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Ventilatory and Cardiovascular Dynamics

» Brooks Chapts 13 and 16

Outline• Ventilation as limiting factor in aerobic performance

• Cardiovascular responses to exercise

• Limits of CV performance

• VO2 max criteria

• CV function and training

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Ventilation as a Limiting Factor in Aerobic Performance at Sea Level (Chapt 13)

• Ventilation not thought to limit aerobic performance at sea level. capacity to ventilation (35x) with exercise is greater than the

capacity to Cardiac Output (6x) considerable ventilatory reserve exists to oxygenate blood

passing through the lungs

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Ventilation Perfusion Ratio - VE/CO

• Linear in ventilation with in exercise intensity. As exercise intensity reaches maximal levels there can be a

non-linear increase in ventilation. Ventilation at rest ~ 5 L/min Maximal levels ~ 190 L/min (35x)

Linear in cardiac output with in exercise intensity. Cardiac Output at rest ~ 5 L/min Maximal levels ~ 30 L/min (6x)

Pulmonary minute ventilation (VE) to Cardiac Output is ~1 at rest and 5 - 6 fold during maximal exercise. One reason why pulmonary ventilation is not thought to limit

aerobic performance.

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• Ventilatory Equivalent VE/VO2

VO2 at rest 0.25 L/min, VE/VO2 = 20

VO2 max ~ 5 L/min, VE/VO2 = 35

the ability to ventilation is greater than the ability to expand oxidative metabolism

VEmax vs. MVV during exercise MVV- maximum voluntary ventilatory capacity the maximum VE during exercise is less than the MVV another reason why pulmonary ventilation is not thought to

limit aerobic performance

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PAO2(alveolar) and PaO2(arterial) O2 moves from areas of high conc to areas of low conc

during exercise maintain or PAO2 PaO2 in blood is also well maintained

• Alveolar surface area is massive (50m2). only 200ml of blood (4%) is in the pulmonary system during

maximal exercise

• Fatigue of ventilatory muscules. the diaphragm and ventilatory muscles can fatigue during MVV test fatigue at end of the test repeat trials - decreased performance fatigue yes - is it relevant -NO (ultra endurance) athletes post ex can raise VE to MVV

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Pulmonary Limits in Elite Athletes

• Fig 13-2: decline in PaO2 with maximal exercise in some elite athletes (individual variability) may be due to compliance in the ventilatory system may be due to economy (energy cost of breathing) athletes may learn to tolerate hypoxemia to energy cost of

breathing during maximal exercise

• Altitude– experienced climbers breathe more and maintain PaO2 when

climbing at altitude

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Cardiovascular Dynamics During Exercise

Brooks, Chapt 16

• O2 to the working muscles with exercise intensity

Principal Cardiovascular Responses to Exercise

• Increased cardiac output HR (60 to 200bpm) SV (80 to 200ml/beat) O2 and substrate delivery to muscle

remove CO2 and metabolites

skin blood flow regulate temperature

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blood flow to the kidneys– maintain blood volume

blood flow to viscera– reduced gastrointestinal activity

• vasoconstriction in the spleen blood volume

• maintain blood flow to the brain

blood flow to coronary arteries of the heart

blood flow to working skeletal muscle

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• Cardiovascular regulation is directed toward maintaining blood pressure.

• During exercise CV regulation balances the need for more blood to the active tissue with the need to maintain BP and blood flow to the brain and heart.

• Although maximum CO may limit O2 transport capacity, maximal exercise may be terminated by the threat of ischemia to the heart (Noakes).

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• Table 16-1: Cardiovascular changes with endurance training.

Rest Submax Ex Max Ex

HR NC

SV

CO NC NC O2up -

SBP NC

TPR NC NC

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• CV response depends on type and intensity of activity.

dynamic ex: large in HR, CO, SBP (not diastolic) volume load on the heart

strength ex: large in SBP and DBP, mod in HR, CO pressure load on the heart

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Oxygen Consumption

• Oxygen consumption is proportional to exercise intensity.

• Determinants: rate of O2 transport

O2 carrying capacity of blood

amount of O2 extracted

• VO2 = [HR x SV] x (a-v)O2•

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Heart Rate

• HR accounts for 75% of O2 uptake at maximal exercise (most important factor)

with intensity, levels off at VO2max (Fig 16-1)

• Range 70 - 210 bpm due to withdrawal of PNS and SNS stimulation intrinsic HR ~ 100 bpm

• Estimated max HR = 220 - age (+/- 12) influenced by anxiety, dehydration, temp, altitude, digestion,

genetics

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• HR response with strength exercise lower than endurance training with muscle mass used higher with upper body

intrathoracic pressure, smaller muscle mass less effective muscle pump - venous return

Cardiovascular drift during prolonged exercise HR gradually at the same work rate venous return ( blood volume)

Rate Pressure Produce - RPP HR X SBP rough index of coronary blood flow

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Stroke Volume

• SV has major impact on CO (2 x SV; 2 x CO).

• SV during exercise to 25 - 50% of max then levels off. Fig 16-2: SV from 75ml to 110ml/beat

• SV as exercise intensity toward max (variable).

• SV is perhaps the most important factor influencing individual differences in VO2max. max SV sedentary 90ml, athlete 180ml

• Supine exercise: SV does not increase - starts high EDV remains unchanged

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(a-v)O2 difference• Difference increases with exercise intensity

Fig 16-3 : rest 5.6 - max 16 (vol%)

always some oxygenated blood returning to the heart

non active tissue does not extract much O2

(a-v)O2 can approach 100% in maximally working muscle

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Blood Pressure BP must during exercise to maintain blood flow to the

heart, brain and working muscle (Fig 16-4).

