Transcript Blood flow

Ventilation and Cardiovascular Dynamics
Brooks Ch 13 and 16
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Outline
• Is Ventilation a limiting factor in
aerobic performance?
• Cardiovascular responses to exercise
• Limits of CV performance
– Anaerobic hypothesis
– Noakes protection hypothesis
• CV function and training
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Ventilation as a limiting Factor to performance
• Ventilation does not limit sea level aerobic performance
– capacity to inc ventilation is greater than that to inc Q
• Ventilation perfusion Ratio - VE/Q
– Fig 12-15 - linear increase in vent with intensity to vent threshold then non linear
– VE rest 5 L/min -exercise 190 L/min
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Ventilation as a limiting Factor to performance
• Fig 13-2
• Q rest 5L/min - ex 25 L/min
• VO2/Q ratio ~ .2 at rest and max
– VE/Q ratio
• ~1 at rest - inc 5-6 fold to max exercise
– Capacity to inc VE much greater
• Ventilatory Equivalent VE/VO2
– rest 20 (5/.25) ; max 35(190/5)
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VE max vs. MVV
• MVV - max
voluntary ventilatory
capacity
• 1.max VE often
less than MVV
• 2.PAO2(alveolar)
and PaO2
(arterial)
– Fig 11-4 , 12-12
– maintain PAO2 or rises
– PaO2 also well
maintained
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VE max vs. MVV
• 3. Alveolar surface area - is very large
• 4. Fatigue of Vent musculature
– MVV tests - reduce rate at end of test
– repeat trials - shows decreased performance
– Yes, fatigue is possible in these muscles - is it relevant NO
– VE does not reach MVV during exercise, so fatigue less
likely
– Further, athletes post ex can raise VE to MVV, illustrating
reserve capacity for ventilation
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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 vent response blunted, even with
dec 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 diffusion due to very high Q ?
• Altitude
– experienced climbers - breathe more - maintain
Pa O2 when climbing
– Elite - may be more susceptible to impairments at
altitude
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CV Responses to Exercise
• Increase flow to active areas
• decrease flow to less critical areas
• Principle responses
– Inc Q - HR, SV
– Inc Skin blood flow
– dec flow to viscera and liver
– vasoconstriction in spleen
– maintain brain blood flow
– inc coronary blood flow
– inc muscle blood flow
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CV Responses to Exercise
• Table 16-1 - Rest vs acute exercise
• CV response - depends on type and intensity of
activity
– dynamic - inc systolic BP; not Diastolic
• Volume load
– strength - in systolic and diastolic
• Pressure load
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Cardiovascular System
Rest vs Maximal Exercise
Table 16.1
(untrained vs trained)
Rest
UT
T
HR(bpm)
70
63
SV(ml/beat)
72
80
(a-v)O2(vol%) 5.6
5.6
Q(L/min)
5
5
VO2 ml/kg/min 3.7
3.7
SBP(mmHg)
120
114
Vent(L/min)
10.2
10.3
Ms BF(A)ml/min 600
555
CorBFml/min 260
250
Max Ex
UT
185
90
16.2
16.6
35.8
200
129
13760
900
T
182
105
16.5
19.1
42
200
145
16220
940
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Oxygen Consumption
• Cardiovascular Determinants
– rate of O2 transport
– amount of O2 extracted
– O2 carrying capacity of blood
• VO2 = Q * (a-v)O2
• Exercise of increasing intensity
• Fig 16-2,3,4
– Q and (a-v)O2 increases equally important at low
intensities
– high intensity HR more important
– (a-v)O2 - depends on capacity of mito to use O2 - rate of
diffusion-blood flow
• O2 carrying capacity - influenced by Hb content 13
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Heart Rate
• Most important factor in responding to acute demand
• inc with intensity due to Sympathetic stimulation and
withdrawal of Parasympathetic
– estimated Max HR 220-age (+/- 12)
– influenced by anxiety, dehydration, temperature, altitude,
digestion
• 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 - heart rate increases steadily
during prolonged exercise due to decreased stroke
volume
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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
– Is lower in strength training
• Inc with ms mass used
• Inc with percentage of MVC (maximum voluntary contraction)
• estimate the workload on heart , myocardial oxygen
consumption, with
• Rate Pressure Produce - RPP
– HR X Systolic BP
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Stroke volume
• Stroke Volume - volume of blood per heart beat
– Rest - 70 - 80 ml
– Max - 80-175 ml
• Fig 16-2 - increases with intensity to ~ 25-50% max
- levels off
– inc EDV (end diastolic volume)
– high HR may dec ventricular filling
– athletes high Co due to high SV
• supine exercise – SV does not increase - starts high
• SV has major impact on Q when comparing athletes
with sedentary
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– ~ same max HR - double the SV and Q for athletes
(a-v)O2 difference
• Difference between arterial and venous oxygen content
across a capillary bed
– (ml O2/dl blood -units of %volume also used)
• Difference increases with intensity
– fig 16-4 - rest 5.6 - max 16 (vol %)
– always some oxygenated blood returning to heart - non
active tissue
– (a-v)O2 can approach 100% in maximally working muscle
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Blood Pressure
• Blood Pressure fig 16-5
–
–
–
–
–
BP = Q * peripheral resistance (TPR)
dec TPR with exercise to 1/3 resting
Q rises from 5 to 25 L/min
systolic BP goes up steadily
MAP - mean arterial pressure
• 1/3 (systolic-diastolic) + diastolic
– diastolic relatively constant
• Rise over 110 mmHg - associated with CAD
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Cardiovascular Triage
• With exercise - blood is redistributed from inactive to active
tissue beds - priority for brain and heart maintained
– sympathetic stimulation increases with intensity
– Causes general vasoconstriction
– brain and heart spared vasoconstriction
– Active hyperemia directs blood to working muscle adenosine, NO - vasodilators
• maintenance of BP priority
– Near maximum, working ms vasculature can be constricted
– protective mechanism to maintain flow to heart and CNS
– May limit exercise intensity so max Q can be achieved
without resorting to anaerobic metabolism in the heart
• Eg - easier breathing - inc flow to ms
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– harder breathing - dec flow to ms
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Cardiovascular Triage
• Eg. Altitude study fig 16-6 - observe a reduction in maximum
HR and Q with altitude even though we know a higher value is
possible - illustrates protection is in effect
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Coronary blood flow
• Large capacity for increase
– (260-900ml/min)
– due to metabolic regulation
– flow occurs mainly during diastole
• warm up - facilitates inc in coronary
circulation
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CV Performance Limitation
• VO2max - long thought to be best measure of CV
capacity and endurance performance
– Fig 16-7
– VO2 max - maximum capacity for aerobic ATP synthesis
– Endurance performance - ability to perform in endurance
events
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CV Performance Limitation
• 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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VO2 max and Performance
• General population - VO2 max will predict endurance
performance - due to large range in values
• elite - ability of VO2 to predict performance is not as
accurate - all have values in 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
• other factors in addition to VO2 max that impact
performance
–
–
–
–
Sustained speed
ability to continue at high % of capacity
lactate clearance capacity
performance economy
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Capacity vs Performance
• Local muscle factors more closely related to
fatigue than Q limitation
– Table 6-3 correlations between ox capacity, VO2 and
endurance
• Lower VO2 max for cycling compared to running
• Running performance can improve without an
inc in VO2 max
• Inc VO2 max through running does not improve
swimming performance
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What limits VO2 max ?
• Traditional Anaerobic hypothesis for VO2max
– After max point - anaerobic metabolism is needed to continue
exercise - plateau
– max Q and anaerobic metabolism will limit VO2 max
– this determines fitness and performance
• Tim Noakes,Phd - South Africa
– re-analyzed data creating Alternate hypothesis for
VO2max
– most subjects did not show plateau bringing anaerobic
hypothesis into question
– Says Q not a limitation
– Rather - neural and endocrine control factors reduce
output before damage occurs in heart
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– Still very controversial - not accepted by most scholars
Inconsistencies in Anaerobic hypothesis
• Q dependant upon and determined by coronary blood flow
– Max Q implies cardiac fatigue - ischemia -? Angina
pectoris?
– this does not occur in most subjects
• Blood transfusion and O2 breathing
– inc performance - many says this indicates Q limitation
– But still no plateau
– was it a Q limitation?
• Blood doping studies
– VO2 max improved for longer time period than
performance measures (eg 10 km time trial)
• altitude - observe decrease in Q
– Yet we know it has greater capacity
– This is indicative of a protective mechanism
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Protection Hypothesis
• 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
• Noakes research suggests peak treadmill velocity
as a good predictor of aerobic performance
– high cross bridge cycling and respiratory adaptations
– Biochemical factors - mito volume, ox enzyme capacity
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are also good predictors of performance
Practical Aspects of Noakes Hypothesis
• Primary regulatory mechanisms of Cardio Resp 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 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
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Changes in CV with Training
• Tables 16-1,2 - training impacts
• Heart - inc ability to pump blood-SV - inc end diastolic
volume-EDV
• Endurance training
– small inc in ventricular mass
– triggered by volume load
• resistance training
– pressure load - larger inc in heart mass
• adaptation is specific to form
– swimming improves swimming
• Interval training - repeated short to medium duration bouts
– improve speed and CV functioning
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– combine with over-distance training
Cardiovascular Adaptations with
Endurance Training
Table 16.2
Rest Submax Ex
(absolute)
HR


