Exercise and Integrated Cardiovascular Response Flashcards

1
Q

Whole body O2 consumption (QO2)

A
  • Rest: 250 ml O2 / min
  • Exercise: 3-5 L / min
  • QO2 is permitted through a parallel increase in cardiac output
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2
Q

Triggers for CV Responses During Exercise

  • Central command
  • Reflexes from skeletal muscle
A
  • Central command
    • Increases HR, contractile force, & vasoconstriction before physical activity is initiated
    • Exhibit similar changes in BP & HR when imagine exercise as when muscle contraction actually occurs
  • Reflexes from skeletal muscle also elicit increases in CO & vasoconstriction
    • Involved muscle afferents
      • Unmyelinated fibers that are sensitive to chemicals produced by contracting muscle
      • Small myelinated fibers that respond to pressure changes during muscle contraction
    • Decrease baroreceptor reflex gain
      • Triggered by inputs from muscle receptors & central command
      • Signals –> nucleus tractus solaritus –> inhibit neurons that receive baroreceptor signals
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3
Q

BP During Exercise

A
  • MAP = CO * TPR
    • CO increases a lot during exercise
    • MAP increases only moderatly during exercise
  • Diastolic vs. systolic pressure during exercise
    • Diastolic pressure doesn’t increase in proportion to systolic pressure
      • Diastolic pressure may drop
    • Decreased vascular compliance –> drop in BP during diastole
    • Decreased TPR –> rapid runoff of arterial blood into capillaries –> large drop in pressure during diastole
  • Decreased peripheral resistance
    • Limits the increase in BP during exercise
    • Vessels dilate to increase perfusion & oxygen delivery
    • Increase in blood flow / perfusoin to skeletal, cadiac muscle, & skin (to dissipate heat)
    • Decrease in blood flow / perfusion to digestive system & kidneys
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4
Q

Factors contributing to exercise-related CV responses: cardiac output

  • Effects of exercise on HR, contractility, & CO
  • Ways to increase HR
  • Max limit on HR
  • Moderately increased HR & stroke volume
  • Stroke volume & cardiac output
  • Factors that contribute less to enhancing venous return
A
  • Exercise –> increased HR & contractility –> increased CO
  • Ways to increase HR
    • Decrease PNS
    • Increase SNS
      • Binding of NE or Epi on autorhythmic cells –> increase firing rate –> increase HR
      • Catecholamines increase conduction through the AV node, bundle of His, & Purkinje fibers
  • Max limit on HR
    • Heart beats too rapidly (170 bpm) –> insufficient filling time
    • Limit is imposed by delay in conduction through AV node & long refractory period of myocardial cells
      • Ensures heart won’t beat too rapidly
    • Increase in HR alone can’t explain increase in CO
  • Why moderately increased HR doesn’t diminish stroke volume
    • Most ventricular filling occurs early during diastole just after the AV valves open
      • Mitigates effects of a shortened diastolic period
    • Increased HR –> increased contraction intensity
      • Enhances ventricular filling
    • Elastic recoil of prevoius ventricular contraction draws blood into relaxing chamber when residual volume is small
    • Bowditch effect: automatically increases contractility as HR increases
  • Stroke volume must increase to increase CO
    • Binding of catecholamines to beta-receptors –> increased contractility
    • Starling’s Law of the Heart: skeletal muscle contractions –> increased venous return –> increased cardiac output
  • Factors that contribute less to enhancing venous return
    • Increased respiratory muscle contractions suck blood into thorax from abdomen
    • Contraction of smooth muscle within veins
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5
Q

Factors contributing to exercise-related CV responses: changes in blood flow

  • SNS outflow during exercise
    • Increased to…
    • Decreased to…
  • Effects of vasoconstriction vs. Epi
  • Major factor contributing ot muscle vasodilation during exercise
A
  • Increased SNS outflow to blood vessels during exercise
    • Not the same in every vascular bed
    • Increased SNS outflow to…
      • Viscera
      • Skeletal muscle
    • Decreased SNS outflow to…
      • Skin (would inhibit cooling of the body)
      • Digestive organs
  • Effects of muscle vasoconstriction is opposed by the release of Epi from the adrenal medulla
    • Epi binding to beta2 receptors in skeletal muscle promotes vasodilation
  • Major factor contributing to muscle vasodilation during exercise: release of paracrines from exercising muscle
    • H+ from acids (lactic acid), K+, adenosine, & CO2 –> vasodilation
    • Regulates blood flow during exercise
    • Ensures only muscles that need a large blood flow to meet metabolic needs will have increased perfusion
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6
Q

What happens in a trained athlete to potentiate the ability to exercise

  • Result of training
  • Marathoner vs. nonathlete
A
  • Training –> increase heart muscle –> increase chamber size –> increase stroke volume
    • HR decreases so MAP will remain normal
    • “Reserve capacity” to increase CO is higher
  • Marathoner vs. nonathlete
    • Decreased resting HR
    • Increased stroke volume
    • During max exercise, HR can rise as much as in a nonathlete while stroke volume is much larger
    • Increased vascularity –> more efficient oxygen delviery to tissues
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7
Q

