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Ventilation and Cardiovascular Dynamics

Brooks Ch 13 Ch 14 - 299-308Ch 15 - 315-316,325-326,329-330Ch 16

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• Cardio-Respiratory responses to exercise• VO2max

– Anaerobic hypothesis– Noakes protection hypothesis

• Limits of Cardio-Respiratory performance• Is Ventilation a limiting factor in VO2max or

aerobic performance?• Cardio-respiratory adaptations to training

Outline

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Cardio-Respiratory Responses to Exercise

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Cardio-Respiratory System Rest vs Maximal Exercise

Table 16.1 (Untrained vs Trained vs Elite athletes) Rest Max Ex Rest Max Ex Rest Max Ex

UT UT T T E EHR(bpm) 70 185 63 182 45 182SV(ml/beat) 72 90 80 105 136 184

(a-v)O2(vol%) 5.6 16.2 5.6 16.5Q(L/min) 5 16.6 5 19.1 5 35

VO2 ml/kg/min 3.5 35.8 3.5 42 3.5 80SBP(mmHg) 120 200 114 200Vent(L/min) 10.2 129 10.3 145Ms BF(A)ml/min 600 13760 555 16220CorBFml/min 260 900 250 940

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• With exercise of increasing intensity, there is a linear increase in O2 consumption

• VO2 = Q * (a-v)O2 (Fick Equation)

• Cardiovascular response determined by

– rate of O2 transport (Q)

– amount of O2 extracted (a-v)O2

• Fig 16-2,3,4– O2 carrying capacity of blood (Hb content of blood)

– Changes in Q and (a-v)O2 important when moving from low to moderate intensities

– changes in HR become more important when moving from moderate to high intensity

Oxygen Consumption

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• important factor in responding to acute demand• HR inc with increasing intensity is due to;

– Sympathetic stimulation (fig 9-11) and Parasympathetic withdrawal– Mechanical (stretch) and chemical (metabolites) feedback to CV control

center– HR response influenced by anxiety, dehydration, temperature, altitude,

digestion– estimated Max HR 220 - age (+/- 12)

• Steady state - leveling off of heart rate to match oxygen requirement of exercise (+/- 5bpm)– Takes longer as intensity of exercise increases, may not occur at very

high intensities

• Cardiovascular drift - HR may increase with prolonged exercise at steady state– may be due to inc skin blood flow with temp– may be due to decreased stroke volume with dehydration or breakdown

of sympathetic blood flow control

Heart Rate

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• HR response :– Is higher with upper body - at same power requirement

• Due to : smaller muscle mass, increased intra-thoracic pressure, less effective muscle pump, feedback to control center

– Is less significant during strength training• Inc with ms mass used• Inc with percentage of MVC (maximum voluntary contraction)

• Rate Pressure Produce - RPP– HR X Systolic BP– Good estimate of the workload of the heart , myocardial oxygen

consumption, with

Heart Rate

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• Stroke Volume - volume of blood per heart beat– Rest - 70 - 80 ml ; Max - 80-175 ml

• Fig 16-3 - SV increases with intensity to ~ 25-50% VO2max - then plateaus

• Fig 14.7 - Factors affecting SV during exercise– Pre load - end diastolic pressure (volume)

• Affected by changes in Q, posture, venous tone, blood volume, atria, muscle pump, intrathoracic pressure.

• Frank Starling Mechanism (fig 14.8)

– After load - resistance to ventricular emptying– Contractility - inc by sympathetic stimulation (fig 14-10)

• SV biggest difference when comparing elite athletes and sedentary population ~ same max HR - double the SV and Q

Stroke volume

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• Difference between arterial and venous oxygen content across a capillary bed – (ml O2/dl blood -units of %volume also used) (dl = 100ml)

• (a-v)O2 difference - depends on – capacity of mitochondria to use O2 – rate of diffusion – blood flow (capillarization)

• (a-v)O2 difference increases with intensity– fig 16-4 - rest 5.6 - max 16 (vol %) (ml/100ml)– always some oxygenated blood returning to heart - non active tissue– (a-v) O2 can approach 100% extraction of in maximally working muscle

