Circulatory responses to exercise

cardiac regualtion

• many coordinating factors that affect the cardiovascular control areas

  • sympathetic tone accelerates and parasympathetic tone bakes system

• vasoconstriction

  • respiratory pump and parasympathetic stimulation

  • in non exercising muscle

    • increased sympathetic outflow

• vasodilation

  • in active muscle

• resetting of baroreceptor control to help regulate BP during exercise

sympatholysis

• opposing sympathetic vasoconstriction

  • ATP, K, Ca, adenosine nad lactate

    • redundant mechanism

cardiac muscle fibres

• muscular fibres pinnation allows for “twist” during contraction

  • more and faster contraction the elastic components reacts

• short muscle fibres connect in tight series 

  • interconnected via intercalated discs 

    • permit transmission of electrical impulses from one fibre to another

    • allow ions to cross from one CV muscle fibre to another 

    • when one heart fibre is depolarized to contract all connecting fibres also become excited and contract as a unit 

• ventricular myocardium in a homogenous muscle containing one primary fibre type 

  • similar to type 1 sk mm 

    • highly aerobic with large number of mitochondria 

      • importance of continuous aerobic metabolism in the heart 

• typically branded 

• involuntary contraction 

structure of the heart

 

• Four chambers descirbed as two pumps in one

  • R atrium and R ventricle form R pump

  • L atria and L ventricle make L pump

• Interventricular septum separates interventricular septum

  • Prevents mixing of blood from 2 sides of heard

• L ventricle accounts for 75-80% total hear mass

  • Needed to pump blood throughout the body under relatively high pressure

  • R ventricle supplies nearby lungs and blood under lower pressure

• Maintain constant blood supply to heart via coronary arteries as heart has high demand for O2 and nutrients

  • Even at rest

  • When disrupted for more than several minutes permanent damage occurs ot hear

    • Ie. MI 

pulmonary circuit

• blood delivered from R heart into lungs 

• O2 is loaded into blood and CO2 released 

• oxygenated blood then travels to L side of heart and pumped to various tissues of body via systemic circuit 

cardiac cycle

• MAP = DBP + 0.33

• PP (pulse pressure) = systolic - diastolic

• as we increase HR heart needs ot unload same amount + a little more unloading than at rest 

• repeated pattern of contraction relaxation of the heart 

  • contraction - systole 

  • relaxation - diastole 

• two step pumping action 

  • L and R atria contract together which empties atrial blood into ventricles 

• at rest - contraction of ventricles during systole ejects 2/3 of blood from ventricles leaving 1/3 remaining in ventricles 

  • ventricles then fill with blood during next diastole

isovolumetric contraction

no change in volume but pressure changes

Pressure changes during cardiac cycle

 

• Pressure within heart chambers rises and falls

  • When atria relaxed blood flows into atria from venous circulation

  • Pressure gradually increase as chambers fill

  • 7-% of blood entering atria during diastole flows directly into ventricles through AC values before atria contraction

  • Atrial pressure rises and forces most of remaining 30% of blood into ventricles following atrial contraction

• Occurrence of lub dub produced by closing of AV values and closing of aortic and pulmonary valves

• Ventricular pressure is low while ventricles fill

  • Increase when atria contracts

• Ventricles contract increase pressure closing AV valve an prevent backflow into atria

• Rise in pressure is is isovolumetric  contraction phase

  • Same volume while pressure rises rapidly

• As ventricular pressure exceed pressure of pulmonary artery and aorta PV and OC open and blood is forced into both pulmonary and systemic circulations

  • Pressure in aorta increased in response to pulse of blood ejected by ventricles

• Following systolic phase of cardiac cycle aortic and pulmonary valves close and ventricular pressure declines

  • Once valve has closed BP within aorta drops to diastolic value

  • Volume of blood in ventricles remains constant - isovolumetric relaxation p

pressure of blood flow

• Pressure head driving blodo flwo in systemic cirucaltory system under resitn condition