Enhanced oxygen delivery to muscle during exercise

A
  • Most oxygen in bloodstream is bound to hemoglobin
    • Local changes in pH & temperature facilitate shedding of oxygen from hemoglobin
  • Increased levels of vasodilating paracrine factors –> relaxed precapillary sphincters –> increased number of open capillaries
    • Increases surface area available for exchange of oxygen b/n blood & tissues
    • CaO2 - CvO2 is larger for working muscles
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8
Q

CV drift during exercise

  • ~10 mins of exercise in a warm environment
  • Sweating
  • Hyperthermia
A
  • ~10 mins of exercise in a warm environment
    • –> decreased stroke volume, CO, & BP
    • –> increased TPR & HR
  • Sweating –> dehydration –> loss of blood volume
    • Decreased venous return –> decreased Starling forces –> decreased CO
    • Increased SNS –> increase HR (to compensate)
  • Hyperthermia enhances muscular activity
    • Increase SNS –> increase HR –> overly increased HR –> not adequate ventricular filling –> decrease stroke volume
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9
Q

Exercise vs. Moderate Hemorrhage for the following Conditions

  • Baroreceptor activity
  • Muscle paracrine factors
  • Angiotensin II levels
  • Vasopressin levels
  • Epinephrine levels
  • Vasoconstrictor activity
  • Diameter of gut arterioles
  • Diameter of brain arterioles
  • Blood pressure
  • Heart rate
A
  • Baroreceptor activity
    • Exercise: elevated BP –> increase, CNS –> decrease
    • Hemorrhage: decrease BP –> increaes hormones like ANG-2 –> increase
  • Muscle paracrine factors
    • Exercise: extreme increase in working muscle
    • Hemorrhage: vasoconstriction –> blood doesn’t get adequate blood flow –> increase
  • Angiotensin II levels
    • Exercise: reduced renal blood flow –> increased SNS –> increase
    • Hemorrhage: hypotension –> extreme increase
  • Vasopressin levels
    • ​Exercise: depends on volume & salt loss from sweating
    • Hemorrhage: decrease blood flow –> increase
  • Epinephrine levels
    • ​Exercise: increase –> vasodilation
    • Hemorrhage: extreme increase –> vasoconstriction b/c high Epi affect alpha receptors
  • Vasoconstrictor activity
    • ​Exercise: increase –> prevent TPR from dropping
    • Hemorrhage: increase –> raise BP
  • Diameter of gut arterioles
    • ​Exercise: constricted
    • Hemorrhage: constricted
  • Diameter of brain arterioles
    • ​Exercise: no difference / normal
    • Hemorrhage: no difference / normal
  • Blood pressure
    • ​Exercise: slightly increase MAP, increase systolic
    • Hemorrhage: no difference / normal
  • Heart rate
    • Exercise: increase
    • Hemorrhage: increase
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10
Q

Exercise vs. Hemorrhage

A
  • Similarities
    • Increased HR
    • Increased vasoconstriction within visceral organ vasculature
    • Increased circulating Epi
  • Differences
    • Higher Epi levels during hemorrhage –> bind alpha receptors
      • Exercise: vasodilatoin
      • Hemorrhage: vasoconstriction
    • Higher antiogensin-2 during hemorrhage
      • Muscle arterioles will constrict, despite paracrines
      • Increase during exercise is just moderate
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11
Q

CV Adaptations During Spaceflight

  • Pressure in arteries
  • Venous circulation
  • Compensatory mechanisms
  • Post-spaceflight orthostatic intolerance
  • Earth analog of CV adaptatoins during spaceflight
A
  • Pressure in arteries
    • Increases as blood goes down w/ gravity
    • Decreases as blood goes up against gravity
    • Earth: 70mmHg in carotid artery, 160mmHg in legs
    • Space: 90mmHg in both carotid artery & legs
  • Venous circulation
    • Earth: venous pooling in legs, little venous pooling in upper body b/c gravity facilitates drainage
    • Space: increase venous return from the lower body, decrease venous return from head b/c no gravity to drive fluid down
  • Compensatory mechanisms
    • Increase venous return –> activate atrial stretch receptors –> increase secretion of atrial natriuretic hormone
    • Increase BP at carotid sinus –> activate baroreceptors –> decrease baroreceptor reflex
    • Increased natriuretic peptides + activated baroreceptors –> decrease vasopression –> inactivate renin-angiotensin system –> decrease plasma aldosterone –> decrease plasma volume
    • Net accumulation of fluid in upper body –> net loss of fluid from CV system
      • When astronaut returns to earth –> bulk of fluid returns to lower body –> hypovolemia
  • Post-spaceflight orthostatic intolerance
    • Can’t stand w/o syncope
    • Loss of plasma volume –> down-regulation of baroreceptor reflex
    • Atrophy of muscles of lower body
      • In 0-gravity, standing provides no loading of muscles –> decrease skeletal muscle pumping
  • Earth analog of CV adaptations during spaceflight
    • Prolonged bedrest induces similar fluid shifts & muscle wasting
    • However, getting out of bed for 1 hour per day circumvents the physiological changes resulting from prolonged bedrest
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