human phys exercise metabolism

exercise

increase atp demand

fuel selection

depnds on intensity and duration

muscle

use stored and circulating fuels

hormones

shift to support energy supply

recovery

has energetic cost

muscle glycogen

supports rapid energy needs

blood glucose

contrirbutes during sustained exercise

fatty acids

support longer duration activity

amino acids

play a minor roel in fuel sources

fuel

changes over time

higher intesity

favors carbohydrate use

longer duration

increase fat contribution

glycogen depletion

shifts fuel selection

training status

affects substrate use

nutrition

alters response

during exercise

insuline decreases

glucagon

supports hepatic glucose output

epinephrine

increase glycogen breakdown

cortisol

supports longer term fuel mobiliztion

hormone

preserve blood glucose during exercise

muscle contraction

activates AMPK and ca2+/calmodulin signaling pthways

AMPK AND ca2+ calmodulin signaling pathways

converge on glut4 vesicles translocation

glucose uptake during exercise

scales w/ exercise intesity

contractionstimulated glut4 translocation

remains intact in insulin resistant muscle

glycogen depletion

after exercise upregulatin glut4 expression an denahnces insulin stimulated translocation

enhance insulin sensitivity

presist 24-48 hrs post exercise in healthy and insulin resistant individuals

effect magnitude

correlated w/ degree of glycogen depletion and total exercise volume

sensitivity enhancement

wanes without repeated bouts

contracting skeletal muscle

secretes cytokine like proteins (IL-6, irisin bdnf, fgf-21 myonectin

exercise derive il-6

stimulates hepatic glucose production and adipose lipolysis acutely

irisin

promotes adipose tissue browning and improves whole body insulin sensitivity

myokines

mediate cross talk btw muscle and brain liver adipose pancrease

myokine secretion

blunted in obesity and T2d reducing systemic exercise signal

obesity

excess adiposity but cardiometabolic risk varies substantially among indiv w/ same bmi

MHO

preserved insulin sensitivity and lipid profiles despite elevated body fat

munw

indiv w/ metabolic dysfunction at low bmi

visceral adiposity

drives cardiometabolic risk more than subcutaneous fat or total body mass

fat distribution and adipose tissue function

matter more than quantity of fat alone

lipid accumulation

in non adipose tissues liver skeletal M pancreas myocardium

DAG and cramide

toxic lipid intermediates

DAG

ACTIVATES NOVAL PKS isoforms PKC theta in muscle

PKCe in liver

that serine phorphorylate IRS-1 blocking insulin signaling

creamide

activates pp2a and pkcgamma directly inhib Akt and promoting beta cell apoptosis

ectopic fat burden

stronger predictor of insulin resitance and T2d risk than bmi or total body fat