4+5. integrative metabolism carbohydrates Flashcards
plasma-derived substrates
glucose and fatty acids
- supply most energy at low intensities
endogenous substrates
glycogen and triglycerides
- more important at higher intensities
- 65% vo2 max
later stages of exercise
- source of energy
plasma source of substrate more important
- endogenous sources decline
higher intensities of exercise
endogenous more important
- CHO
longer duration of exercise
plasma-derived substrates more important
- FFAs
blood glucose concentration regulation
- maintenence value
hepatic glucose production (HGP)
- approx 4-5mM
- tighter compared to FFA (0.2-2mM)
tissues that depend on glucose
neural
- can also use ketone bodies
red blood cells
- lack mitochondria
maximum leg glucose uptake
- problem (total blood glucose content)
~ 2 mM/min
- total blood gluc content only 20mM
- theoretically depleted in 10min
- liver compensates
glycogen bonds
straight
- alpha 1,4 bonds
branching
- alpha 1,6 bonds
enzymes that breakdown glycogen
- pathway and substrate produced
glycogen phosphorylase
- alpha 1,4 bonds
debranching enzyme
- alpha 1,6 bonds
*glycogenolysis produces G6P (glucose-6-phosphate)
G6P in “liver” during exercise
converted to glucose
- exported to systemic circulation
G6P in “muscle” during exercise
used for anaerobic and aerobic metabolism for the muscle
- glycolysis
- converted to pyruvate
*can NOT be converted to glucose
glycogen utilization
- rate of depletion fasting during
onset of exercise
glycogen utilization curve
- duration
- intensity
exponential curves
- decline with time
- incline with intensity
liver glycogen utilization
- how quickly can it be used in 1hr
can utilize 50% in 1hr
glycogen sparing definition
- what improves it
reduced rate of glycogen utilization at “initial period” of exercise
- improved with aerobic training and lipid availability
liver gluconeogenesis with exercise
- increasing intensity
- recovery**
decline gluconeogenesis with increased intensity
- stop exercising, hepatic blood flow rapidly restored
- gluconeogenic precursors still high concentration in blood
- huge “spike” in gluconeogenesis results
liver glycogenolysis and gluconeogenesis with increasing intensities
glycogenolysis (% of blood glucose contribution)
- rest 65-75%
- increase with intensity up to 85-94%
- recovery huge decline 30-60%
*gluconeogenesis huge contribution during recovery
gluconeogenesis (GNG) defn
- substrates
glucose synthesis from non-carbohydrate sources
- pyruvate
- lactate
- glycerol
- some AAs
*muscle does NOT have enzymes for GNG
gluconeogenesis pathway
- starting substrates
- intermediates
start - pyruvate (cytosol) - lactate - aminos intermediates - glycerol - oxaloacetate (mitochondria)
regulation of gluconeogenesis by cAMP
cAMP simultaneously increases GNG and decreases glycolysis
promotes
- pyruvate carboxylase (pyruvate to oxaloacetate)
- fructose 1,6 biphosphatase (F 1,6-P to F 6-P)
inhibits
- pyruvate kinase (PEP to pyruvate)
- phosphofructokinase PFK ( F 6-P to F 1,6-P)
glycolysis produced
pyruvate
anaerobic pathway of pyruvate
anaerrobic “reduction”
- lactate dehydrogenase (LDH)
- lactic acid
- lactate + H ion
aerobic pathway of pyruvate
aerboic “oxidation”
- pyruvate dehydrogenase (PDH)
- acetyl coA (mitochondria)
- citric acid cycle
formation of ATP from pyruvate
substrate level phosphorylation
lactic acid when at pH of 7
in lactate form
importance of lactate production
produces NAD+ when oxygen in short supply
- allows glycolysis to continue
fate of lactate
high levels
- moves from muscle to blood
- liver and heart uptake
- can be used aerobically to produce ATP
- in liver also used in GNG (cori cycle**)
cori cycle
liver GNG
- 2 lactate –> 2 pyruvate –> glucose
- costs 6 atp
what is the cause of muscle soreness
delayed muscle soreness (DOMS)
- inflammatory repair response in muscle
*not lactic acid buildup
lactate threshold (LT)
level of exercise intensity when lactate production exceeds removal from blood
- sharp blood lactate increase
training accelerates lactate clearance
effect of glucose transport with exercise
rapid increase
- persists several hours after post exercise
glucose transport can be stimulated by 2 seperate pathways in skeletal muscle
- activated by?
activated by
- insulin
- contractile activity
additive affect
how insulin and contractile activity effect glucose transport
move GLUT4 receptor to plasma membrane
- distinct pathways
insulin
- binds receptor
- IRS –> PI 3-kinase and so on
- PI 3 kinase depend signals
contraction
- AMPK dependent signals (AMPK alpha, beta, gamma)
- AMPK indepedent signals (Ca2+ activated)
what is AMPK
- how its activated
- what does it do
AMP - activated protein kinase
- responds to decrease energy status
- less ATP, more ADP, AMP, P etc
stimulates atp-producing pathways, simutaneously inhibits ATP consuming pathways
affect of exercise on glut4
rapid increase
- 2fold glut4 mRNA
- 50% protein in membrane
- persists several hours
*why? glycogen replenish
why would too high of skel. muscle glucose uptake be bad
rapid depletion of liver glycogen
- hypoglycemia with continues exercise
- “glycogen sparing”
how to improve glycogen sparing
increase
- mitochondria in muscle
- fat oxidation enzymes