SV


(a-v)O2
0

Q
0
0
VO2
0
0
SBP
0
0
CorBFlow


Ms Bflow(A)
0
0
BloodVol

HeartVol

Max Ex
0




0


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• 0 = no change
CV Adaptations
• O2 consumption
• improvements depend on
– prior fitness, type of training, age
– can inc VO2 max ~20%
– Performance can improve > than 20%
• Heart Rate
– training-dec resting and submax HR
– inc Psymp tone to SA node
• Max HR-dec ~3 bpm with training
– progressive overload for continued adaptation
• Stroke volume - 20% inc - rest, sub and max with training
– slower heart rate - inc filling time
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– inc volume - inc contractility - SV
CV Adaptations
• Stroke volume - cont.
– EDV inc with training - due to inc left vent vol and
compliance, inc blood vol,
– Myocardial contractility increased
• Better release and reuptake of calcium at Sarcoplasmic Reticulum
• Shift in isoform of myosin ATPase
– increased ejection fraction
• (a-v)O2 difference
–
–
–
–
–
inc slightly with training due to ;
right shift of Hb saturation curve
mitochondrial adaptation
Hb and Mb [ ]
muscle capillary density
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CV Adaptations
• Blood pressure - decreased resting and submax BP
• Blood flow
– training - dec coronary blood flow rest and submax
(slight)
• inc SV and dec HR - dec O2 demand
– inc coronary flow at max
– no inc in myocardial vascularity
• inc in muscle vascularity – dec peripheral resistance - inc Q
– dec muscle blood flow at sub max
– inc extraction - more blood for skin...
– 10 % inc in muscle flow at max
• no change in skin blood flow - though adaptation to exercise
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in heat does occur