Cardiovascular and Respiratory Systems: Getting Oxygen From Air to Muscle Integration of Ventilation, Heart, and Circulation

Cardiorespiratory System Functions of cardiorespiratory system:  transportation of O 2 and CO 2  transportation of nutrients/waste products  distribution of hormones  thermoregulation  maintenance of blood pressure

Ability of cardiorespiratory system to maintain high arterial oxygen levels (PaO 2 ) during graded exercise to exhaustion

Critical elements of O 2 Transport Pathway  Ventilation –Moving air in/out of lungs  External respiration –Gas exchange between alveoli and blood  Heart and circulation  O 2 diffusion into mitochondria

Role of the Heart Moving O 2 from lungs to muscle

Oxygen Delivery Determines VO 2 (Fick Principle) VO 2 = Q  (Ca O 2 – Cv O 2 ) VO 2 = [HR  SV]  (Ca O 2 – Cv O 2 ) VO 2 = [BP  TPR]  (Ca O 2 – Cv O 2 )

Cardiac Cycle  systole  diastole  cardiac output (Q) = stroke volume (SV)  heart rate (HR) examples – rest: SV = 75 ml; HR = 60 bpm; Q = 4.5 L  min -1 –exercise: SV = 130 ml; HR = 180 bpm; Q = 23.4 L  min -1

Cardiac output affected by: 1.preload – end diastolic pressure (amount of myocardial stretch) 2.afterload – resistance blood encounters as it leaves ventricles 3.contractility – strength of cardiac contraction 4.heart rate

Muscle pump and one-way valves assist venous return

Cardiac Output Regulation Extrinsic control  autonomic nervous system –sympathetic NS (1  control at HR >100 bpm) NE released as neural transmitter –parasympathetic NS (1  control at HR <100 bpm) ACh released as neural transmitter  hormonal –EPI, NE

Ventilation and External Respiration Getting O 2 from air into blood

A. Major pulmonary structures B. General view showing alveoli and blood vessels C. Section of lung showing individual alveoli D. Pulmonary capillaries surrounding alveolar walls

RBC Single alveoli at rest showing individual RBCs Single alveoli under high flow showing increased RBCs

Lungs and Pulmonary Circulation  alveolar membrane thickness is ~ 0.1 µm  total alveolar surface area is ~75 m 2  80-90% of alveoli are covered by capillaries  pulmonary circulation varies with cardiac output and matched to ventilation rate

Gases Move Down Pressure Gradients

O 2 and CO 2 transit time in lungs (left) and tissue (right) at rest Notice rapid saturation with O 2 by the time RBCs have traveled ⅓ around alveolus

PO 2 in blood returning to the lungs is ____ PO 2 in the alveoli. A.greater than B.less than C.similar to

PO 2 in arterial blood is ____ PO 2 in the mitochondria. A.greater than B.less than C.similar to

PCO 2 in venous blood is ____ PCO 2 in the alveoli. A.greater than B.less than C.similar to

What would be the effect on the saturation of arterial blood with O 2 (SaO 2 ) when pulmonary blood flow is faster than the diffusion rate of O 2 ? A.SaO 2 would remain unchanged B.SaO 2 would be decreased C.SaO 2 would be increased

Rate of gas diffusion is dependent upon pressure (concentration) gradient. Erythrocyte (RBC)  ~98% of O 2 is bound up with hemoglobin (Hb)  Hb consists of four O 2 -binding heme (iron containing) molecules  combines reversibly w/ O 2 (forms oxy-hemoglobin)  1-2% of O 2 is dissolved in plasma

CO 2 + H 2 O  H 2 CO 3  H + + HCO 3 - Transport of CO 2 in blood ~75% ~5% ~20%

Oxygen is transported from lungs to muscle primarily A.dissolved in blood. B.bound to hemoglobin. C.as a bicarbonate ion.

