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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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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
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.
Total CHO: 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.
Training Adaptations # mitochondria • blood lactic acid epi/norepi release during exercise muscle & liver glycogen use intramuscular fat use # MCT’s (via mitochondria) CAT I (ß-oxidation) cAMP
Training Adaptations (cont.) • Two major changes that occur with training • 1.) # mitochondria in muscle cells • can be doubled at most • 2.) epi/norepi release during exercise • training sympathetic activity at any given work load
Benefits of adaptations to training • 1.) Glycolysis • Spares CHO, liver glycogen • maintains blood glucose (CNS) • mechanisms: • catecholamines PFK activity • mitochondria faster ATP generation, [AMP&ADP] PFK activity • 2.) Blood Lactic Acid • keeps blood pH normal • mechanisms: • glycolysis • mitochondria (more MCTs)
Benefits of adaptations to training (cont.) • 3.) Fat use • fat use from adipocytes via epi/norepi • fat use from intramuscular TGs • mechanisms: • mitochondria (via in CAT I activity) • acetyl CoA production PFK glycolysis • Take home point: • *Training glycolysis & Fat use via mitochondria & catecholamines*