ANS Flashcards

1
Q

role of autonomic nervous system

A

maintains organismic homeostasis @ rest + during exercise

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2
Q

what are the two division of the ANS

A

sympathetic (fight or flight)
parasympathetic (rest + digest)

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3
Q

functions of the ANS

A
  • maintains temp @ 37 degreees C
  • HR regulation
  • blood content/hematocrit
  • metabolic adjustments
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4
Q

how does the ANS regulate HR

A
  • can increase HR
  • sympathetic tone –> increase contraction –> increasing venous return –> increase L ventricle SV –> increase in CO –> more blood to working tissues
  • cause vasoconstriction
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5
Q

metabolic adjustments and ANS

A
  • adrenaline release results in nervous input to fat = stimulation of beta-mediated lipolysis
  • stimulation of hepatic glycogenolysis
  • modulation of substrate metabolism like glycogen from non working to working muscles
  • ANS input = alpha adrenergic modulation of lipolysis and hepatic gluconeogenesis
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6
Q

how does the ANS affect maximal aerobic capacity + exercise performance

A
  • more training = more PNS tone to suppress pacemakers
  • can affect resting HR making it lower = more HR reserve
  • regular exercise can modify ANS adjustments to acute exercise
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7
Q

what does a great HR reserve mean

A

larger capacity for heart to increase output during exercise

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8
Q

how to measure ANS activity

A
  • cardiac vagal activity
  • assessment of sympathoadrenal activity
  • assessment of overall ANS effects
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9
Q

cardiac vagal activity measurements

A

looks at muscarinic receptor antagonists
- these receptors when bound to ACh affect HR variability by slowing it down
- it can also be coupled with G protein pathways either increasing cellular effects (Gs) or decreased cellular effects (Gi)

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10
Q

what are muscarinic receptors

A

a type of ACh receptor that also responds to muscarine

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11
Q

assessment of sympathoadrenal activity when measuring ANS activity

A
  • looks at plasma norepinephrine concentrations
  • neuropeptide Y
  • neural recordings of sympathetic NS activity
  • low frequency power of HR variability
  • plasma concentrations + secretion of epinephrine
  • adrenergic receptor antagonists
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12
Q

plasma NE concentrations and spillover

A
  • NE + sympathetic NS = stimulus = body senses stress = increase in HR
  • body doesnt understand specific stress so goes general
  • spillover: the release of NE from the tissues into the bloodstream (increased spillover = increase in sympathetic NS activity)
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13
Q

neuropeptide Y

A
  • released alongside epinephrine + nE under high intensity or prolonged sympathetic stimulation
  • lasts in plasma for longer periods of time than epi or NE so detection in blood indicates the degree of sympathoadrenal activity
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14
Q

how are neural recording used to understand sympathetic NS activity

A

sympathetic tone is very loud and noticeable

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15
Q

what are prescribed to regulate the ANS

A

alpha and beta blockers
- PNS is specifically blocked via beta blockers

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16
Q

how to assess the overall ANS

A
  • surgical ablation of parasympathetic and sympathetic NS structures (removed and looked at)
  • transgenic animals: can be modified to remove genes and helped to better understand receptor density
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17
Q

ANS changes to acute dynamic exercise

A
  • cardiac vagal modulation of HR
  • sympathoadrenal response
  • central and peripheral neural mechanisms
18
Q

cardaic vagal modulation of HR after actue dynamic exercise

A
  • at peak exercuse PNS tone is at a min
  • prolonged or increased intensity of activity results in continued decreased in vagal tone
  • once exercise stops PNS immedielty goes back up
  • atropine and propanol also have an effect
19
Q

how can you rell if PNS health is good

A

look at recovery post exercise it shouldnt take long for HR to return back to normal
(if it takes long could mean too much sympathetic input or adrenaline