Carbon dioxide is transported from muscle to the lungs A.dissolved in blood. B.bound to hemoglobin. C.as a bicarbonate ion. D.all of the above are transport mechanisms for CO 2

Ventilatory Response to Exercise and Control of Blood pH

Minute ventilation (VE) response to different exercise intensities

Ventilatory Control Mechanisms

Current thought is that primary control of ventilation is: from muscle afferents sensory inputs to control arterial PCO 2,(peripheral PCO 2 chemoreceptors) to minimize  in blood pH (peripheral pH chemoreceptors)

Ventilatory responses to incremental exercise Why are there a breakpoints in the linearity of VE and VCO 2 ?

Ventilatory Regulation of Acid-Base Balance CO 2 + H 2 O  H 2 CO 3  H + + HCO 3 -  at low-intensity exercise, source of CO 2 is entirely from substrate metabolism  bicarbonate (HCO 3 - ) buffers H + produced during high- intensity exercise  at high-intensity exercise, bicarbonate ions also contribute to CO 2 production –source of CO 2 is from substrates and bicarbonate ions (HCO 3 - )   blood [H + ] stimulates VE to rid excess CO 2 (and H + ) Can RER ever exceed 1.0? When? Explain

RER = VCO 2 VO 2

What is the primary cause of hyperventilation during incremental exercise? A.muscles cannot get enough O 2 B.sympathetic innervation C.accumulation of lactate ions in blood D.conscious desire to breath harder E.additional stimulation of PCO 2 chemoreceptors

Ventilation Questions 1.Describe how ventilation regulates blood pH. 2.Explain why the ventilatory threshold is related to the lactate threshold 3.Can RER ever exceed 1.0? Under what circumstances? Explain.

Young cowboys in the old west

Matching O 2 delivery to muscle O 2 needs Regulation of cardiorespiratory system

Vascular system aorta  arteries  arterioles  capillaries  venules  veins  vena cava

Vascular smooth muscle allows vessels to constrict in response to SNS stimulation or local factors

Arterioles and Capillaries  arterioles  terminal arterioles (TA)  capillaries  collecting venules (CV)   arterioles regulate circulation into tissues –under sympathetic and local control  precapillary sphincters fine tune circulation within tissue –under local control

Blood vessels are surrounded by sympathetic nerves. A feed artery was stained to reveal catecholamine-containing nerve fibers in vascular smooth muscle cell layer. This rich network extends throughout arterioles but not into capillaries or venules. Local factors that control arterioles PO 2 PCO 2 pH adenosine K + Nitric oxide

Inside of arterioles are endothelial cells that release nitric oxide (NO) in response to sheer stress (increased pressure and flow), which causes vasodilation

Onset of exercise (  1 -adrenergic receptor blocker) 30 s Rapid adaptation of blood flow

Precapillary sphincters fine-tune local blood flow Local control factors PO 2 PCO 2 pH adenosine K + temperature

Blood Distribution During Rest

Blood Flow Redistribution During Exercise

At rest, most blood is found in the ______ while at exercise most blood is in _____. A.venous system; active muscle B.pulmonary circulation; heart C.arterioles; capillaries D.heart; heart E.liver; active muscle

What is the primary mechanism to increase blood flow to working muscle? A.baroreceptors B.sympathetic innervation C.local factors D.epinephrine E.central command

What effect would these local conditions (from resting values) have on arteriole blood flow?  PO 2,  PCO 2,  pH,  temperature A.increase flow B.decrease flow C.no effect on flow D.cannot be determined

O 2 Extraction Moving O 2 from blood into muscle

Factors affecting Oxygen Extraction Fick equation VO 2 = Q   (aO 2 – vO 2 )

O 2 extraction response to exercise Represents mixed venous blood returning to right heart

a-v O 2 difference  Bohr Effect: effect of local environment on oxy-hemoglobin binding strength  amount of O 2 released to muscle depends on local environment –PO 2, pH, PCO 2, temperature, 2,3 DPG  2,3 diphosphoglycerate (DPG) –produced in RBC during prolonged, heavy exercise –binds loosely with Hb to reduce its affinity for O 2 which increases O 2 release

Bohr effect on oxyhemoglobin dissociation O 2 loading in lungs O 2 unloading in muscle Oxyhemoglobin binding strength affected by: PO 2 PCO 2 H + temperature 2,3 DPG

