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35 Cards in this Set
- Front
- Back
what are slow twitch Type 1 fibers used for? what are their characteristics?
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long term exercise
small diameter low glycogen high myoglobin, O2 capaciy, resistance to fatigue |
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what are fasttwitch Type 2b fibers used for? what are their characteristics?
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short term energy need
large fiber diameter high glycogen low myoglobin, O2 capacity, resistance to fatigue |
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How do cardiac muscles get energy? What are their characteristics?
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oxidative phosphorylation (except when well fed)
rich in mito little glycogen |
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How does smooth muscle get energy? What does it do?
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maintains tension for a long period of time
does not need much energy |
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what are 3 types of muscle weakness?
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insufficient energy supply (not enough ATP)
impaired neurological control (not enough intracellular Ca++) deficiency in muscle strucutral proteins |
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what are examples of deficiencies in muscle structural proteins?
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muscular dystrophies (Duchenne, Becker)
(Dystrophin deficient - links muscle fibers to sarcolemma) cardiomyopathies |
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what are examples of deficiencies in muscle energy supply?
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ichemia (lack of O2) like myocardial infarction
genetic diseases of fuel metabolism, like McArdle (Glycogen), Carnitine (FA) |
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what are examples of deficiencies in muscle Ca+=supply?
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myasthenia gravis
neurocontrol compromised acetylcholine receptors |
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What are the 2 major sources of ATP in muscles (metabolic pathways)? What molecules do they use?
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Glycolysis - glucose - from glycogen or blood glucose
Oxidative Phosphorylation - NADH and FADH2 from TCA cycle, B oxidation FAs, oxidation of branched chain AAs like Ile, Leu, Val, conversion lactate to pyruvate |
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What is the role of creatine phosphate in muscle energy metabolism?
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way to store high energy phosphate (ATP)
creatine --creatine phospokinase --> creatine phosphate |
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why cant ATP be stored as it is?
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is an allosteric regulator of many enzymes
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what do increased blood creatine levels indicate?
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impaired kidney function
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How is ATP regenerated?
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adp --adenylate kinase --> ATP + AMP
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What does AMP upregulate?
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glycolysis
glycogenolysis B oxidation of FAs |
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Which disease would cause an increase in creatine kinase levels in a patient's blood?
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McArdle Syndrome
usually not secreted in circulation unless muscle is damaged |
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What is the key regulated enzyme in glycolysis?
How does its regulation differ in liver, skeletal and cardiac muscle? |
Phosphofruktokinase 2 (PFK2)
liver - glucagon/epinephrine -> phosphorylate PFK2 > downregulate glycolysis skeletal - no phosphorylation > no regulation at PFK2 level > glycolysis just occurs cardiac - insulin/epinephrone, AMP -> phosphorylation PFK2 -> glycolysis upregulated |
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What is the major regulated step of B oxidation?
what inhibits it? |
Carnitine palmitoyl transferase 1 (CPT1)
inhibited by malonyl coA (cant get into mito matrix) High ACC2 = high MCoA = CPT1 inhibited and cant degrade FAS High MCoADC = low MCoA = FA degradation |
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how is energy produced in the heart when fasting blood glucose levels?
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degradation of long chain fatty acids
> high levels acetyl coA and citrate > limit energy production from glucose through glycolysis (PFK1 and PDH inhibited) favors TCA not glycolysis |
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how is energy produced in the heart when high blood glucose levels?
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increase glycolysis through insulin (GLUT 4 uptake)
> activates PFK2 > activate PFK1 > activates glycolysis |
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When you eat carbs, what enzyme is activated by phoshorylation throug h action of insulin in heart muscle?
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PFK-2
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What is the effect of ischemia in cardiac muscle (cant get O2 to muscle)?
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no O2 > mito ATP synthesis and B oxidation FAs inhibited
> elevated AMP/ATP ratio > glucose uptake, PFK1 and PFK2 activation > glycolysis > pyruvate converted to lactate |
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what is the source of energy for resting skeletal muscle?
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aerobic metabolism = oxidative phosphorylation, FA oxidation
high blood glucose > glycogen high branched AAs> make energy high citrate > reduced glycolysis (reduce PFK1) and B oxidation FAs (activate ACC2) |
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what is the source of energy for fasting skeletal muscle?
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glucose uptake downregulated (GLUT 4 levels decrease)
FA used as fuel low ATP > high AMP > activate AMP-PK > deactivate ACC2 > low malonyl coA > B oxidation FAs > actyl coA . inhibit pyruvate dehydrogenase > limit use of glucose as energy source |
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what is the source of energy for onset exercise of skeletal muscle?
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first minute = anaerobic glycolysis > quick ATP supply
then glucogenolysis and glycolysis activated (need O2) by AMP and increased Ca++ |
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What is the most sensitive reflection of energy in skeletal muscles during exercise?
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AMP
changes more than ADP or ATP do when resting and exercising |
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What changes in metabolite levels of skeletal muscle would be observed after sprinting?
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decreased ATP
decreased creatine phosphate increased lactate |
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what provides energy during high intensity exercise?
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B oxidation of FAs and TCA cycle
not fast enough > AMP still high > activate PFK1 > anerobic glycolysis > pyruvate which cant enter TCA cycle because it is blocked up > lactate |
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Why cant high intensity exercise be maintained for a long time?
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musle glycogen stores depleted
lactic acidosis |
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what happens to lactate in resting skeletal, cardiac muscle, and liver?
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liver > cori cycle > gluconeogenesis > glucose others can use
muscle > lactate dehydrogenase converts it back to pyruvate if low NADH/NAD ratio > energy |
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what compensates for lactic acidosis during exercise?
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purine nucleotide cycle accelerated
> fumarate > TCA cycle and AMP > IMP which produces NH3 > transported fro muscle (glutamine) to kidney (glutamine) > NH3 helps to excrete protons in urine |
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what is the source of energy for long term exercising skeletal muscle?
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aerobic oxidation of FAs and glucose (BOTH)
less lactate made 40 min > liver flycogen 4 hours> gluconeogenesis increases, glucogenolysis decreases then use FAs from fat |
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What do muscles preferentially get energy from?
when dont they? |
fatty acids
except right after eating |
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What relies on glucose for energy?
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anaerobic glycolysis like at start of exercise or high intensity
long term exercise fast twitch muscles (limited oxidative supply) |
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what enzymatic modification is most characteristic in liver of marathon runner 35 min into race?
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phosphorylation of glycogen phosphorylase (epinephrine)
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What is the most characteristic metabolic change in fast twitch muscles of the legs of a sprinter during a 100 m event?
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Increased glycogen degradation
normal B oxidation |