1
Q
basics of hemodynamics
1. Ohm’s law
2. Posieuille’s law
3. conductance vs. compliance
A
- voltage = current * resistance is analogous to change in MAP = Q * TPR (tone); relationship is generally the same for systemic and local circulation; resistance is how hard it is for blood to flow through BV, greatest factor affecting resistance is radius; pressure decreases throughout the systemic vasculature to maintain driving pressure for BF, increased pressure with smaller diameter is cancelled out by increase in CSA
- pressure at local level can decrease due to increase in viscosity and length which increase resistance but radial changes are still the major factor
- conductance is how easily blood flows through sys based on how mechanically constricted or dilated of smooth muscle in BV, is inversely proportional to resistance; compliance is a physical property due to elastin and collagen in BV that allow them to distend and change vol in response to pressure
2
Q
vascular compliance
1. vascular anatomy
2. windkessel vessels
3. flow through compliant vs. rigid BV
A
- bigger vessels are thicker with smooth muscle and greater compliance due to higher amounts of elastin and collagen; capillaries with only one endothelial cell layer are not compliant and thus are fragile; mammal capillaries are similar in size since RBC do not scale
- highly compliant, elastic properties allow distention then recoil to drive BF and maintain BP by absorbing pressure to dampen pulsatile flow gen by cardiac cycle to protect microvessels
- with age rigid BV less elastin and collagen, unable to distend and recoil, decreasing DBP and flow is inconsistent since unable to distend to maintain driving pressure
3
Q
pressure waveforms
1. overview
2. augmentation
3. vascular stiffening
4. age on blood pressure
5. factors of vascular complicance
A
- unabsorbed pressure reflects off BV; more constriction the greater the amplitude of pressure wave, less compliance the faster the wave reflects back
- moving away from heart, waves peaks more as faster reflections summate; with age and disease states, less compliance, faster reflections will summate with incoming waves to form higher peaks resulting in higher BP with greater peaks earlier in sys vasculature, use pulse wave velocity as clinical measure of stiffness
- age will increase vascular stiffening but to a higher degree in hypertensive individuals
- less stretch results in less distension for less damping, increasing SBP; less recoil thus less difference between systole and diastole for smaller pulse pressure (sys - dia) and lower DBP
- exercise is the leading factor in improving vascular compliance in all age groups but genetics, fetal life, sociodemographic, and lifestyle all contribute to vascular aging
4
Q
BF changes with exercise
1. Local BF change
2. Functional/Exercise hyperemia
3. Redistribution of BF during exercise
4. BF increase response
A
- local BF increases linearly with workload; Increased BF using vasodilation decreases pressure; find balance between BF and pressure using selective vasoconstriction and dilation
- increased BF in response to contraction
- more fit person has higher max Q; most BF gets redirected towards skeletal muscle during exercise, more abs Q for heart, and decrease abs Q for viscera
- immediate increase in BF following contraction to working muscles
5
Q
Q vs. Conductance
1. Q on limiting VO2max
2. Mechanical constraints on CO
A
- Q limits VO2max since O2 uptake is dependent on O2 delivery in blood; max Q of heart is 25-30L but would require much more for all muscle therefore Q has a limit at a global level; so must rely on vascular conductance to meet local demand when CO limited
- the more stretch of the walls of the heart, the greater the contraction and thus SV (Frank-Starling Law); the amount the heart can expand is limited by the pericardium, therefore SV and Q are mechanically constrainted
6
Q
Control of muscle BF
1. Ohm’s Law
2. Factors involved in vasomotor control
3. Mechanical factors
A
- instantaneous flow = change in pressure x vascular conductance (resistance)
- mechanical factors, neural, and biochem
- muscle pump squeeze and collapse veins, dropping venous pressure to zero increases the pressure gradient between arterial and venous circ, sending more blood back to heart; increase in arterial pressure is sensed by the arterioles, decrease radius using myogenic effect to maintain flow and protect capillaries
7
Q
biochemical factors controling muscle BF
1. metabolic hypothesis
2. endothelial hypothesis
3. RBC
4. role of K+
A
- muscle waste metabolites such as adenosine and Ach bind to receptors and trigger prostacyclin G-protein signal pattern to increase NO synthase activity in endothelium to increase NO production for vasodilation; when blocking Ach in animal models decreases BF with lesser changes in smaller vasculature but in humans blocking both NO and Ach does not have a great effect on BF
