Transcript Ventilatory and Cardiovascular Dynamics

Ventilatory and
Cardiovascular Dynamics
• Brooks Ch 13 and 16
• OUTLINE
• Ventilation as limiting factor in
aerobic performance
• Cardiovascular responses to
exercise
• Limits of CV performance
– anaerobic hypothesis
– protection of heart and muscle
• CV function and training
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Ventilation as a limiting
Factor to performance
• Ventilation not thought to limit
aerobic performance at sea level
– capacity to inc ventilation with ex
– relatively greater than that to inc CO
• Ventilation perfusion Ratio - VE/CO
– Fig 12-14
– linear increase in vent with intensity to
vent threshold - then non linear
– VE rest 5 L/min - exercise 190 L/min
– Fig 13-1
• CO rest 5L/min - ex 25 L/min
– VE/CO 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
• max VE often less than MVV
• PAO2(alveolar) and PaO2(arterial)
– Fig 11-3 , 12-11
– maintain PAO2 - or rises
– PaO2 also well maintained
• Alveolar surface area - massive
• Fatigue of Vent musculature
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MVV tests - reduce rate at end of test
repeat trials - decreased performance
fatigue yes - is it relevant -NO
VE does not reach MVV
athletes post ex can raise VE to MVV
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Elite Athletes
• Fig 13-2 - observe decline in PaO2
with maximal exercise in some elite
• 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 CO ?
• 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
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Inc CO - 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
• 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 syst and diastolic
• Pressure load
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Cardiovascular System
Rest vs Maximal Exercise
Table 16.1
(untrained vs trained)
Rest
UT
HR(bpm)
70
SV(ml/beat)
72
(a-v)O2(vol%) 5.6
CO(L/min)
5
VO2 ml/kg/min 3.7
SBP(mmHg)
120
Vent(L/min)
10.2
Ms BF(A)ml/min 600
CorBFml/min 260
T
63
80
5.6
5
3.7
114
10.3
555
250
Max Ex
UT
T
185
182
90
105
16.2
16.5
16.6
19.1
35.8
42
200
200
129
145
13760
16220
900
940
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Oxygen Consumption
• Determinants
– rate of O2 transport
– O2 carrying capacity of blood
– amount of O2 extracted
• VO2 = Q * (a-v)O2
• Exercise of increasing intensity
• Fig 16-1,2,3
– CO 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 - Hb content
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Heart Rate
• Most important factor
• inc with intensity, levels off at
VO2max range 70 - 200 bpm
– increase due to withdrawal of Psymp
and symp stimulation
• estimated Max HR 220-age (+/- 12)
– influenced by anxiety, dehydration,
temp, altitude, digestion
• Less HR response with strength exer
– increases with muscle mass used
– higher with upper body - at same power
– inc MAP, peripheral resistance,
intrathoracic pressure
– less effective muscle pump - venous
return
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HR and Stroke volume
• Rate Pressure Produce - RPP
– HR X Systolic BP
• estimate of cardiac load - O2
• Stroke Volume
• Fig 16-2 - increase 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 CO
– same max HR - double the SV and CO
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(a-v)O2 difference
• Difference increases with intensity
– fig 16-3 - rest 5.6 - max 16
– always some oxygenated blood
returning to heart - non active tissue
– (a-v)O2 can approach 100% in
maximally working muscle
• Blood Pressure fig 16-4
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= CO * peripheral resistance (TPR)
dec TPR with exercise to 1/3 resting
CO rises 5-20 L/min
systolic BP goes up steadily
MAP - mean arterial pressure
• 1/3 (systolic-diastolic) + diastolic
– diastolic relatively constant
• rise - associated with CAD
• Over 110 mmHg
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Cardiovascular Triage
• With exercise - blood redistributed
from inactive to active tissue
– brain and heart spared vasoconstriction
– symp stim inc with intensity
• maintenance of BP priority
– working ms can be constricted
– protective mechanism - maintain flow
to heart and CNS
– limits exercise intensity - max CO can
be achieved with out resorting to
anaerobic metabolism
• Eg - easier breathing - inc flow to ms
– harder breathing - dec flow to ms
• Eg. Altitude study fig 16-5
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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 and endurance capacity
– Fig 16-6
– VO2 max - maximum capacity for aerobic
ATP synthesis
– Endurance performance - ability to
perform in endurance events
• Anaerobic hypothesis
• After max point - anaerobic metabolism
needed to continue exercise - plateau
– max CO and anaerobic metabolism will
limit VO2 max
– this determine fitness and performance
• Tim Noakes - South Africa
• re-analyzed data from classic studies
– most subjects did not show plateau
bringing anaerobic hypothesis into
question
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Inconsistencies with
Anaerobic hypothesis
• CO dependant upon and determined
by coronary blood flow
– Max CO implies cardiac fatigue coronary ischemia -? Angina pectoris?
• Blood transfusion and O2 breathing
– inc performance - still no plateau
– was it a CO limitation?
• Blood doping studies
– VO2 max improved for longer time
period than performance measures
• altitude - observe decrease in CO
– indicative of protective mechanism
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VO2 max and Performance
• General population - VO2 max will
predict endurance performance
– high VO2 max for elite performance 65-70 ml/kg/min
• elite - ability of VO2 to predict
performance is not as accurate
– world records for marathon
– male 69ml/kg/min female 73 ml/kg/min
– male 15 min faster
• other factors in addition to VO2 max
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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 CO 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
• CO depends on coronary blood flow
– Max CO implies cardiac fatigue,
coronary ischemia and angina pectoris
– This does not occur in healthy
individuals
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Protection of Heart and
Muscle
• 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 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 are also good
predictors of performance
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Practical Aspects of
Noakes Hypothesis
• Primary reg mech 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;
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muscle power output capacity
substrate utilization
thermoregulatory capacity
reduce work of breathing
• These changes will reduce load on
heart
– allowing more intense exercise before
protection 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 bloodSV - inc end diastolic volume-EDV
• Endurance training
– small inc in ventricular mass
– triggered by volume load
• resistance training
– pressure load - larger inc in mass
• adaptation is specific to form
– swimming improves swimming
• Interval training - repeated bouts of
short to medium duration
– improve speed and CV functioning
– combine with overdistance training
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Cardiovascular Adaptations with
Endurance Training
Table 16.2
Rest Submax Ex
(absolute)
HR


SV


(a-v)O2
0

CO
0
0
VO2
0
0
SBP
0
0
CorBFlow


Ms Bflow(A)
0
0
BloodVol

HeartVol

Max Ex
0




0


• 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 > 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
– inc volume - inc contractility - SV
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CV Adaptations
• Stroke volume - cont.
– EDV also inc with training - inc left
vent vol and compliance, blood vol,
– Myocardial contractility increased
– release and tx of calcium from SR
– isoform of myosin ATPase
– inc ejection fraction
• (a-v)O2 difference
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inc slightly with training
right shift of Hb saturation curve
mitochondrial adaptation
Hb and Mb [ ]
muscle capillary density
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CV Adaptations
• Blood pressure - dec resting and
submax
• 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 –
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dec peripheral resistance - inc CO
dec musc blood flow at sub max
inc extraction - more blood for skin...
Max - 10 % inc in musc flow
• no change in skin blood flow
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