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Brooks ch 9 p181-191;197-201 Some small sections already covered Outline

Neural - Endocrine Control. Brooks ch 9 p181-191;197-201 Some small sections already covered Outline Maintenance of Blood Glucose during exercise Feed forward Control - SNS Feed back Control - ratio of insulin / glucagon Control of Gluconeogenesis - Ca++, cAMP. Neural - Endocrine Control.

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Brooks ch 9 p181-191;197-201 Some small sections already covered Outline

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  1. Neural - Endocrine Control • Brooks ch 9 p181-191;197-201 • Some small sections already covered • Outline • Maintenance of Blood Glucose during exercise • Feed forward Control - SNS • Feed back Control - ratio of insulin / glucagon • Control of Gluconeogenesis - Ca++, cAMP

  2. Neural - Endocrine Control • During exercise, the maintenance of homeostatic levels is important, particularly blood glucose • Blood glucose is maintained at 4-5.5 mM (90-100mg/dl) • Fig 5.5

  3. Neural - Endocrine Control • During exercise glucose uptake into muscle is stimulated in order to maintain ATP homeostasis • Blood glucose is maintained through release from the liver and kidneys and the mobilization of alternate fuels • Response to maintain blood glucose is governed by the endocrine system and the Sympathetic NS • Via feed-forward and feed-back control mechanisms • Glucose homeostasis is important for CNS metabolism and the anaplerotic effect of carbohydrates on fat metabolism

  4. Glucose Appearance • Several ways to increase blood glucose • Release from gut (prior meal) • Release from glycogen stores • Gluconeogenesis - production of glucose from precursors in kidney and liver - lactate, pyruvate, glycerol, alanine • Body also raises levels of alternative substrates and delivers them to active tissue • fatty acids, TG, lactate, leucine • Which serve to spare glucose use and postpone hypoglycemia and fatigue • Growth Hormone and Catecholamines mobilize FFA and TG

  5. Fasting State fig 5-3b

  6. Feed forward Control • During exercise the rise in glucose uptake is primarily in the active tissue beds • Fig 9-2 • the addition of arm exercise, further increases whole body uptake but blood glucose rises due to high Hepatic Glucose Production (HGP) • stimulated by increased catecholamines and decreased insulin (fig 9-3) • This is a feed forward response, as blood glucose did not drop

  7. Role of the Liver • Liver is essential to the regulation of blood glucose • Uptake and storage when levels are high • Release when levels are low • Uptake and Release are driven by [ ] gradients • In and Out through high Km GLUT 2 (20mM) • Insulin stimulates glucokinase synthesis which phophorylates glucose preventing its efflux and keeping the [ ] gradient high - glucose then stored or metabolized • When there is a fall in [glucose] in liver • Activity of GK (also known as high Km HK) falls • Activity of G6Pase inc, forming glucose for release

  8. Energy Storage • Storage of glycogen is limited to 5-6% of liver by weight (5g/100g) • As G6P builds up in the liver during the fed state, it stimulates glycolysis and formation of acetyl-Co-A, then FFA and the synthesis of TG • TG packaged into VLDL and circulated to adipose • Low insulin and blood glucose in fasting state stimulates FFA release and a decrease in glycolysis through glucose-fatty acid cycle (discussed earlier) • Acetyl co A inhibits PDH • Citrate inhibits PFK • G6P inhibits HK and glucose uptake (skeletal ms)

  9. Insulin and exercise • Insulin falls during exercise - likely due to rise in epinephrine (both changes result in increased HGP) • With aerobic training • Decreased release of glucagon and catecholamines and an reduction in the fall in insulin at a given relative intensity • Fig 9-7

  10. Glucagon • Glucagon enhances glycogenolysis (glycogen breakdown) and gluconeogenesis through adenylate cyclase • Alanine released from muscle after prolonged exercise also stimulates glucagon • Increases amino acid uptake for gluconeogenesis • Glucagon response to exercise is also dampened with training - Fig 9-8

  11. Gluconeogenesis in Liver • Glucose produced from lactate, pyruvate or alanine through the use of bypass steps for the irreversible steps of Glycolysis • Pyruvate carboxylase (PC) and Phophoenolpyruvate carboxylase (PEPCK) reverse PK through Malate shuttle - Fig 9-15 • Fructose-1,6-Bisphosphatase reverses PFK • Glucose 6 Phosphatase reverses HK (GK) • These enzymes are mainly found only in liver and kidneys

  12. Control of Gluconeogenesis • cAMP and Calcium thought to play important roles in stimulation of gluconeogenesis • PK-L liver type PK can be phosphorylated and inhibited by Ca++ and cAMP dependant protein kinases • This will inhibit glycolysis and favour glucose release • Fructose 2,6 Bisphosphate (present after eating) will activate glycolysis and inhibit gluconeogenesis • Activates PFK- and inhibits F 1,6 BPase • PFK-2 in liver can act as either kinase or phosphatase (reverse) • cAMP dependant protein kinase will inhibit PFK-2 kinase function and activate PFK-2 phoshorylase function

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