- mechanical transduction of shear stress of contraction of smooth muscle on endothelium triggers endothelium to release NO, PG, and Ach to relax smooth muscle
- RBC detect O2 levels and produce vasodilators; release ATP and No to signal vasodialation
- rapid release of K+ from muscle hyperpolarizes outside the muscle membrane, relaxing and vasodialating the BV
8
Q
Endothelium
1. Importance
2. Ascending vasodilation
A
- effectiveness of exercise and vascular aging often target endothelium, is good indicator of CVD health and future health risk; able to use doppler ultrasound to img layers of BV and id reactivity to different stimuli to determine health of BV
- RBC in capillary close to SM can sense change in metabolism, SM can send signal from myoendothelial gap junctions to the endothelium, signal travel through endothelial gap junctions up the vascular tree to vasodilate, decreasing resistance and increasing BF to capillaries
9
Q
Vasodilatory pathways
1. Nitric oxide
2. Ach
3. Prostaglandin
A
- endothelial glycocalyx (glycoproteins) breakdown due to increased BF via shear, increase in Ca2+ levels, activates eNOS which uses O2 and L-Arginine to produce NO which diffuses across endothelial and SM membrane to increase cGMP and cause vasodilation
- Ach also increase Ca2+ in endothelium to trigger increased eNOS activity; L-NAME and L-NMMA are eNOS inhibitors
- shear stress induce endothelial glycocalyx (glycoproteins) breakdown; activating arachidonic acid which is converted into PG via cyclooxygenase in endothelium, PG binds to recptors on smooth muscle and increase cAMP to vasodilate
10
Q
Assessing endothelial function
1. process
2. results
3. factors affecting shear
A
- reactive hyperemia method allowing to isolate for endothelial func; Inflate cuff above systolic BP to cut off blood flow to extremity causing downstream ischemia; deflate cuff to cause high increase in BF (velocity) causing shear; check endothelium response to lvl of shear 40-45 sec after release as increase in brachial artery diameter (FMD response); 30-90s delay for change in diameter due to time for mech signal to change into chem signal
- should be 5%-10% increase for healthy; 5% or less increase is indicator of CVD; higher FMD indicate better vascular health and recover from CV events
- amt shear is proportionally related to how long cuff was on; 5 mins is standard
11
Q
Nitric oxide blood flow regulation
1. different intensities
2. effects of aging and exercise
A
- with injection of LNMMA at rest and heavy, BF drops sig, thus endothelium plays a major role in maintaining resting BF and during maximal exercise; even with LNMMA not much change from baseline, role of NO less prominent as other redundant factors become more prominent
- age impairs endothelial function but not much difference between young and older trained individuals; can also increase endothelial function through training from sedentary state
12
Q
red blood cells regulation of BF
A
- sesnse decrease in O2, releases ATP which binds to P2Y receptors on the endothelium
- endothelial intracellular Ca2+ release to increase eNOs activation to dilate smooth muscle
13
Q
cellular basis of vasodilation in smooth muscle
1. Nitric oxide
2. PG
A
- NO binds to NO receptors on smooth muscle, increase cGMP activity in muscle cell which blocks phospholipase C (stim SR release of Ca2+ for CBC); decreasing intracellular Ca2+, blocking contraction from occuring, dilating the vessel
- Prostaglandins bind to EP2 on smooth muscle, increase cAMP which blocks phospholipase C, dilating the vessel
14
Q
hemodynamics at different exercise intensities
1. changes in CO, BP, and conductance
2. limitation of vasodilation
A
- CO increases and starts to decrease at high intensity; BP increases and starts to increase greatly at high intensity, total vascular conductance starts to decrease at high intensity
- vasodilation has limit before maximal exercise, to maintain BF, vasoconstrict to increase BP and thus increase flow; at low intensity VC play big role in increasing BF but at high intensity BP drive BF
15
Q
ANS
1. overview
2. major neurotransmitter and targets
A
- SNS preG short, synapsing close to spinal cord at sympathetic chain ganglia, releasing Ach to nicotinic receptors on postG neurons; postG long, synapse with effector organs; PNS preG long, synapse and release ACh to nicotinic receptors on postG near effector organs; postG release Ach to muscarinic receptors on the heart and BV
- SNS postG release NE, Epi, NpY, and ATP (bind to P2X receptor on smooth muscle) to heart and BV; SNS preG connect to adrenal medulla, adrenal medulla directly release NE and Epi as hormones into blood to act on effector organs