• 20 vol %

(a-v)O2 difference

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• Blood Pressure fig 16-5– BP = Q * total peripheral resistance (TPR)– dec TPR with exercise to 1/3 resting cue to vasodilation in active

tissues– Q rises from 5 to 25 L/min– systolic BP goes up steadily with intensity– MAP - mean arterial pressure

• 1/3 (systolic-diastolic) + diastolic

– diastolic relatively constant• Rise of diastolic over 110 mmHg - associated with CAD

Blood Pressure

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• With exercise - blood is redistributed from inactive to active tissue beds

• the priority for brain and heart circulation are maintained

• Skeletal muscle blood flow is influenced by balance between metabolic factors and the maintenance of blood pressure

• Fig 17.3 a,b Exercise Physiology , McCardle, Katch and Katch

Circulation and its Control

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• Metabolic (local) control is critical in increasing O2 delivery to working muscle– sympathetic stimulation increases with intensity

• Causes general vasoconstriction in the whole body• brain and heart are spared vasoconstriction

– Active (exercise) hyperemia - directs blood to working muscle - flow is regulated at terminal arterioles and large arteries

– vasodilators decrease resistance to flow into active tissue beds• adenosine, low O2, low pH, high CO2, Nitric Oxide(NO), K+, Ach, • Figs 9.3 and 9.4 (Advanced cv ex physiology - 2011- Human Kinetics)

– Increases capillary perfusion– Increases flow in feed arteries through conducted vasodilation

• Vasodilation in distal vessels spreads proximally through cell to cell communication between endothelial cells and smooth ms cells

Circulation and its Control

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• maintenance of BP priority “cardiovascular triage”– Near maximum exercise intensities, the working muscle

vasculature can be constricted– This protective mechanism maintains blood pressure and

blood flow to the heart and CNS– This may limit exercise intensity so max Q can be achieved

without resorting to anaerobic metabolism in the heart

• Experimental Eg - changing the work of breathing alters blood flow to active muscle

Circulation and its control

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• Experimental Eg. Altitude study fig 16-6 - observe a reduction in maximum HR and Q with altitude – illustrates protection is in effect as we know a higher value is possible

Cardiovascular Triage

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• Experimental Eg - – one leg exercise - muscle blood flow is high– two leg exercise - muscle blood flow is lower– to maintain BP, vasoconstriction overrides the local chemical signals in the active muscle for vasodilation

Cardiovascular Triage

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• Large capacity for increase – (260-900ml/min)– due to metabolic regulation– flow occurs mainly during diastole– Increase is proportional to Q

• warm up - facilitates increase in coronary circulation

Coronary blood flow

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• Maximal rate at which individual can consume oxygen - ml/kg/min or L/min

• long thought to be best measure of CV capacity and endurance performance– Fig 16-7

VO2max

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• Criteria for identifying if actual VO2 max has been reached– Exercise uses minimum 50% of ms mass– Results are independent of motivation or skill– Assessed under standard conditions– Perceived exhaustion (RPE)– R of at least 1.1– Blood lactate of 8mM (rest ~.5mM)– Peak HR near predicted max

VO2 max

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• Traditional Anaerobic hypothesis for VO2max– After max point - anaerobic metabolism is needed to continue

exercise - we observe a plateau (fig 16-7)

– max Q and anaerobic metabolism will limit VO2 max

– this determines fitness and performance

• Tim Noakes,Phd - South Africa (1998)– Protection hypothesis for VO2max

– CV regulation and muscle recruitment are regulated by neural and chemical control mechanisms

– prevents damage to heart, CNS and skeletal muscle– regulates force and power output and controls blood flow– Still very controversial - not accepted by many scholars

What limits VO2 max ?

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• Q dependant upon and determined by coronary blood flow– Max Q implies cardiac fatigue - ischemia -? Angina

pectoris? - pain does not occur in healthy subjects• Blood transfusion and O2 breathing

– inc performance - many says this indicates Q limitation– But still no plateau, was it actually a Q limitation?