  • MAP is 100 mmHg

    • Pressure of blood in aorta

  • Pressure in R atrium is 0 ,,Hg

• Dirivng pressure acorss the circualtry system is 100 mmHg

• The flow of blood thrgh the systemic circuit is dpeednent on pressure difference between aorta and R atrium

• pressure drops due to function of vessels 

  • buffers some energy form large vessels 

    • due to increased surface area creates reduction 

  • at the capillary level RBC move through 1 at a a time 

  • directionally of vein in closed systems continues to push returning blood to heart

flow rate

• Through vascular system is proportional to pressure difference across the system

  • Inversley proporitonal to the resisitance

  • When vascualr resisitance increases blood flow decrease

    • Inversely proportional

• Blood flow can be icnrease by either na increase in BP or a decrease in resistance

• 5 forld increasei n blood flow could be gerated by 5 fold increase in pressure

  • Although hasardous to health

• Increase in blood flow during exericse ahcived by primarly by decreasr in resistance with small rise in BP

contributing factors of blood flow

• Directly proportional to length of vessel and viscosity of blood

• Diameter of blood vessel

  • Vascualr resistance inversley proportional ot 4th power of raidus of vessel

    • Increase in either vessel length or blood viscosity resultsi n proprotion icnrease in resisitance

how do we assess MAP during exercise

non-invasive blood pressure cuff to measure systolic and diastolic pressure during exercise, and then calculate MAP using the formula MAP = Diastolic Pressure + 1/3(Systolic Pressure - Diastolic Pressure)

contributing factors of blood flow

• Directly proportional to length of vessel and viscosity of blood

• Diameter of blood vessel

  • Vascualr resistance inversley proportional ot 4th power of raidus of vessel

    • Increase in either vessel length or blood viscosity resultsi n proprotion icnrease in resisitance

sources of vascular resistance

• Length of blood vessel does not change in normal phys

• Blood viscosity tpyically remans unchanged at rest

  • Only slightly altered by acute bout of exercise

• Priamry regualting factor of blood flow through organs is diameter of blood vessel

  • Small vasocontrcition results in large vascualr resisitance and decreaser in lbood flow

  • Effect of changes in radius have magnified impact on blood flow rate

    • Blood can be diverted from one organ systme to another

      • Variyng thr amount of vasocontricitino and vasodialtion

• Udirng heavy exercise altered vascualr rsistance explains how blood is diverted toward contracting sk mm and away from less acitve tissue

• Greaest vlasucalr resistance in blood flow occurs in arteiroles

  • Large dopr in arteiral pressure occurs across artierioes - 70-80% of decline in MAP

Cardiac output equation

Q = ABP - RAP / TPR

blood flow equation

• blood flow = change in pressure / resistance 

Poiselles equation

• flow = change in pressure X pi X r^4 / 8nl

  • change in radius causes 4 fold increase in pressure 

pressure regulation

• MAP determined by 2 factors

  • Q and TVR

  • MAP = Q x TVR

• Increase in ethier factor results in an icnrease in MAP

• Depedns on variety of physioglcial factros

  • Q

  • Blodo volume

  • Resistnace ot flow

  • Blood viscosity

• Increase in any of these vairbles results in increase in arterial BP

  • Decrease in any of the variables cuases decrease in BP

• stroke volume increases 

  • volume of flow out of ventricle increases 

• peripheral resistance increases 

  • constriction of non exercising muscles 

    • ie. splanchnic 

      • increase in flow increases resistance

 

regulation of BP

• Acute regualtion from sympathetic NS

• Long temr regualtion function of kineys

  • Regulate BP by controlling blood volume

cardiovascular control centre

• Baroreceptors (pressure receptors) in carotid artery and aorta are snesntive ot change in artrial blood pressure

• Increase in arterial pressure triggers recpetors to send impusles to CV control centre