16
Q
neural control of SNS
A
- central oscillator comp medulla integrates signals about homeostatsis to increase or decrease SNS activity to maintain homeostasis through reflexes
- cortical autonomic network can also influence homeostasis; can increase sympathetic activity in anticipation of stress
17
Q
SNS local BF control: varicosities
1. SNS neurotransmitter release
2. negative feedback
A
sympathetic neurons in tunica media innervating smooth muscle cells form a net around the muscle, have bumps (varicosities) containing vesicles with different distributions of neurotransmitter types; when AP pass through varicosity, activate vesicle to dock at the edge of varicosity and release neurotransmitters, resulting in different vascular effects
2. neurotransmitters can also bind back onto varicosity; NPY bind on Y2, ATP bind to P2y on varicosity, and NE on alpha 2 to inhibit further release of SNS neurotransmitters
18
Q
3 fates of NE after binding to effector
A
- Shuttled back into varicosity and repacked into vescicle for release
- NE diffuse into blood (NE spill over, v. Little)
- Taken up by varicosity and broken down into monoaine oxidase
19
Q
sympathetic innervation across vascular tree
A
- arteries and arterioles have high density innervation,
thick muscular layer to change diameter, high innervation; thick muscle = stiff + SNS vasoconstriction = limit BF (restraint mech) - capillaries have no muscle cannot change diameter, no innervation
- venules have low density innervation
- veins have high density innervation; hydrostatic gradient when standing, blood pool in lower extermity, sense drop, baroreceptor reflex increase SNS to vascoconstrict veins to pump blood up and back to heart to prevent fainting
20
Q
sympathetic tone
A
SNS activity is present at baseline (50% of baseline contractile state or vascular tone is due to SNS); for more increase SNS tone and decrease PNS signal in anticipation of or presence of stressors
21
Q
SNS neural discharge patterns
A
SNS discharge patterns release different neurotransmitters; at low freq (rest) release more ATP than NE, at mid freq (low intensity) release ATP and NE, at high frequency (high stress) release ATP, NE, and NPY
22
Q
mechanism of SNS neurotransmitters on vasoconstriction
A
- Force corresponds to constriction, when ATP bind to p2x to open membrane Ca2+ channel, increasing intracellular Ca2+ in smooth muscle for fast constriction but with less force bc limited Ca2+
- continued stim release NE and NPY which bind to receptor and trigger G pro signalling to increase phospholipase C and induce SR release of Ca2+ for constriction, greater change in force but longer time for effect
- NE bind to alpha 1 and 2 adenergic receptor (through G pro sys)
23
Q
SNS mediated constraint of muscle BF during exercise
1. microneurography
2. sympathetic control vs intensity
3. changes in BF due to SNS activity
A
- measure neuronal firing of SNS neurons; high plasma NE indicate high SNS; high plasma renin when high SNS
- Before 90 bpm, increase in HR is due to withdrawal of PNS, Increase intensity past 90 bpm, decrease splanchnic and renal BF by increasing SNS activity, vasoconstrict and increase HR
- BF increase after prazozin (block alpha 1 receptor) injection; increase BF after bretylium (inhibit NE at varicosity), NE constriction at rest and exercise
24
Q
distribution of SNS receptor type throughout vasculature
A
heterogenous distribution of different receptors at different parts of the vascular tree
1. Alpha receptors predominate at bigger arteries
2. Y1 and P2x predominate in smaller vessels
25
neural reflex control of circulation
1. overview
2. pathophysiology
1. sensory receptors detect changes in internal and external factors and send efferent signals to medulla, supra meduallary regions of autonomic control also send signals to medulla to reg homeostasis, central oscillator of medulla intergrates signals and sends out appropriate afferent response to change SNA to maintain homeostasis
2. Control at any level of ANS, disease/condition can affect how brain signalings to ANS causing autonomic dysfunction; why those with certain conditions find it difficult to do dynamic activities
26
baroreceptor brainstem autonomic reflexes
1. baro, metabo, and chemoreceptors send info to nucleus tractus solitarius in brainstem
2. high stretch send signal to nucleus ambiguous and dorsal motor nucleus to inhibit PNA to increase HR and in BP
3. if low stretch NTS send signal to caudal ventrolateral medulla which inhibits signalling to rostral ventrolat medulla (increase SNA to drive up BP) to decrease SNA
4. supermeduallary input integrating perception and experience can send both inhibitory and excitatory signals to NTS to change SNA to certain stimuli