• DCA improves VO2max without changing muscle oxygenation– Stimulates pyruvate dehydrogenase

• altitude - observe decrease in Q (fig 16-6)– This is indicative of a protective mechanism

• Discrepancies between performance and VO2 max– Elite athletes, changes with training, blood doping

Inconsistencies in Anaerobic hypothesis

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• regulatory mechanisms of Cardio Respiratory and Neuromuscular systems facilitate intense exercise– until it perceives risk of ischemic injury– Then prevents muscle from over working and potentially

damaging these tissues

• Therefore, improve fitness / performance by;– muscle power output capacity– substrate utilization– thermoregulatory capacity– reducing work of breathing

• These changes will reduce load on heart – And allow more intense exercise before protection is instigated

• CV system will also develop with training

Practical Aspects of Noakes Hypothesis

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• Endurance performance - ability to perform in endurance events (10km, marathon, triathlon)

• General population - VO2 max will predict endurance performance - due to large range in values

• elite - ability of VO2max to predict performance is poor– athletes all have values of 65-70 + ml/kg/min– world record holders for marathon– male 69 ml/kg/min female 73 ml/kg/min - VO2 max– male ~15 min faster with similar VO2max

• Observe separation of concepts of VO2max / performance– Lower VO2 max recorded for cycling compared to running– Running performance can improve without an increase in VO2 max– Inc VO2 max through running does not improve swimming

performance

VO2 max versus Endurance Performance

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• other factors that impact endurance performance– Maximal sustained speed (peak treadmill velocity)– ability to continue at high % of maximal capacity– lactate clearance capacity– performance economy– Thermoregulatory capacity– high cross bridge cycling rate– muscle respiratory adaptations

• mitochondrial volume, oxidative enzyme capacity

VO2 max versus Endurance Performance

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• Relationship between Max O2 consumption and upper limit for aerobic metabolism is important

1. VO2 max limited by O2 transport

• Q and Arterial content of O2

• ? or protection theory

2. Endurance performance limited by Respiratory capacity of muscle (mitochondria and enzyme content)

• Evidence• Fig 33-10 restoration of dietary iron

– hematocrit and VO2 max responded rapidly and in parallel– muscle mitochondria and running endurance - improved more slowly, and in

parallel

VO2 max versus Endurance Performance

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• Table 6.3 - Correlation matrix – VO2 and Endurance Capacity .74– Muscle Respiratory capacity and Running endurance.92– Training results in 100% increase in muscle mitochondria and 100 %

inc in running endurance– Only 15% increase in VO2 max– VO2 changes more persistent with detraining than respiratory

capacity of muscle– Again illustrating independence of VO2 max and endurance

VO2 max versus Endurance Performance

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• Ventilation (VE) does not limit sea level VO2max or aerobic performance in healthy subjects

• There is sufficient ventilatory reserve to oxygenate blood passing through the lungs

• The following evidence comes from investigating the rate limiting factor in the processes of oxygen utilization

• 1. Capacity to increase ventilation is greater than the capacity to increase Q or oxygen consumption

• 2. Alveolar surface area is extremely large compared to pulmonary blood volume.

• 3. Alveolar partial pressure of O2 (PAO2) increases during exercise

• 4. arterial partial pressure of O2 (PaO2) is maintained• 5. Alveolar - arterial O2 gradient widens during max effort• 6. Ventilatory capacity may not even be reached during max

exercise

Is Ventilation a limiting Factor?

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• 1. Capacity to increase ventilation is greater than the capacity to increase Q or oxygen consumption

• Fig 13-2 VO2/Q• Q rest 5L/min - ex 25 L/min• VO2/Q ratio ~ .2 at rest and max

– Oxygen use and circulation increase proportionally with exercise

• Ventilation perfusion Ratio - VE/Q– VE rest 5 L/min - exercise 190 L/min– VE/Q ratio

• ~1 at rest - inc 5-6 fold to max exercise

– Capacity to inc VE much greater than capacity to increase Q

Is Ventilation a limiting Factor?

