Ventilatory and Cardiovascular Dynamics Brooks Chapts 13 and

Ventilatory and Cardiovascular Dynamics » Brooks Chapts 13 and 16 Outline • Ventilation as limiting factor in aerobic performance • Cardiovascular responses to exercise • Limits of CV performance • VO 2 max criteria • CV function and training 1

Ventilation as a Limiting Factor in Aerobic Performance at Sea Level (Chapt 13) • Ventilation not thought to limit aerobic performance at sea level. capacity to ventilation (35 x) with exercise is greater than the capacity to Cardiac Output (6 x) considerable ventilatory reserve exists to oxygenate blood passing through the lungs 2

Ventilation Perfusion Ratio - VE/CO • Linear in ventilation with in exercise intensity. As exercise intensity reaches maximal levels there can be a non -linear increase in ventilation. Ventilation at rest ~ 5 L/min Maximal levels ~ 190 L/min (35 x) · Linear in cardiac output with in exercise intensity. Cardiac Output at rest ~ 5 L/min Maximal levels ~ 30 L/min (6 x) · Pulmonary minute ventilation (VE) to Cardiac Output is ~1 at rest and 5 - 6 fold during maximal exercise. One reason why pulmonary ventilation is not thought to limit aerobic performance. 3

• Ventilatory Equivalent VE/VO 2 at rest 0. 25 L/min, VE/VO 2 = 20 VO 2 max ~ 5 L/min, VE/VO 2 = 35 the ability to ventilation is greater than the ability to expand oxidative metabolism · VEmax vs. MVV during exercise MVV- maximum voluntary ventilatory capacity the maximum VE during exercise is less than the MVV another reason why pulmonary ventilation is not thought to limit aerobic performance 4

PAO 2(alveolar) and Pa. O 2(arterial) O 2 moves from areas of high conc to areas of low conc during exercise maintain or PAO 2 Pa. O 2 in blood is also well maintained • Alveolar surface area is massive (50 m 2). only 200 ml of blood (4%) is in the pulmonary system during maximal exercise • Fatigue of ventilatory muscules. the diaphragm and ventilatory muscles can fatigue during MVV test fatigue at end of the test repeat trials - decreased performance fatigue yes - is it relevant -NO (ultra endurance) athletes post ex can raise VE to MVV 5

Pulmonary Limits in Elite Athletes • Fig 13 -2: decline in Pa. O 2 with maximal exercise in some elite athletes (individual variability) may be due to compliance in the ventilatory system may be due to economy (energy cost of breathing) athletes may learn to tolerate hypoxemia to energy cost of breathing during maximal exercise • Altitude – experienced climbers breathe more and maintain Pa. O 2 when climbing at altitude 6

Cardiovascular Dynamics During Exercise Brooks, Chapt 16 • O 2 to the working muscles with exercise intensity Principal Cardiovascular Responses to Exercise • Increased cardiac output HR (60 to 200 bpm) SV (80 to 200 ml/beat) O 2 and substrate delivery to muscle remove CO 2 and metabolites • skin blood flow regulate temperature 7

• blood flow to the kidneys – maintain blood volume • blood flow to viscera – reduced gastrointestinal activity • vasoconstriction in the spleen – blood volume • maintain blood flow to the brain • blood flow to coronary arteries of the heart • blood flow to working skeletal muscle 8

• Cardiovascular regulation is directed toward maintaining blood pressure. • During exercise CV regulation balances the need for more blood to the active tissue with the need to maintain BP and blood flow to the brain and heart. • Although maximum CO may limit O 2 transport capacity, maximal exercise may be terminated by the threat of ischemia to the heart (Noakes). 9

• Table 16 -1: Cardiovascular changes with endurance training. Rest Submax Ex Max Ex HR NC SV CO NC NC O 2 up SBP NC TPR NC NC 10

• CV response depends on type and intensity of activity. dynamic ex: large in HR, CO, SBP (not diastolic) ¶ volume load on the heart strength ex: large in SBP and DBP, mod in HR, CO ¶ pressure load on the heart 11

Oxygen Consumption • Oxygen consumption is proportional to exercise intensity. • Determinants: ¶ rate of O 2 transport ¶ O 2 carrying capacity of blood ¶ amount of O 2 extracted • VO 2 = [HR x SV] x (a-v)O 2 • 12

Heart Rate • HR accounts for 75% of O 2 uptake at maximal exercise (most important factor) • with intensity, levels off at VO 2 max (Fig 16 -1) • Range 70 - 210 bpm ¶ due to withdrawal of PNS and SNS stimulation ¶ intrinsic HR ~ 100 bpm • Estimated max HR = 220 - age (+/- 12) influenced by anxiety, dehydration, temp, altitude, digestion, genetics 13

• HR response with strength exercise lower than endurance training with muscle mass used higher with upper body ¶ intrathoracic pressure, smaller muscle mass ¶ less effective muscle pump - venous return Cardiovascular drift during prolonged exercise HR gradually at the same work rate venous return ( blood volume) Rate Pressure Produce - RPP HR X SBP rough index of coronary blood flow 14

Stroke Volume • SV has major impact on CO (2 x SV; 2 x CO). • SV during exercise to 25 - 50% of max then levels off. Fig 16 -2: SV from 75 ml to 110 ml/beat • SV as exercise intensity toward max (variable). • SV is perhaps the most important factor influencing individual differences in VO max. 2 max SV sedentary 90 ml, athlete 180 ml • Supine exercise: SV does not increase - starts high EDV remains unchanged 15

(a-v)O 2 difference • Difference increases with exercise intensity Fig 16 -3 : rest 5. 6 - max 16 (vol%) always some oxygenated blood returning to the heart non active tissue does not extract much O 2 (a-v)O 2 can approach 100% in maximally working muscle 16