27
autonomic problems in maintaining BP
1. exercise induced hypotension
2. orthostatic intolerance
1. >10 mmHg fall in SBP during exercise, symptom of autonomic failure, multiple sys atrophy, and SCI, not related to heart or SM but due to blunted SNA and excessive vasodilation in splanchnic circ, thus less blood to the muscle
2. fainting is inability to maintain BF in response to changes in BP; when standing decreased SV since blood pools in lower extremity, normally increases SNA to vasoconstrict venous circ to increase pressure to drive BF back to the heart but with autonomic problems unable to constrict in time and faint to eliminate gravitation resistance on BF to brain
28
baroreflex
1. baroreceptors
2. negative feedback loop
1. are mechanoreceptors formed from clusters of sensory neurons that sense distension of vessels, arterial high pressure sensors in the carotid sinus and aortic arch, low-pressure sensors in the heart and lungs, greater BP will stretch the vessels more, detect as transmural pressure (intravessel pressure - interstitial/outside pressure) send afferent signal to medulla via glossopharyngeal nerve
2. baroreceptors in the carotid sinus and aortic arch sense transmural pressure; unloading baroreceptor such as when standing, outside < inside P detected as low distension, thus low BP, decrease afferent signal (decreased GPN activity) to medulla, increase efferent SNA, decrease vagal tone to increase HR and constriction to drive increase in BP
3. loading baroreceptor such as during water immersion drive blood back to heart, inside > outside detected as high distension thus high BP, increase afferent GPN signal to medulla, decrease efferent signal to SNA to increase vagal tone to decrease HR and vasodilation to drive decrease BP
29
baroreflex sensitivity and effects of age and training
1. sensitivity is change in time between heartbeats when there is 1 mmHg change in BP
2. phenylephrine bolus technique for measuring BRS blocks a1 receptor to cause vasoconstriction, measured BRS using RR interval on ECG, increase BP due to vasoconstriction, healthy baroreflex will have quick reflexive increase in RR interval to slow HR and decrease BP'
3. age decrease BRS but with exercise improved BRS, middle aged adults able to reach young level of BRS but older could not though there was still improvement with training
30
baroreflex resetting
1. denervated baroreceptors in dogs shows greater variabliity in BP comp normal; thus baroreceptors do not control MAP but maintain BP within range
2. during exercise reset range of acceptable BP to include greater value with a greater homeostatic set point moderated by supramedullary regions and afferent neurons
31
central command
1. overview and first observation
2. effects of central command on SNS
3. effects of central command on HR
1. assoc with effort and influence ANS activity based on experience; when measuring resp, HR, and EMG, increases in resp and HR occurs before the start of the EMG signal (contraction) indicating an anticipatory effect (effort) modulated by central command
2. to isolate for effect on SNA, use curare which is a skeletal muscle nicotinic receptor antagonist that blocks postSGN from SNA to stim paralysis; MSNA and force higher with handgrip, during curare contraction, MSNA is still higher than low intensity due to central command exerting effort but force is low since cannot contract, effort on SNS more important at maximal intensity
3. to isolate for effect on HR, use curare during handgrip, HR increases by 20 bpm at rest, higher than low intensity but matching moderate intensity, effort on HR more important at moderate intensity through PNS withdrawal (PNS withdrawal key factor for change in HR below 90 bpm)
32
supramedullary regions of central command
1. medial PFC (decrease), anterior cingulate cortex (decrease), thalamus (increase), insular cortex (increase), and cerebellar vermis change activity during contraction comp baseline
2. regions with decreased activity responsible for parasympathetic withdrawal
3. regions increasing activity responsible for SNA
33
metaboreflex
1. overview
2. combined effects of central command and metaboreflex
3. metaboreflex only
1. exercise pressure response, combination of type III afferent mechanoreceptor sensing tension and type IV afferent metaboreceptor sensing SM metabolites activate during exercise and send signals to central oscillator to increase SNA
2. normal response increases BP during exercise and drops BP immediately during recovery
3. cuff ischemia greatly increases BP during exercise, post-exercise occlusion during recovery ischemic protocol prevents circulation of metabolites, continued activation of type IV afferents increases SNA and maintains BP at high level, release of cuff allows metabolite circulation and BP drop
