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Ventilation and Cardiovascular Dynamics
Brooks
Ch 13
Ch 14 - 299-308
Ch 15 - 315-316,325-326,329-330
Ch 16
1
Outline
• 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
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3
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
UT
UT
HR(bpm)
70
185
SV(ml/beat)
72
90
(a-v)O2(vol%) 5.6
16.2
Q(L/min)
5
16.6
VO2 ml/kg/min 3.5
35.8
SBP(mmHg)
120
200
Vent(L/min)
10.2
129
Ms BF(A)ml/min 600
13760
CorBFml/min 260
900
Rest Max Ex
T
T
63
182
80
105
5.6
16.5
5
19.1
3.5
42
114
200
10.3 145
555
16220
250
940
Rest Max Ex
E
E
45
182
136
184
5
3.5
35
80
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Oxygen Consumption
• 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
6
Heart Rate
• 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
7
Heart Rate
• 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
8
Stroke volume
• 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
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10
11
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(a-v)O2 difference
• 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 %
13
Blood Pressure
• 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
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Circulation and its Control
• 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
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Circulation and its Control
• 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
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Circulation and its control
• 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
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Cardiovascular Triage
• 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
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Cardiovascular Triage
• 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
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Coronary blood flow
• 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
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VO2max
• 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
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VO2 max
• 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
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What limits VO2 max ?
• 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
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Inconsistencies in Anaerobic hypothesis
• 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
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Practical Aspects of Noakes Hypothesis
• 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
30
VO2 max versus Endurance Performance
• 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
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VO2 max versus Endurance Performance
• 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
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VO2 max versus Endurance Performance
• 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
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VO2 max versus Endurance Performance
• 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
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Is Ventilation a limiting Factor?
• 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
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exercise
Is Ventilation a limiting Factor?
• 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
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Ventilation as a limiting Factor to performance?
• 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)
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Ventilation as a limiting Factor to performance?
• 3,4,5.
PAO2(alveolar)
and PaO2
(arterial)
– Fig 11-4
– PAO2 - rises
– PaO2 well
maintained
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Ventilation as a limiting Factor?
• 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
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Elite Athletes
• Fig 13-3 - observe decline in PaO2 with
maximal exercise in some elite athletes
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Elite Athletes
• 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 ?
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Cardiovascular Adaptations with
Endurance Training
Table 16.2
Rest Submax Ex
(absolute)
VO2
0
0
Q
0
0
HR


SV


(a-v)O2
0

SBP
0
0
CorBFlow


Ms Bflow(A)
0
0
BloodVol

HeartVol

Max Ex


0


0


43
• 0 = no change
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CV Adaptations
• 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
45
CV Adaptations
• 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
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CV Adaptations
• (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
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CV Adaptations
• 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
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CV Adaptations
• 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
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CV Adaptations
• 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
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