Blood Pressure · BP must during exercise to maintain blood flow to the heart, brain and working muscle (Fig 16 -4). • TPR with exercise to 1/3 resting (due to in CO). · SBP steadily during exercise (120 - 180 mm. Hg). · MAP: 1/3 (systolic-diastolic) + diastolic · DBP is relatively constant 17

Cardiovascular Triage • CT: protective mechanisms that prevent coronary and CNS ischemia and maintain central blood volume. • During exercise these mechanisms limit blood flow to muscles when the body cannot meet the needs of the heart and CNS • With exercise blood is redistributed from inactive to active tissue brain and heart spared vasoconstriction SNS stimulation steadily with exercise intensity · At altitude the circulatory system appears to protect the heart by blood flow to the muscles and reduce the work of the heart (Fig 16 -5). 18

• Skin blood flow during submaximal exercise but to resting values during maximal exercise. • Coronary blood flow during exercise from 260 -900 ml/min flow occurs mainly during diastole coronary artery disease may restrict blood flow and cause ischemia a good warm up facilitates an in coronary circulation 19

Limits of CV Performance • VO 2 max has long been considered the best measure of CV capacity and aerobic performance (Fig 16 -6). • VO 2 max = [HRmax x SVmax] x (a-v)O 2 max • VO 2 max is the point at which O 2 consumption fails to rise, despite an power output or intensity. VO 2 PEAK 20

VO 2 max Anaerobic Hypothesis • After reaching VO 2 max exercise intensity is by anaerobic metabolism. max CO and anaerobic metabolism will limit VO 2 max best predictor of performance in endurance sports • Tim Noakes - South Africa re-analyzed data from classic studies found that most subjects did not plateau 21

Inconsistencies with Anaerobic hypothesis • Blood transfusion and O 2 breathing have been shown to performance. was it a CO limitation? • Blood doping studies VO 2 max improved for longer time period than performance measures • There is a discrepancy between VO 2 max and running performance in elite athletes. • At altitude CO indicative of protective mechanism 22

• Lower VO 2 max for cycling compared with running. • Running performance can improve without an in VO 2 max. • VO 2 max through running does not improve swimming. • Local muscle factors often appear to be more closely related to fatigue than a limitation in CO. • CO is dependant upon and determined by coronary blood flow. Max CO implies cardiac fatigue, coronary ischemia and angina pectoris? 23

Protection of Heart and Muscle During Exercise • 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 by Noakes suggests that peak treadmill velocity is a good predictor of aerobic performance. high cross bridge cycling and respiratory adaptations biochemical factors such as mito volume and O 2 enzyme capacity are also good predictors of endurance capacity 24

Practical Basis of the Noakes Hypothesis • Primary regulatory mechanism of the CV and neuromuscular systems facilitate intense exercise until it perceives risk of ischemic injury to the heart, CNS and muscles. • Fitness should be improved by: muscle power output capacity substrate utilization thermoregulatory capacity reduce work of breathing • The CV system develops at the same time that other adaptations occur from training. 25

Criteria for Measuring VO 2 max • Exercise must use at least 50% of the total muscle mass (do not use upper body exercise). • The exercise must be continuous and rhythmical and done for at least 10 minutes. • The test should try to eliminate motivation and skill. • The subject must reach maximum capacity. • The measurement must be made in a controlled environment. • VO 2 max on a bicycle is usually 10 to 15% less than running on a treadmill. 26

VO 2 max and Performance • For the general population VO 2 max will predict performance in an endurance event. • For elite athletes VO 2 max is a poor predictor of performance in an endurance event. male 69, female 73 ml/kg/min: male 15 min faster • Other performance factors: speed ability to continue at high % of capacity lactate clearance capacity performance economy 27

Cardiovascular Adaptations with Endurance Training HR SV (a-v)O 2 CO VO 2 SBP Cor. BF Blood. Vol Heart. Vol Rest NC NC Submax Ex NC Max Ex NC 28

Changes in CV Parameters with Training • Heart ability to pump blood by SV ( EDV). • Small in ventricular mass (volume load) with endurance training. • Strength training produces a pressure load that will LV mass. • Adaptation to endurance training is sport specific. • Interval training – acts as an overload – improve speed and CV functioning – combine with endurance training 29

CV Adaptations • Improvements in VO 2 max depend on prior fitness, type of training, age. can VO 2 max by ~20% • Endurance performance can by much more than 20% by improving mitochondrial density, speed, running economy, and body composition. 30

Heart Rate • Endurance training resting and submax HR by increasing PNS activity to the SA node. may intrinsic HR athlete 40 bpm may be a genetic influence resting HR may be due to disease (sick sinus syndrome) • Max HR may ~3 bpm with training. 31

Stroke Volume • Endurance training can resting and submax SV by 20%. • SV due to in heart volume and contractility. • HR will SV HR allows for filling time (Frank-Starling) • LV compliance allows ventricle to stretch more. • contractility due to in release and transport of Ca from SR. 32

(a-v)O 2 difference • (a-v)O 2 slightly with training difference right shift of Oxy. Hb dissociation curve mitochondrial adaptation Hb and myoglobin conc muscle capillary density • capillarization around muscle fibres is thought to facilitate diffusion during exercise. Blood Pressure • Endurance training resting and submax SBP, DBP and MAP (no change during max ex). 33

Blood Flow • With endurance training coronary blood flow slightly at rest and during submax exercise. SV and HR reduce myocardial O 2 consumption coronary blood flow at max ex with training • supports higher metabolic requirements with CO • Skeletal muscle vascularity with endurance training. peripheral resistance • The trained muscle has an O 2 extraction capacity. • There is no change in skin blood flow with training. 34