Training Adaptations. LIVER. SKELETAL MUSCLE TISSUE. Adrenal Gland. Adipocytes. Mitochondria. TRAINING WILL: Decrease RER Does not effect sub-max oxygen uptake Increases LT and lowers muscle and blood lactate at any sub-max workload.
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SKELETAL MUSCLE TISSUE
Does not effect sub-max oxygen uptake
Increases LT and lowers muscle and blood lactate at any sub-max workload
However, when express per gram of mitochondrial protein training does not alter specific activity.
Aerobic training can cause 50-100% increases in mitochondrial mass per gram of skeletal muscle.
Pre = 145 umol/min
Post = 100 umol/min
or a 50% decrease
This is due to decrease reliance on blood glucose and muscle glycogen
Training decreases Ra(rate of appearance) of glucose from the liver. This means less glycogen depletion in liver.
With training you can double your mitochondrial mass, thus at any giving work load each mitochondrion will only be working (ie producing ATP) at half the rate it was before training. The main stimulus for increases in oxidative phosphorylation is ADP. Therefore the increase in intracellular ADP must be less in trained individuals.
epi/norepi release during exercise
muscle & liver glycogen use
intramuscular fat use
# MCT’s (via mitochondria)
CAT I (ß-oxidation)