  • Wirhin medulla oblongata

• Responds by decreasing sympathetic acitvity to heart and blood vessels

• Reduction in sympathetic acitvity may lower Q and/or lower vascualr reisistance

  • Lowers BP

• Decvrease in BP reslts in reduction of baroreceptro activity sinalling in brain

  • Causes CV control ceentre ot respond by increase in sympathetico utflow

  • Raises BP back to normal

• Integrated control of BP udring exercise regualted at higher set point comapred ot rtest

• Baroreceptor control is altered during exercise by higher systolci BP nedded to support increase Q udring intense exercise

regulatory reflex of baroreceptors at R atrium

• Increase in R atrial pressure singals CV control centre

  • Icnrease in venous occurred to prevent a backup of blood in systmic venous system

    • Increased Q must result

• CV control centre repsonds by sending symapthetic accelratro nerve impulses to the heart

  • Increase HR and Q

• Resuslts in increase in Q lowers R atrial pressure back to normal

  • Venous BP si reduced

influence of body temp on HR

• Increase in body temp above normal resutls in increasevs HR

• Lowering of body temp below normal causers recuction in HR

  • Exercise in a hot enviro results in increase body temp and higher HR than if performed in cool enviro

autonomic control of heart

• Quantity of blood pumped by heart must change in accorance with elevated SK mm O2 demand

  • SA node controls HR - changes in HR influences SA node

    • Parasumaptic and symapthetic hcanges of ANS

• Both branches are essnetioal for integrated control of CV fucntion

  • At rst normal balance of parasymapthetic tone and symapthetic acitviy to hear maintained by Cv control centre in medulla oblonaga

    • Recived impulses from vairous parts of cirucalory system relative ot changes in parameters - ie. BP etc.

    • Relays motor impulses ot hear in repsonse to changing CV need

      • Increase in resitng BP sitmuatres baroreceptors in carotid arteires and arch of arotia sending impusles to CV control centre

        • Increases parasymapthetix acitivy ot heart to lsow HR and recucde Q

          • Reduction in Q causes BP to lower back to normal

parasympathetic control of heart

• Parasympathetic

  • Fibres thati nnervate hear from neruons in CV control centre in medulla bolongata

    • Make up portion of vagus nerve

  • Fibres make contact with both SA and AV node

    • When sitmuated nerve endings release Ach cuasing a decrease in acitvity of both SA and AV nodes due to hyperpolarixation

      • End result is reduced HR

        • Braking system to slow HR

  • At rest vagus nerve carries impusles to SA and AV nodes

  • Infleunce of vagus nervie refered to as parasympathetic tone

  • Changes in parasympathetic acitiy can cuase HR ot icnrease or decrease

    • Decrease in PS tone to heart can increase HR

    • Increase in PS acitvity causes slowed HR

• carotid baroreceptors regulates HR 

  • afferent feedback from barorecpetos

• aortic baroreceptors regulates pressure

sympathetic control of heart

• Reach hearty by means of caridac accelratory nerves

  • Innervate both Sa node and ventricles

• Endeings of these fibres relsease NE upon stimuaiton

  • Act on beta receptors in heart and cause increase in toh HR and forve of myocardia conttroaion

• Increased frequency and force of heart beats increases metaboic rate

  • In many patients altering autonmuc influence on heart metabolci rates preserves proper caridac fucntion

Heart rate regulation

• regulates coronary vessels 

  • without would decrease flow in coronary vessels 

• parasympathetic blockers show similar results to moderate intensity exercise 

• Intial increase in HR udring low intensity exercise is d/t withdrawls of parasymapthetic tone

  • Initial increase in HR due to intrisic firing without PS neural input ot slow SA node

• At ihger work rate stimuation of SA and AV ndoes via SNS responsible for increases in HR

  • Sympathetic outflow

Stroke volume 

• regualted by 3 factors

  • EDV

    • Volume of blood in ventricles at end of diastole

    • Referred to as "prelaod"