• TPR with exercise to 1/3 resting (due to in CO).

SBP steadily during exercise (120 - 180mmHg).

MAP: 1/3 (systolic-diastolic) + diastolic

DBP is relatively constant

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Cardiovascular Triage

• CT: protective mechanisms that prevent coronary and CNS ischemia and maintain central blood volume.

• During exercise these mechanisms limit blood flow to muscles when the the body cannot meet the needs of the heart and CNS

• With exercise blood is redistributed from inactive to active tissue brain and heart spared vasoconstriction SNS stimulation steadily with exercise intensity

At altitude the circulatory system appears to protect the heart by blood flow to the muscles and reduce the work of the heart (Fig 16-5).

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• Skin blood flow during submaximal exercise but to resting values during maximal exercise.

• Coronary blood flow during exercise from 260 -900 ml/min flow occurs mainly during diastole coronary artery disease may restrict blood flow and cause

ischemia a good warm up facilitates an in coronary circulation

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Limits of CV Performance

• VO2 max has long been considered the best measure of CV capacity and aerobic performance (Fig 16-6).

• VO2max = [HRmax x SVmax] x (a-v)O2max

• VO2max is the point at which O2 consumption fails to

rise, despite an power output or intensity. VO2PEAK

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VO2max Anaerobic Hypothesis

• After reaching VO2max exercise intensity is by anaerobic metabolism. max CO and anaerobic metabolism will limit VO2 max best predictor of performance in endurance sports

• Tim Noakes - South Africa re-analyzed data from classic studies found that most subjects did not plateau

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Inconsistencies with Anaerobic hypothesis

• Blood transfusion and O2 breathing have been shown to performance. was it a CO limitation?

• Blood doping studies VO2max improved for longer time period than performance

measures

• There is a discrepancy between VO2max and running performance in elite athletes.

• At altitude CO indicative of protective mechanism

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• Lower VO2max for cycling compared with running.

• Running performance can improve without an in VO2max.

VO2max through running does not improve swimming.

• Local muscle factors often appear to be more closely related to fatigue than a limitation in CO.

• CO is dependant upon and determined by coronary blood flow. Max CO implies cardiac fatigue, coronary ischemia and

angina pectoris?

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Protection of Heart and Muscle During Exercise

• Noakes (1998) alternative to anaerobic hypothesis.

• CV regulation and muscle recruitment are regulated by neural and chemical control mechanisms prevent damage to heart, CNS and muscle by regulating force and power output and controlling tissue

blood flow

• Research by Noakes suggests that peak treadmill velocity is a good predictor of aerobic performance. high cross bridge cycling and respiratory adaptations biochemical factors such as mito volume and O2 enzyme

capacity are also good predictors of endurance capacity

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Practical Basis of the Noakes Hypothesis• Primary regulatory mechanism of the CV and

neuromuscular systems facilitate intense exercise until it perceives risk of ischemic injury to the heart, CNS and muscles.

• Fitness should be improved by: muscle power output capacity substrate utilization thermoregulatory capacity reduce work of breathing

• The CV system develops at the same time that other adaptations occur from training.

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Criteria for Measuring VO2max

• Exercise must use at least 50% of the total muscle mass (do not use upper body exercise).

• The exercise must be continuous and rhythmical and done for at least 10 minutes.

• The test should try to eliminate motivation and skill.

• The subject must reach maximum capacity.

• The measurement must be made in a controlled environment.

• VO2max on a bicycle is usually 10 to 15% less than running on a treadmill.

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VO2 max and Performance

• For the general population VO2max will predict performance in an endurance event.

• For elite athletes VO2max is a poor predictor of performance in an endurance event. male 69, female 73 ml/kg/min: male 15 min faster

• Other performance factors: speed ability to continue at high % of capacity lactate clearance capacity performance economy

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Cardiovascular Adaptations with Endurance Training

Rest Submax Ex Max ExHR NCSV

(a-v)O2 NC CO NC NC VO2 - - SBP NCCorBF BloodVol HeartVol

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Changes in CV Parameters with Training

• Heart ability to pump blood by SV ( EDV).

• Small in ventricular mass (volume load) with endurance training.

• Strength training produces a pressure load that will LV mass.

• Adaptation to endurance training is sport specific.

• Interval training– acts as an overload

– improve speed and CV functioning

– combine with endurance training

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CV Adaptations

• Improvements in VO2max depend on prior fitness, type of training, age. can VO2max by ~20%

• Endurance performance can by much more than 20% by improving mitochondrial density, speed, running economy, and body composition.

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Heart Rate

• Endurance training resting and submax HR by increasing PNS activity to the SA node. may intrinsic HR athlete 40bpm may be a genetic influence resting HR may be due to disease (sick sinus syndrome)

• Max HR may ~3 bpm with training.

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Stroke Volume

• Endurance training can resting and submax SV by 20%.

SV due to in heart volume and contractility.

HR will SV HR allows for filling time (Frank-Starling)

LV compliance allows ventricle to stretch more.

contractility due to in release and transport of Ca from SR.

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(a-v)O2 difference

• (a-v)O2 slightly with training difference right shift of OxyHb dissociation curve mitochondrial adaptation Hb and myoglobin conc muscle capillary density

capillarization around muscle fibres is thought to facilitate diffusion during exercise.

Blood Pressure• Endurance training resting and submax SBP, DBP

and MAP (no change during max ex).

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Blood Flow

• With endurance training coronary blood flow slightly at rest and during submax exercise. SV and HR reduce myocardial O2 consumption

coronary blood flow at max ex with training • supports higher metabolic requirements with CO

• Skeletal muscle vascularity with endurance training. peripheral resistance

• The trained muscle has an O2 extraction capacity.

• There is no change in skin blood flow with training.