34
metaboreflex and neural signalling during exercise
1. experimental design
2. MSNA
3. HR
4. BP
5. CO and TPR
1. baseline, handgrip (central command and exercise pressor), metaboreflex only during post-exercise occlusion, and recovery
2. 30-sec delay after start of contraction before increase in MSNA due to time for metabolite buildup, MSNA still high post-exercise occlusion due to metaboreflex but drop during recovery when metabolites wash out
3. Immediate change in HR due to PNS withdrawal from central command during exercise, HR drops immediately after exercise due to lack of central command
4. with exercise, immediate BP increase due to HR increase (MAP = CO*TPR), higher comp baseline during occlusion due to metabolite buildup (metaboreflex), release of cuff during recovery metabolites about to washout and BP drop
5. MAP gen by handgrip sustained during PECO despite CO return to baseline but no increase in TPR thus constriction must be occurring elsewere
35
Segmental model of neurogenic control
1. Leg vascular control
2. Kidney
3. Portal vein
4. Mesentary
5. Spleen
6. Coronary circ
7. Summary
1. During handgrip, large increase in BP and SNA but no change in TPR despite large increases in BF
2. Increase exercise increases res to vasoconstrict renal artery
3. During handgrip constrict (more res) portal vein, during PECO no constriction, metaboreflex not effecting portal vein
4. With increased duration of exercise, mesenteries exp more vasoconstriction (res); phentolamine is a1 receptor blocker, less change in res with phentolamine > sympathetic mediation of vasoconstriction in mesenteries (NE big role in increases res in mesentary)
5. Splenic vol decreases with handgrip, Decreases with lower body neg pressure (supine with vaccum around legs, turning on vacumm pools blood in the legs up to -80mm Hg, fainting may indicate autonomic disorder), valsava manuver and cold pressor also decrease splenic vol indicate that vasoconstriction (res) in spleen is due to sympatho-excitatory reflexes
6. intensity increase coronary vascular resistance to allow for greater shunting of blood from the outside to inside of the heart for perfusion of myocardium and increase CO, BF to heart as whole does not change!
7. During vol handgrip vasoconstrict everywhere except extremities (SM)
36
Respiratory muscle metaboreflex
1. Overview
2. Changes in work of breathing
3. Evidence supporting diaphragm metaboreflex on SM BF
1. Respiratory muscle chan redirect BF from SM by producing metabolities and sending signals to brain via afferent to vasoconstrict and limit SM BF, protection mech of lungs competition
2. Work of breathing is how hard it is to breathe can change by breathing through straw or normally, plateau CO by maintaining steady state at 85% VO2max, increase work of breathing, lungs work harder and produce more metabolites, SM BF decreases due to vasocontriction (increased vascular res); vice versa when easier to breathe; no change SM BF due metaboreflex when cardiac output changing, but change when Q maintained
3. Increase in AP of type III and IV diaphragm afferent recordings to increase SNA in lungs in rodents; MSNA studies in humans show that change in work of breathing increases right phrenic nerve activation (innervates the diaphragm); greater fatigue of diaphragm decreases limb vascular conductance (vasodilation) in dogs
37
Splanchnic and thoracic hemodynamic changes during exercise
1. Blood volume
2. Impedance
1. During exercise more Bvol in thoracic then increase CO and venous return, BV decrease in visceral/splanchnic
2. impedance (res) increase in splanhnic during exercise and decreases in thoracic, both have quick increase/decrease at start of exercise and quick return to baseline at end of exercise
38
Modifying sympathetic vascular control during exercise
1. Importance
2. Physiological control of sympathetic vasomotor impact during exercise
1. Req balance between BP reg and perfusion to meet metabolic demand for all organs during exercise, vasoconstriction operates through different levels of SNS control
2. 2 forms of control: prejuntional control of neurotransmitter release when adrenergic neurotransmitters (ATP, NPY, NE) binding back to preSN inhibits further release of neurotransmitters, and prevent more vasoconstriction independent of exercise; or through functional sympatholysis
39
Functional sympatholysis
1. Overview
2. Assessing sympatholysis
1. Reduction of sympathetic vascular control to decrease in SNA during SM contraction (functional) in SM, indirect vasodilators effect to allow perfusion in SM