    • Infleunces SV

      • Strength of ventricular contraction increased with an enlargement of EDV

        • Frank-starling law of heart

    • Increase in EDV results in lengthening of CV fibres which improves force of ocntraction similar to that of sk mm

    • Influence of CV fibres optimzies the nubmer of myosin cross bridge interactions within actin

      • Elevated force production

      • Rise in caridac contraciltiy results in increase blood pumped per beat

    • Princiapl viarialbe is rate of venous retunr to heart

      • Icnrease in venous return resuts in a rise in EDV

        • Increase in SV

      • Increased venous return and resutling icnrease in EDV plays role in icnrease in SV observed during upright exercise

  • Average aortic blood pressure

  • Strength of ventrivular ocntraction

sympathetic control

• sympathetic nerves increase contractility of muscle control HR impacting SV and improve contracittliy through increased Venus return increasing SV

• SNS control Q but also SV

  • Improve contracitltyi of caridac mm so that cardiac mm can contract nad expand  more rapidly imprvoing filling time

    • Bigger stretch and better contraction

      • Sturcture and fucntion

  • Not just HR

heart rate regulation during exercise

• Braking aciton

  •  Reduction of peripheral nerve acitivty

• OC/Mechano/CBR (carotid baraceptor resetting)

  • Central command

    • Act of preparing to exercise

      • Efferent signal changes HR

  • Mech stimulation inceases HR

  • carotid baraceptor resetting

    • Helps to reduce variabltiy

    • Want ot be in a mcuh lower level

• At rst there is more variability

  • HRV is variable at rest

  • As we begin ot exercise as we remove parasympathetic activity the HR becomes less variable

• Further loss of cardiac parasymapthetic acitvity as we increases intensiy

  • Increase in ScaridacNA

• Arterial barocerecptor resets from central command simialr to HR

  • Don’t want BP to have lg fluctuation

    • Want ot be stable

• Metaboreflex/symaptthetic (adenergic) responses

  • Close ot max HR and intensity

  • When SNS is stimualted provokign adrenergic molecules from adrenal medulla to cirucalte humorally dirving increases in HR

    • Heart transplant will decrease nervous connections of heart

      • HR folowing heart rnasplant is much higher

        • Increased HR with exercise is humoral not neural

heart rate regualtion as we recover

• Mechanical recpetors stop stimulation

• Arterial barorecptors start ot retun to regualtroy factors

• Metabolic, symapthetic adrenergic and thermal conditions

  • Have ot maintian higher HR so blood flow gets to warm areas - allwong for cool off

• Return in PN acitivty and reduction of SNS acitivty

  • Know of this thorugh post-exercise msucle ischemia

    • Get tired aqs exercise icnreases

      • Right as we are done - pump of BP cuff to trap metabolites and stop of exercise

      • Increase in HR nadm etabolites in arm

      • When we stop HR drops and plateuas as metabolites send sigals thorugh G4 afferents

reactors that impact EDV

1. venocosntirction 

2. muscle pump 

3. respiratory pump

venoconstriction on EDV

• drives blood back towards heart by contracting veins

  • decrease in size 

• Increase venosu return by decreasing diamaeter of vessels in increaseing peressure in vein

• Invreased vneous pressire drves blood back toweards the heart

• Occurs via symapthetic reflex control within blood vessels of SK mm

• Symapthetic constriction of smooth mm in vein accelerated return of blodo to earty

• Effects are integrated features of CV control centre in medulla

muscle pump on EDV

• biomechanical venous compression helping blood return to heart 

• Result of mechanical action of rhythmic sk mm contraction

• When mm contract during exercise compress veins and expedite return of blod to heart

• Between contration blood refills veins and process is repeated

• Blood is prevneting form flowing aaway from heart between contractions bty 1 way vlaves located in large veins

