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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 1 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) 2 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 – – – – – 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 3 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 4 CV Responses to Exercise • Increase flow to active areas • decrease flow to less critical areas • Principle responses – – – – – – – 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 5 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 6 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 7 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 8 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 9 (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 – – – – – = 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 10 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 11 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 12 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 13 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 14 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 – – – – speed ability to continue at high % of capacity lactate clearance capacity performance economy 15 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 16 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 17 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; – – – – 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 18 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 19 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 20 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 21 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 – – – – – inc slightly with training right shift of Hb saturation curve mitochondrial adaptation Hb and Mb [ ] muscle capillary density 22 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 – – – – 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 23