2. When infusing phenylephrine (a1 agonist causing vasoconstriction), less increase in vasoconstriction with increasing intensity compared to rest in leg SM; same effect with clonidine (a2 agonist) and with Y1 and P2X receptor stimulation indicating there is a mechanism that breaks down the SNA effects during exercise to moderate vasoconstriction at the local level of SM
40
Mechanisms of sympatholysis
1. constriction and dilation overview
2. Metabolites
1. Shear induce dilation through NO release, adrenergic neurotransmitter causes constriction, myogenic response senses increase intravascular pressures due to mechanical distension in smooth muscle caused increase muscular constriction to bring flow back, metabolites activate metaboreflex for constriction
2. Metabolites increasing during exercise (functional) can also interfere with normal vascular constriction response to adrenergic neurotransmitters by inhibiting binding at VSM receptor to decrease constriction (sympatholysis)
41
Mechanisms of sympatholysis
1. Nitric oxide
2. K+
1. NO released from the increased shear during exercise inhibits adrenergic neurotransmitters to decrease constriction; in animals studies LNAME infusion reduced NO production and reduced sympatholysis but no changes shown in human LNAME infusion thus role of NO in sympatholysis is species dependent
2. Alpha receptor stimulate increase in Ca2+ in VSM via voltage gated Ca2+ channel on cell membrane, metabolites in smooth muscle open K+ channel, outflux of K+ hypopolarizes Ca2+ channel, decreased stimulation of constriction in VSM; decrease sympatholysis with higher intensity compared to baseline; glyburite inhibiting K+ channel restores sympathetic constriction in the exercising limb no change in the non-exercising limb
42
IP3 in sympatholysis
1. in smooth muscle phospholipase C activates IP3 to stim SR release of Ca2+ for constriction
2. IP3 can exit through myoendothelial junction and exit smooth muscle cells and bind to endothelial IP3 receptors, increasing Ca2+ in endothelium, Ca2+ bind to Ca2+ gated K+ channel, increase K+ outflux of endothelial cell by opening K+ channel, hyperpolarizing smooth muscle cell, decreasing sympathetic tone for constriction since harder to contract as moderation of vasoconstriction in smooth muscle
43
PNS and ANS innervation of the heart
ANS emerging from sp cd innervate SA node for rhymicity, at baseline vagal dominate and PNS slow HR between baseline levels and 100 bpm, SNS dominate past 100 bpm to accelerate HR
44
PNS control on HR
1. rapid HR response to vagal stim
2. fast increase HR due PNS withdrawal from acetylcholinesterase (breakdown Ach at muscarinic receptor to decrease PNS effects)
3. fast decrease in HR due to muscarinic-activated K channels (K channel linked to Ach, binding of Ach to muscarinic receptors allows quick outflux of K+ for hyperpolarization to slow pacemarker cell to slow contraction and HR)
45
SNS control on HR
SNS has slow HR response since Epi/NE bind to beta receptors on heart and use G PRO signalling pathways to increase Ca2+ influx for contraction of myocardium
46
intrinsic control on HR
SA node depolarizes when Na+ leaks through funny channels (constant leak to keep ions flowing through cell) to threshold, Ca2+ enters cardiac cells to depolarize for myocardial contraction, K+ outflux repolarizes
47
age on control of HR
1. HR variability is time between HR (RR interval) and can measure PNS or SNS dominance
2. How well RR interval is able to change with BP is indicator of baroreflex sensitivity, slower change in increase in RR interval in older adults comp young, suggests more SNS dom with age due to impaired PNS function thus less withdrawal in older people; older people also have higher resting SNS
48
mPFC on HR
Handgrip at 5% and 35% MVC; out of motor cortex, insula, and posterior cingulate, only mPFC able to differentiate between two intensities with inverse relation between HR and mPFC activity, thus mPFC involved in PNS withdrawal during exercise for early HR changes to exercise
49
exercise induced bradycardia
1. overview
2. isolating for intrinsic rhythm
3. role of funny channels
1. Bradycardia (reduction in HR) common in athletes and common in those who go from sedentary to training
2. Give sedentary people atrophine (blocks muscarinic receptors/PNA to increase HR) and propranolol (block beta receptors/SNA to decrease HR) to isolate for intrinsic rhythm at 100 bpm; same trial in athletes show intrinsic rhythm is lower at 80 bpm, therefore training bradycardia is likely due to decrease in intrinisic rhythm than enhanced PNS, but ANS adaptations is still possible
3. Stain for funny channel HCN4, less stain in trained mice, indicating training downregs HCN4 making it harder to depolarize cardiac cell bc less leaking, thus exercise play role in intrinsic rhythm
CV Exercise Physiology
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