Muscle at Rest/Exercise - Abali 3/17/16 Flashcards Preview

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Flashcards in Muscle at Rest/Exercise - Abali 3/17/16 Deck (19):

health adv of regular exercise

  • lower CVD risk
    • obesity
    • bp
    • lower blood glucose (better response to insulin)
  • lower stress
  • higher immune fx (to a pt, past which it can ding your immune fx )


AMP-activated protein kinase pathway

stimulation of energy production in low energy/stress states


  • cell stress causes energy consumption to outpace energy production
    • ATP falls, ADP rises
    • ADP → ATP [adenylate kinase]
  • rise in AMP + drop in ATP → activation of AMPK
    • AMPK stimulates catabolism (more ATP) and puts a hold on ATP-consuming processes (synth pathways)


AMP kinase


+ : AMP

- : ATP

pathways it affects:

  • upreg GLUT4 activity → more glucose transport into cells
  • upreg sk muscle FA oxidation
  • downreg synthesis: TAG/glycogen/protein/chol/FA/insulin secretion


recall: hormonal reg of glycolysis/gluconeogenesis


insulinactivates glycolysis, inhibits gluconeogen

  • dephosphorylates PFK2 → fructose 2,6 bisphosphatase made
    • F2,6BP → activates PFK1 (activates glycolysis)
    • F2,6BP → inhibits F1,6BPase (no gluconeo)

glucaconinhibits glycolysis, activates gluconeogen

  • phosphorylates PFK2 → NO fructose 2,6 bisphosphatase made
    • no F2,6BP → PFK1 not activated (no glycolysis)
    • no F2,6BP →  stops inhibition of F1,6BPase (activates gluconeo)


effect of epinephrine on glycolysis

accelerates glycolysis in muscle

epi → P of glycogen phosphorylase, more glycogen degradation → more F6P → more F2,6P [PFK2], activating glycolysis

  • F2,6P is allosteric activator of PFK1, glycolysis

epi inhibits glycolysis in liver


regulation of beta oxidation of FA in muscle

occurs at level of fatty acyl CoA entry into muscle mitochondria

malonyl CoA inhibits CPT1

low energy state indicated by rise in AMP → activation of AMP-protein kinase


high energy/low AMP, AMPK inactive

  • ACC (acetyl CoA carboxylase) converts acetyl CoA into malonyl CoA → inhibits CPT1, entry of fatty acyl CoA for beta ox

low energy/high AMP, AMPK active

  • ACC downreg'd
  • MCoADC (malonyl CoA decarboxylase) upreg'd, converts malonyl CoA into acetyl CoA → undoes inhibition of CPT1, clears the road for fatty acyl CoA
  • muscle now able to generate ATP from FAs!


adipose tissue: glyceroneogenesis

adipose tissue doesnt have glycerol kinase (cant pick up glycerol from TAGs in circ)

  • needs to make its own glycerol3P through glycolytic intermediates


during lipolysis (stimulated by epi, cortisol), HSL is active → glycolysis is inhibited → DHAP not available to make glycerol3P!

enter...glyceroneogenesis (fx: convert  pyruvate → DHAP)

  • reason why adipose cells express pyruvate carboxylase  and PEP-CK even though they dont make glucose!



why do you need glyceroneogenesis to occur when you have lipolysis?

(seems counterintuitive)

TGs and FAs shuttle between liver and adipose tissues to maintain high lipid turnover rate in blood: FA-TG cycle

adipose TG broken down in excess of amount needed → liver repackages FA in VLDL, sends it back to adipose tissue

the process...

  • uses energy (but no more than 5%)
  • conserves FAs not used for ox

glyceroneogenesis allows you to pick up and store the excess FAs released during exercise or fasting


how is blood glucose maintained over long periods of exercise?

liver glycogenolysis

liver gluconeogenesis

  • initially, much greater contribution from glycogenolysis than from gluconeogenesis
  • over several hours, becomes almost 50:50 contribution


alanine-pyruvate cycle

net transport of nitrogen from BCAAs (Iso, Leu, Val) to liver, but no net production of glucose

  • in liver, Ala → NH3 + pyruvate
  • pyruvate converted to glucose, heads back to muscle cell and is recycled through


will happen during strenuous exercise and also during starvation


biological energy systems used by muscle

phosphagen system (creatine phosphate)

  • anaerobic
  • bursts of heavy activity (exhausted in ~15s)
  • active at the start of all exercise (regardless of intensity)


  • breakdown of carbs (either stored glycogen or delivered through circ)
  • fast (anaerobic) and slow (uses oxphos)

oxidative system

  • primary source of ATP at rest/low-int exercise
  • uses mainly carbs (oxphos) and fats (beta ox)


**all three active at any given time; extent to which each is used depends on activity intensity and duration


energy system selection

phosphagen system: short duration, high intensity

glycolytic system: short-med duration, mod-high intensity

oxidative system: long duration, low intensity

  • both beta-ox and glycogen through beta ox (?)


rate of energy demand and power output will determine when you incorporate one system or another


phosphagen system

used for short bursts of high intensity training

active at the start of all exercise regardless of intensity (exhausted in <30s)


creatine is a reservoir of high-egy P that can be used to get ADP → ATP

  • carries high egy P from mitochondria to myosin filaments where ATP is used for contraction
  • ADP + creatine phosphate → ATP + creatine [creatine kinase]

creatine stocks

  • muscle only stores a small amt; working out more increases size of muscle creatine store
  • reformation of PC requires ATP - only occurs during recovery


utility of anaerobic glycolysis to a muscle cell in high exertion

rate of ATP production from glycolysis is approx 100x as fast as oxphos!

fast glycolysis: pyruvate → lactic acid

  • energy produced RAPIDLY

slow glycolysis: pyruvate moves to mito for oxphos


ranking of ATP generating processes by...

  • rate of energy production
  • amt of ATP produced

inverse relationship: fastest rate = lowest yield and vice versa

in order of fast → slow (or low yield → high yield):

1. phosphagen

2. fast glycolysis

3. slow glycolysis

4. oxidation of carbs

5. oxidation of fats/proteins


energy systems used by different muscle types

slow twitch

  • slow contraction
  • slow oxidative energy production
    • not a lot of glycogen
  • high capacity for aerobic metabolism
  • high myoglobin/ability to store O2
  • red muscle

fast twitch

  • fast contraction
  • fast glycolytic energy production
    • lots of glycogen
  • low capacity for aerobic metabolism
    • more sensitive to fatigue
  • white muscle


factors affecting fuel selection

1. intensity

high → low intensity : more carbs → more FAs

2. duration

long → short duration : more FAs → more carbs


main source of FAs - free FAs released from adipose cells

main source of carbs - muscle glycogen stores


phosphagen depletion/repletion

creatine phosphate decreases by 50-70% during high intensity exercise, but can be near completely eliminated in cases of exhaustion

muscle ATP drops no more than 60% even during high intensity ex


replenishment of phosphagen system occurs post-exercise:

  • regen of ATP in 3-5 min
  • complete resynth of creatine phosphate in 8 min

**resistance training → increase in resting conc of phosphagens! 


glycogen depletion/repletion

liver glycogen: key during low intensity ex

muscle glycogen: key during med-high intensity ex


repletion of muscle glycogen is linked to post exercise carb consumption

  • can get complete replenishment within 24h on sufficient carb diet

**anaerobic training → increases glycogen stores!