Ventilation and Cardiovascular Dynamics
Brooks Ch 13 and 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
2
3
Cardio-Respiratory Responses to Exercise
• Increase Respiratory Rate and Depth
• Increase blood flow to active areas
• decrease blood flow to less critical areas
• Principle CV responses
–
–
–
–
–
–
–
Inc Cardiac Output - 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
4
Cardio-Respiratory 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
5
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
6
Ventilatory Response
• Fig 12-15 - linear increase in ventilation with intensity
to about 50-65% VO2 max - then non linear
• With training, ventilatory inflection point shifts to right
(delay)
7
Oxygen Consumption
• 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 mitochondria to use O2 rate of diffusion - blood flow
• O2 carrying capacity - influenced by Hb content
8
9
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
10
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
11
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 have high Q due to high SV
• supine exercise – SV does not increase - starts high
• SV has major impact on Q when comparing athletes
with sedentary
12
– ~ 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) (dl = 100ml)
• 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 * 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 of diastolic over 110 mmHg - associated with CAD
14
15
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 are spared vasoconstriction
– Active hyperemia - directs blood to working muscle
- adenosine, Nitric oxide - vasodilators
16
17
18
Cardiovascular Triage
• 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 working ms
– harder breathing - dec flow to working ms
• 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
19
20
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
21
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
22
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
23
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
24
What limits VO2 max ?
• Traditional Anaerobic hypothesis for VO2max
– After max point - anaerobic metabolism is needed to continue
exercise - 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
– prevent damage to heart, CNS and muscle
– regulate force and power output and controlling tissue
blood flow
– Still very controversial - not accepted by most scholars
25
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?
• altitude - observe decrease in Q (fig 16-6)
– Yet we know it has greater capacity
– This is indicative of a protective mechanism
26
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
27
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 VO2 to predict performance is not as accurate
- 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 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
28
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
29
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
2. Endurance performance limited by Respiratory capacity
of muscle (mitochondria and enzyme content)
• Evidence
– anemic blood replaced with healthy blood containing red
blood cells
– immediately raises Hb - and restores VO2 max to 90% of
pre anemic levels
– running endurance was not improved
30
VO2 max versus Endurance Performance
• Davies - CH 6 - Correlation's
– 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
31
VO2 max versus Endurance Performance
• Second Davies study iron deficiency
• 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
32
Is Ventilation a limiting Factor to performance?
• Ventilation (VE) does not limit sea level aerobic performance
– capacity to increase ventilation is greater than that to inc Q
• Ventilation perfusion Ratio - VE/Q
– VE rest 5 L/min - exercise 190 L/min
• 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
33
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)
34
Ventilation as a limiting Factor to performance?
• MVV - maximum
voluntary ventilatory
capacity
• 1. VE max often
less than MVV
• 2. PAO2(alveolar)
and PaO2
(arterial)
– Fig 11-4 , 12-12
– maintain PAO2 or rises
– PaO2 also well
maintained
35
36
Ventilation as a limiting Factor to performance?
• 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 exhaustive exercise can still raise
VE to MVV, illustrating reserve capacity for ventilation
37
Elite Athletes
• Fig 13-3 - observe decline in PaO2 with
maximal exercise in some elite athletes
38
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 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
39
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
40
– 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


41
• 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
42
– 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
43
44
45
46
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
47
in heat does occur