lsm3212_lecture 12 ans-cvs

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.

lsm3212_lecture 12 ans-cvs

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