Cardiorespiratory Responses to Exercise

Question 1

blood pressure
1. BP overview
2. pressure changes at rest in vasculature
3. mean arterial and pulse pressure

Answer 1

1. avg F exerted by blood against vasculature; primarily determined by Q (flow) and total peripheral resistance, P = flow*resistance, when pressure is too high risk of stroke/hemorrhage increase, when too low faint
2. at rest 120/80, systolic BP during contraction decrease greatly moving from aorta to vena cava, diastolic during relaxation smaller change throughout vasculature, measures LV pressure
3. avg driving pressure during cardiac cycle, MAP = DBP + 1/3 (SBP-DBP), closer to DBP because spend more time in diastole at rest, pulse pressure is SBP-DBP

Question 2

BP response to exercise
1. dynamic exercise
2. resistance exercise and valsalva maneuer
3. estimating workload of heart
4. changes in whole body hemodynamics

Answer 2

1. SBP increase by ~100 mmHg, DBP no change in healthy individual, increase DBP indicate increase in resistance in vasculature during relaxation
2. SBP increase by ~200 mmHg, DBP increase greatly due to occlusion of BV by muscle; Valsalva maneuver is forced expiration against closed of glottis to stabilize thoracic muscles and protect spine, occludes BV
3. double product = HR*SBP, dynamic exercise DP 21000, hypertensive dynamic exercise DP 28000, resistance exercise DP 56000
4. Q increase 4-5x, MAP increase 30%, resistance (TPR) decrease 4x overall; active tissue vasodialate to decrease resistance, inactive tissue constrict to increase resistance, allow redirection of Q

Question 3

measuring BP

Answer 3

1. cuff around brachial artery not inflated, cuff pressure 0, laminar BF, no sounds
2. when cuff filled to completely occlude artery BF, cuff pressure ~140 mmHg, no sounds
3. as cuff deflates, turbulent BF is partially occluded, blood rushing through occluded artery produce 1st Korotkoff sound (SBP) ~120 mmHg
4. complete deflation to 0 pressure, laminar BF, last sound before disappearance is DBP ~80 mmHg

Question 4

Respiratory basics
1. key terms
2. conducting v. respiratory zone
3. ventilation vol

Answer 4

1. ventilation is total air movement in/out of the lungs, respiration is gas exchange b/w tissues measured via hemoglobin saturation, tidal vol is how much air moved in/out of lungs with each breath (VT), alveolar vol is air that reached alveoli (VA) minus dead space vol (VD, space taken up by respiratory structure)
2. conducting zone is space available for ventilation VD, respiratory zone is space available for respiration VA, VT comp conducting and respiratory zone; in healthy lungs VA is most SA of lungs but in dmg lungs such as smoking, VA smaller thus have to have VT to provide sufficient gas exchange
3. total lung capacity (7L) is total amount of space available for air, functional residual capacity is air remaining after quiet inhalation, vital capacity is total amount of air inspired/expired, residual volume is VD

Question 5

ventilation rates
1. rest
2. maximal exercise
3. response to exercise

Answer 5

1. minute ventilation is the amount of air flow per minute (VTfreq = 500 mL12 breaths/min = 6L/min); alveolar ventilation is the amount of fresh air flow per min (VAfreq = 350 mL12/min = 4.2 L/min
2. for average untrained male, minute ventilation increase x20 comp rest and VA increase x27 comp rest; great increase in ventilation indicate high lung reserve, why cardiorespiratory func is key factor in determining VO2
3. ventilation increases as intensity increases, increase just before exercise because anticipation of exercise activates SNS (increased catecholamine)

Question 6

ventilatory regulation in exercise
1. overview
2. input to respiratory centre
3. neurohumoral control

Answer 6

1. freq and depth (VT) of ventilation influenced by many controls, compensate for each other if any are dmg/lost; respiratory control centre in the brainstem; inspiratory centre influenced by chemreceptors, voluntary control, and mechanoreceptors control activity of diaphragm and external intercostals; expiratory center controlled by lung stretch receptors to control activity of intercostal and abdominal muscles
2. central chemoreceptors in medulla oblongata sense PCO2 and H+ in CSF, peripheral in aortic and corotid bodies sense PCO2, PO2, and H+ in arterial blood, primary driver of breathing is increase of PCO2; neural control is key stimulus adjusting ventilation to intensity in exercise via motor cortex voluntary control and mechanoreceptors signalling increase ventilation with motion
3. in anticipation to exercise SNS activation increase catachoamine to increase glycogen and lactate (slight increase H+), after exercise begins rapid rise due to mechanoreceptor detection of motion with higher intensity increasing ventilation faster to maintain PAO2, PO2/PCO2 no change in arterial blood if there is proper lung func thus p. chemoreceptors not much of role, with humoral control fine tunes response, rises slowly before leveling off towards end of exercise

Question 7

1. 3 factors affecting gas exchange
2. partial pressure
3. main gases in atmospheric air
4. effect of water vapour

