1 Ventilation and Cardiovascular Dynamics Brooks Ch 13 and 16

2 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 Outline

3

4 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 Ventilation as a limiting Factor to performance

5 Fig 13-2 Q rest 5L/min - ex 25 L/min VO 2 /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/VO 2 –rest 20 (5/.25) ; max 35(190/5) Ventilation as a limiting Factor to performance

6 MVV - max voluntary ventilatory capacity 1.max VE often less than MVV 2.PAO 2 (alveolar) and PaO 2 (arterial) –Fig 11-4, –maintain PAO 2 - or rises –PaO 2 also well maintained VE max vs. MVV

7 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 VE max vs. MVV

8 Fig observe decline in PaO 2 with maximal exercise in some elite athletes Elite Athletes

9 may see vent response blunted, even with dec in PaO 2 –may be due to economy –extremely high pulmonary flow, inc cost of breathing, any extra O 2 used to maintain this cost –? Rise in PAO 2 - was pulmonary vent a limitation, or is it diffusion due to very high Q ? Altitude –experienced climbers - breathe more - maintain Pa O 2 when climbing –Elite - may be more susceptible to impairments at altitude Elite Athletes

10 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 CV Responses to Exercise

11 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 CV Responses to Exercise

12 Cardiovascular System Rest vs Maximal Exercise Table 16.1 (untrained vs trained) Rest Max Ex UTTUT T HR(bpm) SV(ml/beat) (a-v)O 2 (vol%) Q(L/min) VO 2 ml/kg/min SBP(mmHg) Vent(L/min) Ms BF(A) ml/min CorBFml/min

13 Cardiovascular Determinants –rate of O 2 transport –amount of O 2 extracted –O 2 carrying capacity of blood VO 2 = Q * (a-v)O 2 Exercise of increasing intensity Fig 16-2,3,4 –Q and (a-v)O 2 increases equally important at low intensities –high intensity HR more important –(a-v)O 2 - depends on capacity of mito to use O 2 - rate of diffusion-blood flow O 2 carrying capacity - influenced by Hb content Oxygen Consumption

14

15 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 Heart Rate

16 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 Heart Rate

17 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 Stroke volume

18 Difference between arterial and venous oxygen content across a capillary bed –(ml O 2 /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)O 2 can approach 100% in maximally working muscle (a-v)O 2 difference

19 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 Blood Pressure

20 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 Cardiovascular Triage

21

22

23 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 Cardiovascular Triage

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

25 VO 2 max - long thought to be best measure of CV capacity and endurance performance –Fig 16-7 –VO 2 max - maximum capacity for aerobic ATP synthesis –Endurance performance - ability to perform in endurance events CV Performance Limitation

26 Criteria for identifying if actual VO 2 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 CV Performance Limitation

27 General population - VO 2 max will predict endurance performance - due to large range in values elite - ability of VO 2 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 - VO 2 max –male ~15 min faster with similar VO 2 max other factors in addition to VO 2 max that impact performance –Sustained speed –ability to continue at high % of capacity –lactate clearance capacity –performance economy VO 2 max and Performance

28 Local muscle factors more closely related to fatigue than Q limitation –Table 6-3 correlations between ox capacity, VO 2 and endurance Lower VO 2 max for cycling compared to running Running performance can improve without an inc in VO 2 max Inc VO 2 max through running does not improve swimming performance Capacity vs Performance

29 Traditional Anaerobic hypothesis for VO 2 max –After max point - anaerobic metabolism is needed to continue exercise - plateau –max Q and anaerobic metabolism will limit VO 2 max –this determines fitness and performance Tim Noakes,Phd - South Africa –re-analyzed data creating Alternate hypothesis for VO 2 max –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 What limits VO 2 max ?

30 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 O 2 breathing –inc performance - many says this indicates Q limitation –But still no plateau –was it a Q limitation? Blood doping studies –VO 2 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 Inconsistencies in Anaerobic hypothesis

31 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 Protection Hypothesis

32 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 Practical Aspects of Noakes Hypothesis

33 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 Changes in CV with Training

34 Cardiovascular Adaptations with Endurance Training Table 16.2 Rest Submax Ex Max Ex (absolute) HR   0 SV    (a-v)O 2 0    Q 0  0   VO  SBP 0  0  0 CorBFlow    Ms Bflow(A)  0  0  BloodVol  HeartVol  0 = no change

35 O 2 consumption improvements depend on –prior fitness, type of training, age –can inc VO 2 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 CV Adaptations

36 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)O 2 difference –inc slightly with training due to ; –right shift of Hb saturation curve –mitochondrial adaptation –Hb and Mb [ ] –muscle capillary density CV Adaptations

37 Blood pressure - decreased resting and submax BP Blood flow –training - dec coronary blood flow rest and submax (slight) inc SV and dec HR - dec O 2 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 CV Adaptations