Extremes of Metabolism Flashcards
how do we generally classify muscle fibres? which do each type use for fuel?/ stores
- type 1: slow twitch fibres - FA for energy (& glucose)
•Can sustain contraction for longer and more often, but with less force.
•Are rich in mitochondria and myoglobin (hence the characteristic red colour) with rich capillary supply
•Have large triacylglyceride stores
- *- type 2: fast twitch fibres: glycogen for energy:**
- Have few mitochondria and myoglobin (hence the pale colour).
- Have large glycogen stores for rapid anaerobic respiration.
i) type 2A: IIa aka Fast Twitch Oxidative:- have myoglobin
ii) type 2B- IIb aka Fast Twitch Glycolytic
* *-** rely on anaerobic glycolysis
- the most specialised form for anaerobic respiration.
why are slow twitch muscle fibres slow?
what type of runnng are slow twitch muscles good for?
why are fast twitch muscle fibres fast?
type 1 / slow twitch: get their energy from fatty acids. have to go through whole TCA cycle & ETC = slow process !! so not good for short bursts, but they are good for slow release energy
slow twitch would be good for long distance running
type 2 / fast twitch: rely on glycogen for energy
type 2A:
i) glycogen breakdown in muscle avoids going into the TCA
ii) but have myoglobin - so undergo some oxidative phosphorylation.
- *type 2b:**
- rely an anaerboic glycolysis - v quick !!
how do metabolic demands change during exercise?
metabolic demands during exercise
- first source: ATP. but runs out v quickly
- second source: creatine phosphate. also quickly runs out
- third source: aerobic or anaerobic glycolysis (depening on exertion (if you can get oxygen in to do TCA)
- 4th aerobic lipolysis. also requires O2 !
(not all secular)
short term energy requirements / short term exercise:
- which energy source is used for short term exercise ? (e.g. 100m sprint)
- whats the MoA of this occuring?
(what is released that signal ATP to be released for muscle contraction?
short term exercise
- uses ATP
- *MoA:**
- Ca2+ released due to nerve signalling from the :
i) adrenaline starts chain reaction
ii) IP3 causes release of Ca2+ from ER
iii) Ca2+ switches on calmodulin & PKC
iv) calmodulin binds to calmodulin dependent kinase
v) causes the phosphorylation of glycogen synthase (inhibits it) & phosphorylase kinase (activates)
vi) phosphorylase kinase switches on glycogen phosphorylase
vii) causes glycogen -> glucose-1-phosphate
remember that P on synthase & phosphorylase has antagonisitc effect !!
how is the TCA cycle controlled in response to exercise?
(3)
1.
- Ca2+ is an allosteric keeps the pyruvate deyhyrogenase complex activated.
- *- therefore causes quicker conversion of pyruvate -> acetly co-A**
- increases TCA to occur more
(PDH controls the entry to the TCA, it’s activity is regulated. The enzyme is phosphorylated and dephosphorylated depending on whether it is active or inactive. The calcium is promoting essentially the active state of PDH, by influencing PDH phosphatase (this PDH phosphatase will remove phosphates from the PDC and activate it)
2:
- calcium and ADP drive activity of two dehydrogenase enzymes in the TCA to maintain high ATP production
3.
Low levels of ATP/NAD pushes Pdh into its active state.
how does AMP regulate exercise? (3)
- during exercise, ATP runs low & AMP levels start increasing
AMP stimulates:
- increases recruitment of GLUT4 tranpsorter to membrane of muscle cells
- allosterically activates inactive glycogen phosphorylase
- allosterically activates phosphofructokinase-1 (PFK-1) (drives glycolysis)
high levels of AMP also activates an important kinase anzyme: AMPKinase.
AMP kinase has 3 major effects. what are they?
- promotes the recruitment of GLUT4 tranporters to the membrane of muscle cells. important: insulin-independint effect !!
- Activates phosphofructokinase 2, (PFK2). PFK2 strong allosteric activator of PFK-1 (to make fructose 1,6 BP -> glycolysis). only happens in cardiac muscle !!!
- shifts from glucose to fatty acid break down as a source of ATP:
i) phosphorylase acetyl co-A carboxylase (which makes FAs)
ii) stops the production of malonyl-CoA (normally inhibits carnitine shuffle. cartinine shuffle is needed in FA break down)
what happens when u have muscle fatigue / hit the wall?
(4)
in order, you run out of:
1. run out of ATP & CP
- **run out of glycogen
- switch to FA.**
but they take longer to break down (beta ox, TCA etc). requires more oxygen than glycolysis = has a limited energy output of 60% at maximum rate.
AT THE SAME TIME:
- lactic acid builds up: decreases the pH in muscles and slows glycolysis and ox. phos
what causes decreased mt?
- mt lessen with age - :(
- obesity. increased by training
what is the priority of ur body when undergoing starvation? (2)
- priotity = maintain blood glucose for ur brain!!
change in basal metabolic rate (how much energy u need to just survive)
what are the step changes in metabolism that undergo during starvation? (5)
- glucose starts falling; insulin goes down, glucagon up
- glycogen can keep brain alive for 2/3 days / 30 hrs
- swith to FA break down = energy for 2-3 days due to gluconeogenesis
- FA then switches to ketone bodies. (ketone bodies can go into brain - important !)
- final resource = break down proteins to release amino acids for gluconeogenesis
what is the common pathway used to break down alcohol?
* what is an important product of alchohol break down? *
most common pathway:
i) ethanol ⇌ acetaldehyde (via enzyme alcohol dehydrogenase (ADH))
ii) acetaldehyde –> acetate (ketone body - so can be used to make energy !) via enzyme ALDH2
acetate can then be converted into (acetyl co-a
important product: NADHs produced !! remember
why do people of asian decent have a predisposition to hangovers?
have a decficiency in ALDH2 enzyme. so cant convert acetaldehyde to acetate
alcohol metabolism produces increased what? (2)
what three things do ^ cause to occur?
- alcohol metabolism produces increased NADH & acetyl co-A (from acetate)
- NADH & acetyl co-A play roles in end product inhibition, & as a consequence:
i) inhibit GAPDH & pyruvate dehydrogenase enzymes (TCA) -> generally inhibits glycolysis
ii) activates lactate dehydrogenase (drives lactic acid)
iii) inhibits malate dehydrogenase (inhbits gluconeogenesis)
(so shifting lots of metabolism away from glycolysis to alcohol met)
explain how two pathologies occur from xs alchohol consumption !
- excess alchohol consumption leads to excess acetyl co-A
- excess acetyl co-A:
i) produces lots of ketone bodies: acidic –> metabolic acidosis
ii) gets converted to fats -> fat & obese
-
fatty liver:
- XS acetly co-A converted to fat & stays in liver.
- often have low food intake - poor protein intake = low albumin. = fat not transported
- get scar tissue forming
- results in cirrhosis
