Exercise Metabolism Flashcards
effect of excercise on glucose/insulin
resting hyperglycemia not much better but response to glucose is not as drastic-cells more insulin sensitive and faster to resting glucose levels
@ excercise-insulin secreiton in people with abnornal glucose will increase almost to normal levels
excercise effect on immune function
increase to a point where too much excercise
what pathway is for excercise
AMPK
- decreases ATP consumption (not use ATP for synthesis)
- increase catabolism
- AMP accumulates=low energy within the cells-activates AMPK
Physiologic targets of AMPK
GLut4 (muscle and adipose tissue)-take glucose in tnto these organs
SM FA ox, and increases gluocse uptake here-again GLUT4
Inhibits TAG syn, glocyogen syn, protein syn, cholesterol syn, FA syn, and insulin syn (req energy/ATP)
PFK 2 on when … activates and how activate
-same for off
Off when dephosphorylated by Insulin
-results in gluconeogenesis
On when glucagon phosphorylates it
-results in glycolysis
PFK2 off downstream
Fructose 2,6 bisP activated
- PFK1 is active
- gluconeogenesis
PFK2 on downstream
Fructose 2,6 P bisP inhibited
- FBP1,6ase is active
- glycolysis
epi effects on muscle and liver gycolysis
accerates glycolysis in muscle
inhibits glycolysis in liver
how does epi secretion increase glycolysis rate in muscle
epi phosphorylates gluycogen phosphorylase
- glycogen deg pathway
- get glucse 6p to fructose 6p
- Either PFK2 makes fructose 2,6bis P-activates PFK 1
- —-or makes PFK1 directly
PFK1 results in glycoslysis increase or fructose 1,6 bisP
ACC2
inhibits CPT thereby blocking FA CoA entry to mito
-inactivated by AMPK
MCoADC
Maloyl CoA to acetyl CoA
-activates by AMPk
Where get DHAP from
-and where not from (2)
@lipolysis, glycolysis is inhib
@adipose cells-no glycerol kinase to make glycerol 3 P (made when DHAP made)
Use glyceroneogenesis
GLyceroneogenesis
(basically shortened gluconeogenesis in liver/adipose)
Pyruvate to DHAP
Gluconeogenesis vs glycogenolysis @ excercise
start with much more glycogenolysis
-over time decrease, adn increase gluconeogenesis
Alanine cycle
- what happens
- extra things made
breakdown of glucose to alanine, then alanine regenerates glucose in liver
Uses BCAA and ALT to generate alanine
Alanine to glucose also makes ammonia
phosphagen system
anerobic, creatine phosphate
quick was of getting energy for a few seconds
glycolysis
fast and slow
breakdown of carbs, either glycogen stored in muscle or deleivered in blood to produce ATP
-anerobic is 100x faster than aerobic
oxidative system
primarily at rest and low energy
- uses carbs and fats as substrates
- ox phos and beta ox
high intestity for short duration
low intensity for long duration
mod to high intesnity for short to medium duratin
phosphocreatine-for burst of heavy activiy
FA, ketone bodies, blood glucose
creatine but also muscle glycogen to lactate
-creatine doesnt last that long
anerobic vs aerobic
-time
-demand
shorter time, more anerobic vs aerobic
higher dmage (100m dash/weight lifting)-more anerobic
Creatine shuttle=
phosphagen system
can psosbile increase creatine storage through excercise
why use anerobic glycolysis during exertion vs ox phos
ATP generated at 100x faster rate-for fast glycolysis
fast glycolysis vs slow glycolysis
glucose, pyruvate, lactate (faster ATP yield rate)
sloww-glucose, pyruvate, TCA cycle
pruvate to mito-for TCA=slow
Rank ATP production vs capactiy for ATP production
there exist in inverse
phosphogen=fastest fast (anerobic) glycolysis slow (Aerobic/TCA) glycolysis oxidation of carbs ox of fats and proteins