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• Ventilatory Equivalent VE/VO2

– Fig 12-15 - linear increase in vent with intensity to ventilatory threshold - then non linear

• VE rest 5 L/min - exercise 190 L/min• VO2 .25 L/min - exercise 5 L/min

– VE/ VO2 : rest 20 (5/.25) ; max 35(190/5)

Ventilation as a limiting Factor to performance?

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• 3,4,5. PAO2(alveolar) and PaO2 (arterial)– Fig 11-4 – PAO2 - rises– PaO2 well

maintained

Ventilation as a limiting Factor to performance?

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• 6. Capacity of Ventilation• MVV - maximum voluntary ventilatory capacity

– VE at VO2max often less than MVV

– athletes post exhaustive exercise can still raise VE to MVV, illustrating reserve capacity for ventilation

• MVV tests – With repeat trials - performance decreases

• while fatigue is possible in these muscles, it may not be relevant

– If VE does not reach MVV during exercise, fatigue and rate limitation is less likely

Ventilation as a limiting Factor?

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• Fig 13-3 - observe decline in PaO2 with maximal exercise in some elite athletes

Elite Athletes

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• may see ventilatory response blunted, even with decrease in PaO2

– may be due to economy – extremely high pulmonary flow, inc cost of

breathing, any extra O2 used to maintain this cost

– ? Rise in PAO2 - was pulmonary vent a limitation, or is it a diffusion limitation due to very high Q ?

Elite Athletes

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Cardiovascular Adaptations with Endurance Training

Table 16.2

Rest Submax Ex Max Ex (absolute)

VO2 0 0 Q 0 0 HR 0SV (a-v)O2 0 SBP 0 0 0CorBFlow Ms Bflow(A) 0 0 BloodVol HeartVol

• 0 = no change

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• O2 consumption • improvements depend on

– prior fitness, type of training, age– can inc VO2 max ~20%– Performance can improve much more than 20%– Impacts are sport specific

• Cardiac Output (Q)– Same for a given absolute submaximal workrate

(VO2), – Q increases dramatically at maximal exercise due

to increased stroke volume

CV Adaptations

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• Heart Rate– training-decreases resting and submax HR– Increased Psympathetic (vagal) tone to SA node

• Observed after 4 weeks of brisk walking• faster recovery of resting HR evidence of improved PS tone

– Max HR may decrease ~3 bpm with training (not significant)

• Stroke volume - 20% increase -at rest, sub and maximal after training

– End Diastolic Volume increases with training - • inc blood volume (20-25%) - increases venous return• slower heart rate - increases filling time• inc left vent volume and compliance

– Myocardial contractility increases• Better release and reuptake of calcium at Sarcoplasmic Reticulum• Shift in isoform of myosin ATPase to V1• Improves Q by about 15 to 20%

– increased ejection fraction

CV Adaptations

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• (a-v)O2 difference

– inc slightly with training due to ;– right shift of Hb saturation curve– mitochondrial adaptation– Hemoglobin mass increases 25%– muscle capillary density

CV Adaptations

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• Heart • Endurance training (increased pre load)

– small inc in ventricular mass - sarcomeres added in series

– triggered by volume load

• resistance training (increased after load)– pressure load - larger inc in heart mass – Sarcomeres added in parallel- increased relative

wall thickness

CV Adaptations

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• Blood pressure -

• Fig 10.2 Advanced CV Ex Phys (2011)– decreased resting and submax Systolic BP– Increase in maximal systolic pressure– Slight decrease in Diastolic BP

CV Adaptations

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• Blood flow– training - dec coronary blood flow rest and submax (slight)

• inc SV and dec HR dn BP - decreases O2 demand

– inc coronary flow at max – Changes in myocardial vascularity depend on study

• Muscle Blood Flow – Selective increase in perfusion of high oxidative fibers– dec vascular resistance - improved release of vasodilators

• Inc eNOS expression and activation– Inc Nitric Oxide production in endothelial cells

– Larger arterial diameter in trained limbs– Angiogensis - capillary growth– 10 % inc in muscle blood flow at max

CV Adaptations