1. Ventilation and Cardiovascular Dynamics
Brooks Ch 13 and 16

2. Is Ventilation a limiting factor in aerobic performance?
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

4. 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 linear increase in vent with intensity to vent threshold - then non linear
VE rest 5 L/min -exercise 190 L/min

5. 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)

6. 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

7. 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

8. Elite Athletes
Fig observe decline in PaO2 with maximal exercise in some elite athletes

9. 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

10. 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

11. CV Responses to Exercise
Table 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

12. Cardiovascular System Rest vs Maximal Exercise Table 16
Cardiovascular System Rest vs Maximal Exercise Table (untrained vs trained)
Rest Max Ex
UT T UT T
HR(bpm)
SV (ml/beat)
(a-v)O2(vol%)
Q(L/min)
VO2 ml/kg/min
SBP(mmHg)
Vent(L/min)
Ms BF(A)ml/min
CorBFml/min

13. Oxygen Consumption Cardiovascular Determinants VO2 = Q * (a-v)O2
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

15. 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

16. 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

17. Stroke volume Stroke Volume - volume of blood per heart beat
Rest ml
Max ml
Fig 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
~ same max HR - double the SV and Q for athletes

18. (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 rest max 16 (vol %)
always some oxygenated blood returning to heart - non active tissue
(a-v)O2 can approach 100% in maximally working muscle

19. 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

20. 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
harder breathing - dec flow to ms

23. Cardiovascular Triage
Eg. Altitude study fig observe a reduction in maximum HR and Q with altitude even though we know a higher value is possible - illustrates protection is in effect

24. Large capacity for increase
Coronary blood flow
Large capacity for increase
( ml/min)
due to metabolic regulation
flow occurs mainly during diastole
warm up - facilitates inc in coronary circulation

25. 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

26. 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

27. 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 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

28. 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

29. Traditional Anaerobic hypothesis for VO2max
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
Still very controversial - not accepted by most scholars

30. 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

31. 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 are also good predictors of performance

32. 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

33. 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
combine with over-distance training

34. Cardiovascular Adaptations with Endurance Training Table 16.2
Rest Submax Ex Max Ex
(absolute)
HR   0
SV   
(a-v)O2 0   
Q 0  0  
VO 
SBP 0 0 0
CorBFlow   
Ms Bflow(A) 0 0 
BloodVol 
HeartVol 
0 = no change

35. CV Adaptations O2 consumption improvements depend on Heart Rate
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

36. CV Adaptations Stroke volume - cont. (a-v)O2 difference
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

37. 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 in heat does occur