Chapter 3 Flashcards
Functional Sympatholysis
Is an inhibition of the sympathetically mediated vasoconstrictor response in active muscles as long as blood pressure is maintained. This is due to substances produced in the contracting muscle that inhibit substances released from nerve terminals.
This is necessary to override active muscle vasoconstriction in attempt to match the blood flow to metabolic demand while maintaining blood pressure.
Impact of muscle pump play on muscle blood flow during exercise.
Through ecercise blood flow increases in working muscles, varying by work load (linear relation ship). Blood available for exercise is not limitless, if workload exceeds the hearts capacity to supply.
-If muscles works at high intensity for long duration and there is limited blood available they might undergo vasoconstriction in order to maintain blood pressure.
Role of Nitric Oxide during exercise
NO is most effective when blocked DURING exercise.
Not involved in blood flow changes from one intensity to another.
NOS inhibitors return blood flow to baseline levels faster after exercise.
-NO signaling pathway leads to vasodilation.
Role of Adenosine during ex
Responsible for 20%-40% of maintained phase of exercise hyperemia.
Originates from AMP released by muscle fibers converting it to adenosine.
It is important in determining blood flow heterogenetiy in human muscle during ex.
When adenosine receptors are blocked blood flow is more homogeneous.
Prostaglandins in ex
Prostaglandins not involved in changes in blood flow when exercise intensity changes.
Prostaglandins produced by factors that increase calcium levels, exert their effect on smooth muscle which results in decreased calcium levels.
Potassium during ex
Potassium is release from muscle fibers during activity. When accumulated it can effect the blood flow with interaction of the vasculature. Vascular smooth muscle hyperpolarization is prevented by potassium infusion. Potassium increase effect of other vasodilators.
ATP during exercise
(adenosine triphosphate)
contributes to exercise hypermia by binding to purinegic receptors, can result in release of substances.
Help control of blood flow with release of ATP, in porportion to oxygen released.
AMPK role on muscle metabolism
AMPK seen as the thermostat that can control energy flux aka metabostat.
AMPK is a kinase activated under metabolic stress/exercise.
AMPK activates catabolic pathways that generate, consume and conserve ATP.
Causes:
Increased Catabolism (increase glucose, glycolysis etc.)
Decreases Biosynthesis: (decreased protein synthesis, glucogen, fatty acid and cholestoral.)
Compare and contrast insulin promoted glucose uptake vs exercise induced uptake of insulin
Insulin promoted glucose uptake:
works by activating the insulin receptor phosphorylates the insulin receptor substance (IRS), that bind to other target proteins when phosphorylated. When proteins are activated results in facilitating glucose entry.
Exercise induced uptake of insulin:
Muscles have an increased sensetivity to glucose occurs during exercise, with type 2 diabetes. AMPK and increased calcium enhances glucose uptake. Sensetivity is increased during and after exercise.
Insulin Resistance and impact of chronic exercise.
This is when the body looses the ability to clear a glucose load from circulation in response to insulin. Originates in the tissue. Happens due to a disconnect between fatty acid uptake and oxidation in muscle cells.
Obese/Diabetic people have permanent relocation of fatty acid transporters to the plasma membrane with out increased expression, meaning, a greater fatty acid uptake for any given level circulating.
Chronic exercise reduces insulin resistance. Stimulates gene expression.
