activation and inhibition in muscles
Activated by high concentrations of - AMP - Ca2 - Epinephrine Inhibited by high concentrations of - Insulin - Glucose 6-P - ATP
53
Glycogen synthase activation and inhibition in muscles
Active by large contractions of - Glucose 6-P - Insulin Inhibited by large concentrations - Epinephrine
54
Glycogen synthase inhibition and activation in liver
Active by large concentrations of - G6P - Insulin Inhibited by large concentrations of - Glucagon - Epinephrine
55
Glycogen phosphorylase activation and inhibition in liver
Activation occurs in high concentrations of - Epinephrine - Glucagon Inhibition occurs in high concentrations of - G6P - Glucose - ATP - Insulin
56
Lysosomal (a) 1,4-glucosidase
Product of a housekeeping gene Degrades Glycogen at optimal pH of 4.5 Deficiency causes Type 2 Pompe disease
57
Type 2 Pompe disease
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
Type 5 McArdle syndrome
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
Type 6 Hers disease
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
Type 3 cori disease
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
Inhibitors of Complex 5
Oligomycin
62
Cytochrome C
Acts on caspase to initate apoptosis.
63
CPT - 2 deficiency
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
Insulin affects on muscle
Turns on AkT and inhibits glycogen degradation as well as turns on glycogen synthesis
65
Epinephrine affects on muscle regulation
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
Allosteric regulation of calcium in muscle
Free calcium in muscles bind to calmodulin. Calmodulin activates phosphorylase kinase B phosphorylase kinase B stimulates glycogen degradation.
67
Type 4 Andersen disease
Branching enzyme deficiency in muscle Causes infantile hypotonia, cirrhosis and death Glycogen having few branches is the pathological confirmation
68
CPK/CK 1
Creatinine kinase founds only in the Brain
69
CPK/CK 2
Creatinine found only in the Heart *presence in blood/urine signals a myocardial infarction*
70
CPK/CK 3
Creatinine kinase found in both skeletal and cardiac muscle
71
Type 2 oxidative muscle fibers
Fast-twitch red fibers High myoglobin content and use oxidation to generate energy Average resistance to fatigue Large fiber diameter (2nd fastest movement)
72
Type 2 glycolytic muscle fibers
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
Type 1 muscle fibers
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
Myoglobin
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
AMP activates what in muscles?
GLUT 4 transporters FA transporters Glycogenolysis and glycolysis
76
Ca2+ activates what?
Glycogenolysis PDH complex activation CTC cycle
77
Timing of both creating phosphate and ATP in exercise
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
Carbs and FA usage in exercise
Carbs: used in vigorous contractions and explosive forces Fatty acids: used in low intensity exercises
79
Aerobic vs anaerobic exercise
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
The athlete paradox
Lipid droplet accumulation in muscle cells that are used as energy actually cause increased insulin sensitivity in athletes rather than insulin resistance.
81
Sarcopenia
Age-related skeletal and muscle mass decline/function Affects nearly 50% of all 70+ people. Idiopathic etiology and is multifactorial
82
Cachexia
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
Cardiac muscle cells characteristics
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
Why does blood flow increase in aerobic exercise?
Lactate relaxes blood vessels

Musculoskeleton (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions