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8/3/2019 LSM3212_Lecture 12 Ans-cvs
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Applications in Exercise and Sports Performance
A/Prof Lim Chin Leong FabianBSc(PE), MSc(PE), MBA and PhD
Programme Director,Combat Protection and Performance
Head, Military Physiology LaboratoryDMERI, DSO National Labs
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Healthy and at rest
Physical exertion
Extreme Performance
Illness /
Injury
Over exertion
The Dimensions of Physiological State and Homeostasis
Challengeto regulate
Limits of regulation
Dysregulation
Non-survival /Chronic injury
Shift in baseline physiology tosurvive at a new state ofexistence. Key issues:
Acute adaptationChronic adaptation
Variations in adaptationLimits of adaptationsMechanisms of adaptationInterpretation of physiology
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Comprises the heart and all the bloodvessels in the body
Arteries
Veins
Aterioles
capillaries
Primary role is the delivery of inertbiochemical products to target cellsand removal of biological wastes fromthese sites. e.g.,
Respiratory system
Immune system
Metabolic system
Endocrine system
Thermoregulation
Influence on metabolic system playkey roles in exercise performance.
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Determining VO2 measurement by the Fick equation:
VO2 = Cardiac Output x A-VO2 Difference
Stroke Volume x Heart RateEnd diastolic volume
End systolic volume
Ventricular compliance
Contractility
Ventricular volumeBlood pressure
Peripheral O2 ExtractionVascularization
Mitochondria volume
Citric acid cycle enzymes
Muscle type
Pre-ETC events.
X
Delivery of Oxygen Extraction andutilisation of oxygen
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The Cardiovascular System during Exercise
Stroke volume:End-diastolic volume
End-systolic volumeEjection fraction
Venous return
Heart rate:Baroreflex
Autonomic stimulationArterial pressure
Blood volume
Cardiac output
Oxygen delivery toactive muscles
Aerobic metabolismKreb cycle
Electron transport chain
Sustained physical work
ATP
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Blood Distribution during Exercise
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CVS Response during Exercise
HR, SV, EDV and Q increases withincreasing exercise intensity
SV and EDV starts to plateau atabout 50W (power output)
SV and EDV decreases when nearmaximal exercise due to lowervenous return and shorter cardiac
cycle
HR increases acutely to sustain Qcardiovascular drift.
Q may also decreases near maximalexercise due to reduced SV and EDV
A drop in Q may be the limiting factorto intense exercise performance
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CVS Adaptation to Chronic Endurance Exercise
Heart size athletes s heart
Larger LV volume
Larger wall thicknessHigher LV mass
Higher SV at rest and peakexercise
Lower HR at rest andsubmaximal workload
Faster recovery HR
Higher Q due to increase in
SV
Higher Plasma volume
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Cardiac Compliance influence Stroke Volume
No difference in cardiac
contractility (End systolic volume)between endurance trained anduntrained subjects
Significant difference in cardiaccompliance (End diastolic volume)
between trained and untrained
subjects (Frank-Starlingmechanism)
Heart also needs to fill the LV veryquickly during maximal exercise(CV drift);
ET athletes are able to fill their LVrapidly at maximal exercise.
Levine BD J Physiol, 586.1, 25 34, 2008
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CVS functions and fatigue during exercise
Gonzalez-Alonso et al. J Physiol 586.1: 45-53, 2008 Gonzalez et al. JAP 86: 1032-1039, 1999
BF demand > BF supply
during maximal exercise
Rate of rise in muscle BFand O2 delivery attenuated
at 50% VO2max ; Qplateaus at 90% VO2max
Limitation in muscle BFmay be due to insufficient
Q at maximum exercise
During heat stress, fatigueoccurs at Tc of about 40oC.
Occurrence of fatigue isassociated with decreasedQ and SV
Decreased CVS functionsmediates fatigue duringexercise
Systemic
Peripheral
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CVS, Aging and Endurance Performance
Drop on CVS functions contribute todecrease in endurance performancewith age
Tanaka and Seals. J Physiol, 586.1: 55-63, 2008
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Regulates automatedphysiological processes for dailyfunctions and physicalperformances
Essential for regulation ofphysiological homeostasiswhich are important for survivaland physical exertion.
The ANS stimulates the targetorgans mainly throughneurotransmitters.
The ANS comprises theparasympathetic and thesympathetic nervous systems
Spinal cord
Lower brain
Higher brain
Autonomic
nervoussystem
Centralnervo
ussystem
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The Autonomic Nervous System
Parasympatheticnervous system
promotes restingstates and functionse.g., sleep and and
digestion.
Sympathetic nervous
system promotes thefight or flight response
e.g., aggression,motivation and drive
Increase:Arterial pressure
BF to active musclesMetabolic rateBlood glucose levels
GlycolysisMuscle strength
Mental drive
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Parasympatheticneurons
Sympatheticneurons
ACH ACH ACH NEpi
Cell of target organ
-receptors -receptors
Transmitters act on the cellmembrane by changing itspermeability to ions
ACH promotes the entry of Cl inheart muscles, which lowersresting potential
NEpi promotes the entry of Na+
and Ca2+ in the heart musclemembrane, which increases heart
rate.
Sympathetic NS stimulatessecretion of Epi and NEpi from the
adrenal medulla
NEpi is attracted to -receptors
Epi is attracted to both - and -receptors
Adrenergic receptors and functions
VasoconstrictionVasodilation 2Cardiac acceleration 1Increased myocardial contractility 1
Bronchodilation 2Glycogenolysis 2Lipolysis 1Intestinal relaxation
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How does exerciseaffect catecholamine
response?
No effect at low intensity unlessblood glucose level falls
Acute increase in catecholaminesat 50% - 60% VO2max
Training suppressescatecholamine responses inmoderate intensity exercise
Catecholamine concentrations are
higher in trained than untrained
individuals at high / maximalintensity exercise
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Catecholamines and Glucose Homeostasis during Exercise
Substrate availability is key togood endurance performance
Glucose paradox liverprefers lactate to ingestedglucose
60% of liver glycogen isconverted from lactate.
Ingested glucose is stored
primarily in muscles.
Muscle glycogenolysis is theprimary sources of metabolic
substrate in the first 60 min ofexercise
Epinephrine activates
adenylate cyclase that drivesmuscle glycogenolysis
Norepinephrine stimulatesliver glucose production
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Catecholamine andLipolysis during Exercise
Substrate crossover during exercise occurs atabout 50% to 70% VO2max.
Utilisation of FFA as substrate leads to glycogensparing, which is crucial for enduranceperformance
Epinephrine stimulates HSL during moderate
intensity exercise, leading to lipolysis
Epinephrine triggers lipolysis by activating 1receptors. Fat deposit sites with more
1receptors will be more responsive to fat lossfollowing a period of exercise
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Optimal exercise intensity for fatoxidation occurs between 55%and 70% VO2max and between
65% and 80% HRmax
Exercise programme targetingat inducing weight/fat lossshould be kept within theseintensity zones
A high VO2max
does notnecessarily correspond withmore efficient fat utilisation.
Peak fat utlisation occurs atVO2max of about 50 mL/kg/min
The shift towards more efficientfat utilisation occurs at > 60mL/kg/min of VO2max
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Autonomic Regulation of Blood Circulation during Exercise
Blood pressure is a function of blood volume andtotal peripheral resistance
Blood distribution is regulated primarily by pressuredifferential within the circulation
Sympathetic (heart and blood vessels) andparasympathetic (heart) tones are the basal statesof the physiology under ANS influence at rest.
During exercise blood is shunted from the visceralorgans (vasoconstriction) to the exercising muscles
(vasodilation) by controlling local blood pressure.
The shunting of blood increases delivery ofsubstrates and oxygen to, and the removal of heat,metabolic products and CO2 from the exercisingmuscle.
When core temperature rises to a threshold, SNSincreases blood flow to the skin for heat dissipationvia evaporation, convection and conduction.
Muscle competes for blood flow with the skin whenexercising in the heat.
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Physicalexertion
Muscular
heat
production
Convective
heat removal
via blood flow
Heat is
transported to
the skin surface.
Sweatproduction
Low RhEvaporationof sweat
Significantheatdissipation
High RhSweatdrippedoff
Minimumheatdissipation
Decreasedplasma volume
-ve fluidreplacement
MAP / CVP
VasoconstrictionCardiac output (SV)Muscle blood flowTemperatureHeart rate
-ve fluid intake
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Fluid in the circulation
(extracellular)
IntracellularIntercellular
Kidney Bladder
Excess Fluid
Able to defend up to 2% BW fluid deficit
Osmotic gradientHydrostatic gradient
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Heat Exhaust ion or CVS Failur e?
Heat Exhaustion
Brain
Heart
Muscle
Heartpumpsbloodsupply tomuscle
Musclepumpsbloodback tothe heart
=
Maintain blood
pressure & flow
Blood circulation
during exercise Heat stress
Sweat loss
Blood volume
Bloodpressure
Intense Exercise
M. FatigueBlood pooling
Peripheralresistance
and venousreturn
Force output
Collapsed
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Autonomic Regulation of Heart Rate during Exercise
Intensity
Start exercise Submaximal exercise Maximal exercise / recovery
PNS withdrawal
PNS SNS balance
Total PNS withdrawaldoes not occur evenat maximal exercise
Recovery HR:
PNS reactivated < 1 min post-exIncreased PNS until 4 minPNS remain constant for 10 minWithdrawal of SNS
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Autonomic Regulation of Heart Rate during Exercise
Before ETAfter ET
Intensity
Start exercise Submaximal exercise Maximal exercise / recovery
PNS withdrawal
PNS SNS balance
Total PNS withdrawaldoes not occur evenat maximal exercise
Lower RHR may bereversed after 8 wks
moderate intensitytraining
6 12 wks3 to 5 X/wk30 min 4h> 70% VO2max
> 85% HRR
ET may decreaseMHR by 5 13 bpm
post-training
Recovery HR:
PNS reactivated < 1 min post-exIncreased PNS until 4 minPNS remain constant for 10 minWithdrawal of SNS
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Autonomic Regulation of Heart Rate
ET reduced HR response
in normal combat attirebut not in protective suits
HA did not reduce HRresponse when working inprotective suits in hotconditions in both groups.
ET did not reduce HR
response in both normalcombat attire andprotective suit.
HA reduced HR responseof UT to that of the ETsubjects
Autonomic adaptation inHR regulation to exerciseand heat stress
Aoyagi et al, EJAP 68:234-245, 1994
8 weeks ET versus UT 6-day HA
Combat attirebefore ET/HA
Combat attireafter ET/HA
NBC attireafter ET / HA
NBC attirebefore ET / HA
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I nt egr at ion of Physiological Syst ems
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The CVS play the key role of
transportation / communication
between various physiologicalsystems. Such a role allows eachorgan / system to influence target
organs / cell located at different sitesin the body.
Changes in cardiac output could be a
key limiting factors in enduranceexercise performance, especiallyunder hot conditions.
Cardiac output changes are influencesby SV, EDV, blood volume, andvenous return.
The heart adapts to chronic exercise
by changing in size and contractility,which enhances its functions during
intense exercise.
The ANS regulates many of the
voluntary functions that supports our
survival and physical exertion
The ANS act on target organs directlythrough neurotransmitters i.e.acetylcholine and norepinephrine
Besides innervating the target organs
directly, the ANS also regulatesphysiological functions throughepinephrine and norepinephrine thatare secreted in the adrenal medulla.
Epinephrine and norpeinephrine
influence exercise performance by
regulating body temperature,glycogenolysis, lipolysis, sweating,
hepatic glucneogenesis, and theconversion of lactate to glucose in the
liver.