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
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
- Involved muscle afferents
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
- Diastolic pressure doesn’t increase in proportion to systolic pressure
- 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
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
- Most ventricular filling occurs early during diastole just after the AV valves open
- 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
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
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
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
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
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
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
- Higher Epi levels during hemorrhage –> bind alpha receptors
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