20
Q

sympathoadrenal response to acute dynamic exercise

A
  • vagal tone is withdrawn followed by an immediate increase in HR to meet the needs of the body
  • increase in intensity = increase in SNS input and catecholamin levels
  • plasma lactate response and sympatholysis occurs
21
Q

plasma lactate response in the sympathoadrenal response to acute dynamic exercise

A
  • adrenaline/adrenal activity inversely realted to [lactate] in blood
  • due to metabolism (more mitochondria activity and increase adrenaline = more metabolism of pyruvate = decrease in lactate acid)
22
Q

sympatholysis in sympathoadrenal response to acute exercise

A

process where local metabolic and mechanical factors in active muscle soveride sympathetic vasoconstriction
- working tissues need/want blood so don’t want vasoconstriction

23
Q

what are factors of change for ANS during acute dynamic exercise

A
  • absolute vs realtive exercise intensities
  • sex of individual
  • size of active muscle mass
  • ambient temp + internal temp
  • hydration
  • body position
  • diet
  • hypoxia vs hyperozia
  • modulatory factors
24
Q

how does sex factors affect the ANS changes to acute dynamic exercise

A

women have more SNS tone + men more PNS tone bc men have larger hearts so need more to help control

25
how does the size of active muscle mass affect ANS in acute dynamic movements
- greater muscle mass = more adrenaline needed - more activity/training = more adrenergic receptors
26
how is hydration affect ANS changes to acute dynamic exercise
hydration = more plasma volume = less SNS tone bc more venous return
27
how does body position affect ANS changes to acute dynamic exercise
standing = blood pools = SNS tone increases to increase venous return
28
how does hypoxia and hyperoxia affect ANS in acute dynamic exercise
hyperoxia = less input hypoxia = more input
29
what are modulatory factors to changes in AND to acute dynamic exercise
brain regions and neuromodulators involved in ANS control help to maintain function during stress - parts like the insular cortex, diencephalon, midbrain + pons, medulla
30
how are central and peripheral neural mechanisms changed during acute dynamic exercise
central command - active muscle reflexes through muscle thermoreflexes (automatic responses), mechanoreceptors, chemoreceptors - arterial baroreflex - cardiopulmonary baroreflex - arterial chemoreflex - lung inflation reflex
31
muscle mechanorecptors in response to acute dynamic exercise
stretching/changes in tendons increase response in skeltal muscle through golgi tendon organs - highly loaded positions also allow for antagonist golgi tendon bodies to respond = get out position faster
32
muscle chemoreceptors in response to acute dynamic exercise
muscle decreases activity when out of fuel - too acidic will stop - too basic will reduce activity
33
what senses pH changes in the blood
arterial chemoreflex
34
how does breathing affect HR
highly linked HR increase with inhalation and slows with exhalation
35
how does the ANS function and controlled
like a feed forward controller with a feedback controller - feedback controller: autonoic pathways --> affecting heart and vasculature --> arterial BP --> baroreceptors to make changes
36
how does ANS change with chronic exercise
- cardiac vagal modulation - sympatoadrenal activity - central and peripheral neural mechanisms - endurance training + tissue responsiveness
37
cardiac vagal modulation and chronic exercise
lower resting HR, faster vagal withdrawl at exercise onset, lower HR at submaximal intensities, faster recovery
38
sympathoadrenal system activity with chronic exercise
- at rest theres lower SNS tone, lower resting BP - during acute: delayed + lower SNS activity - adaptations to regulate and optimize functions within the body - resistance training: catecholamine plasma concentration remains elevated for longer, greater muscle recruitment (higher epi and NE release)
39
central + peripheral nerual mechanisms with chronic exercise
- ANS changes at rest - ANS adapataions during submaximal exercise
40
how is endurnace training and tissue responsiveness affected with chronic exercise
adrenergic stimulation seen by more receptors being available even tho there are less neurotransmitters - alpha adrenergic: lower catecholamine response to a given workload - beta adrenergic = greater glucose uptake, increased mitochondrial function