• Sustained msusucalr contractions (ismetric exercise) msucle pump cannot perate and venous return to heart is reduced

respiratory pump on EDV

• rhythmic breathing pattern provides mechanistic pump promoting venous return

• During inspriation pressure w/I thorax decreases and abdominap ressure icnrease

  • Venous return is promoted because chest pressure are slighlty lower than pressure in abdominal avity

• Rest aids in vneous return

  • Rolew of resp pump is enhanced during exercise due to greaster RR and depth

• Dominant factor that promotes venous return to heart udring upright exercise

Aortic pressure (MAP)

• Pressure genrateed by L ventricle must exceed pressure in aorta

• Represents barrier to ejection of blood from ventricles

• SV inversley proportional to afterlaod

  • Increase in MAP produces decrease in SV

• Incease in MAP during CGV exercise is not problematic for ehatlhy heart

  • Counteracted by cardiact contractiltiy icreased udirng exercise d/t increasers symapthetic stimaution of heart and Frank-Starling effecvt

• Minimzed udirng bout of exericse beucase of artoerle dialation

  • Makes it easiler for heart ot pump a larger volume of blood despite rise in ststolic BP experienced during exericse

SV regulated by 3 factors

1. EDV

2. Cardiac contracitlyi

3. Cardiac afterlaod (MAP)

• During upright exercise exercise induced increases in SC occcur d/t both increases in EDV and cardiac contraciltiy due ot circualting catecholamines and/or sympathetic stimulation

• Increase in MAP results in decrease in SV during resting conidtions where various infleunceso n cardiac contracitltiy are not at work

circulating catecholamines

• E + NE 

  • Both increase entry of extracellular calium into cardiac mm fibre

    • Increase cross-bridge acitvation and force prduction

• Infleunce of catacholamines compeltments direct stimulation of heart by cariac accelerator nerves

• Increase cariac contractitlyi by increasing amount of claicum avaialbe to cardiac msucle fibrees

• Increase symapthetic stimaution of heaet increases SV at any level fo EDV

blood flow to mm and brain during exercise

• At rest 15-20% of total Q direct ot sk mm

• During max exercise 80-85% of total Q goes ot contracting sk mm

  • Trnaistion from rest ot max exercise is an increaser in both volume and % of total Q that SK mm recives

• Increase in blood flow to sk mm is necessary ot meet large increase in O2 requirements udirng intese exercise

• Although % of total Q recived by brain is reeuced during max exercise comapred ot rest absolute volume of blood is slightly increases above resitng values

  • Increase in overall supply of blodo due to elevated Q during PA

    • Physi9olkgical improtance of continued brain fucntion during exercise

  • Form 15% to 3-4% during max exericse

blood flow to organs during exercise

• Volume nad percantage of blodo allocated ot heart udring max exercise is unique

• % of total Q that reaches myocaridum is same at rest and max exercise

  • 4-5%

  • Virtually identical due to metaoblic rate of the heart percicly controlled at all times to ensure shifitng energy demands of body can be met rpadily

• Total coronary blood flow is increased ot match elevated Q udirng insnse exercise

Blood flow to sk mm during exercise

• Some ittsuses recies less blood

  • Reduced blodo flow to abdominal organs

    • Improtant means of shifting Q aeay from less active tissues

• Higher Q results in only slightly reduced volme of blood reaching organs

• Skin blood flow decreases during max exercise to support msucualer owkr

  • Reduction in skin lbood flow is not problematic in terms of theraml regualtion

  • Skin blood flow increased in trnaisiotn from rest during both light nad moderate exercise to dissipate heat

redistribution of blood flow to active vs inactive tissues

• shows sympathoylsus 

  • change in increase in volume and increases mm blood flow

• crease musclalr blod flow while reducing blood flwo to less actibe organs

  • Such as liver, kidnets and GI tract

• Change in blood flow to mm and splachnic circualtion dictatedby exercise inteitity - metaoblic rate

• Increase in mm blood flow udring exercise and decrease in splacnic blood cflow changes as linear function of % VO2 max