Answer 7

1. partial pressure gradient of gas, decrease in atmospheric pressure decrease pressure grad making it harder to diffuse, diffusion capacity/solubility of gas, characteristics of barrier
2. a gas as portion of total pressure
3. N2 is 79.03% conc, O2 =20.93%, CO2 = 0.03%, PO2 in dry air at sea lvl is 0.2093*760 mmHg =159 mmHg
4. water molecules disperse gas, increase total vol of air while decrease gas PP, conducting zone clean, warm, and humidify air, PO2 in alveoli lower than atmosphere at 149 mmHg due to moisture

Question 8

PO2 and PCO2 changes in body

Answer 8

1. atmosphere starting PO2 est ceiling (min 150-160 mmHg to est driving pressure)
2. small decrease as water vapour is added in trachea
3. sig drop PO2 to 105 in alveoli as venous and arterial blood mix, PCO2 = 40
4. slight decrease in arterial blood PO2 to 100 but about the same when proper ventilation/perfusion (gas exchange) as alveoli to drive hemoglobin saturation, PCO2 at 40
5. large decrease as O2 used in tissue cells, greater metabolism greater decrease,
6. venous blood PO2 depends on O2 leftover from metabolism, PO2 40 (15 during heavy exercise), PCO2 slightly increase to 46 (60 during heavy exercise) since it is highly diffusible, there is little change
7. lungs able to fill up O2 in one pass even under heavy exercise since it has high reserve, why arterial O2 does not change when lungs functioning properly

Question 9

Blood O2 transport
1. Importance of alveolar PO2
2. Hemoglobin
3. Determining blood O2 content

Answer 9

1. PAO2 sets ceiling, PaO2 (arterial) est arterial saturation (SaO2), est arterial O2 content
2. Hemoglobin comp 4 heme groups, each can bind one oxygen, blood saturation is average saturation of all hemoglobin, approx 97% (195 mL) in arterial blood since some venous blood is shunted directly to arteries with out deoxygenating at lungs and mismatch between ventilation and perfusion in different areas of the lungs (top higher ventilation, bottom higher perfusion)
3. Females have lower hgb conc, [Hgb] in g/100 mL blood, normal is 15 g%, 1g Hgb binds 1.34 mL O2 at 100% saturation; blood O2 = [Hgb]* 1.34* %sat, can artificially increase [Hgb] by sup EPO to increase blood O2 content, 3 mL/L dissolved in plasma

Question 10

oxyhemoglobin disassociation curve
1. overview
2. shifts in curve

Answer 10

1. how much saturation per PO2, at high saturation high affinity for O2 creates a safety margin to tolerate a great drop in O2 before offloading, arterial PO2 is 97 mm Hg (more O2 bound to hgb), venous PO2 around 40 mm Hg (low PO2 less O2 bound)
   at low PO2 small decreases in PO2 allow for great offloading
2. shift curve left increase affinity less offload, shift right decreased affinity higher offloading, decrease temp shift left, increase temp shift right; increase pH shift left decreased pH shift right (increase offloading O2 in response to increased H+ as metabolic by-product)

Question 11

1. muscle O2 transport and myoglobin
2. blood CO2 transport

Answer 11

1. myoglobin is globin with a heme group present in muscle which binds O2 tighter than Hgb; PaO2 about 100 O2 transferred from Hgb in blood to mgb in muscle cell with PO2 = 40, mgb transfer O2 into mitochondria where PO2 is very close to 0 (O2 used up in metabolism as soon as it is transported in), leaving PvO2 = 40, decrease during higher intensity exercise
2. carbonic anhydrase facilitates rxn of CO2 and H2O to H2CO3 which dissociates into H+ and HCO3-; CO2 transported into RBC converted to H+ and HCO3-, HCO3 released into blood while H+ stays trapped in RBC to buffer blood pH, in tissues form HCO3-, in lungs RBC take in HCO3-, form CO2 to release it; at altitude hyperventilate breathe off CO2 to decrease H+ and increase pH shift Ohgb curve left for easier O2 offloading at low PO2

Question 12

cardioresp adaptations to trainning:
1. central limitations
2. peripheral limitations
3. changes to SV with training
4. major adaptations to trainning (same abs workload)
5. why isn’t VO2 higher after training if fat use increases?

Answer 12

1. O2 delivery; heart ability for high CO primarily impacted by SV, lung pulmonary exchange capacity increases peak ventilation, and O2 carrying capacity of blood based on number of RBC (hgb conc stays same since more blood)
2. O2 utilization; mitochondrial size and number determines metabolism, capilllary density determines how much O2 extracted by muscle for use (increase capillary number/fibre with aerobic training allow for increase TT and time for O2 exchange)
3. SV = EDV - ESV (no change); EDV increase bc greater ventricle size allow greater filling due to increased blood vol, greater preload for stronger contraction
4. no change VO2rest, n/c VO2submax, increase VO2max; HRrest decrease, HRsubmax decrease, HRmax n/c; SV increases for all intensity, Qrest n/c, Qsubmax n/c, Qmax increase; VErest n/c, VEsubmax n/c, VEmax increase
5. sig change in RER result in minimal change in kcal/min use therefore VO2 change is negilible in measured VO2