A change in the local metabolic environment has occurred: pH and PO 2 have  ; temperature and PCO 2 have . What effect will these changes have on the amount of O 2 released to the muscle? A.increase O 2 release B.decrease O 2 release C.no change in O 2 release D.cannot be determined

A change in the local metabolic environment has occurred: pH and PO 2 have  ; temperature and PCO 2 have . What do these changes in local environmental suggest has occurred? A.the muscles changed from an exercise to a resting state B.the muscles began to exercise C.no change D.cannot be determined

During graded exercise, A.VCO 2 increases linearly B.A breakpoint occurs in VCO 2 that coincides with lactate threshold C.A breakpoint occurs in VE that is caused by increased VO2 D.A breakpoint occurs in VCO 2 that results from increased epinephrine release

Which of the following would NOT cause local vasodilation? A.  PCO 2 B.  PO 2 C.  temperature D.  pH E.  nitric oxide production

Which of the following would NOT cause greater O 2 unloading from hemoglobin? A.  PCO 2 B.  PO 2 C.  temperature D.  pH E.  nitric oxide production

Which of the following adaptations likely had the LEAST influence for explaining why VO 2max increased 12% after completing a cross country season? A.  cardiac output B.  blood volume C.  mitochondrial volume D.  capillary density E.  number of RBC

Which of the following does NOT occur during exercise? A.Vasodilation occurs throughout body. B.Blood is redirected towards exercising muscle. C.Local factors loosen binding of O 2 to hemoglobin. D.Increased venous return causes increased stroke volume. E.There is increased afterload to heart.

Which of the following does NOT occur during moderate-intensity running exercise? A.Sympathetic stimulation increases blood flow to working muscles. B.  PCO 2 causes greater unloading of O 2 to working muscles from hemoglobin. C.Sensory inputs from muscle afferent nerves stimulate ventilation and heart rate. D.PO 2 in alveoli drops to less than the PO 2 in blood returning to the lungs. E.There is little change to diastolic BP.

Control of cardiac function and ventilation Parallel activations

What would be the effect of local arteriole dilation on BP? A.Decrease BP B.Increase BP C.No effect on BP

During running exercise, total peripheral resistance ____ because of _____. A.increases; sympathetic stimulation B.increases; local control factors C.decreases; vasoconstriction D.decreases; local control factors

Reflex control of cardiac output Primary regulators  Central command control center (medulla) –Input from motor cortex parasympathetic inhibition predominates at HR <~100 bpm sympathetic stimulation predominates at HR >~100 bpm –Sensory input from skeletal muscle afferent sense mechanical and metabolic environment Secondary regulator  arterial baroreceptors –Provide input to central command –located in carotid bodies and aortic arch –respond to arterial pressure Reset during exercise

Maintaining Blood Pressure Pressure is Necessary for Blood Flow

Pressure is necessary for blood to flow. Notice that blood flow decreases with BP

Regulation of Blood Flow and Pressure Blood flow and pressure determined by: arterioles B. Pressure difference between two ends A. Vessel resistance (e.g. diameter) to blood flow A A B B cardiac output BP = Q  TPR

Regulation of Blood Flow and Pressure Time 120 Pressure (mm Hg) 80 BP = Q  TPR

At what level is peripheral resistance greatest?

Effects of Exercise on Cardiac Output

Effects of Exercise Intensity on TPR

Effects of Incremental Exercise on BP

Effects of Isometric Exercise on BP

Cardiovascular Response to Exercise Fick equation VO 2 = Q   (aO 2 – vO 2 ) VO 2 = [HR  SV]   (aO 2 – vO 2 ) VO 2 = [BP  TPR]   (aO 2 – vO 2 )

Exercise effects on heart   HR caused by –  sympathetic innervation –  parasympathetic innervation –  release of catecholamines   SV, caused by –  sympathetic innervation –  venous return   cardiac output

Cardiorespiratory adaptations to endurance training How does endurance training affect VO 2max ?

Maximal oxygen consumption (VO 2max ) VO 2max –highest VO 2 attainable –maximal rate at which aerobic system utilizes O 2 and synthesizes ATP –single best assessment of CV fitness intensity VO 2 VO 2max

 VO 2max affected by: –genetics (responders vs. nonresponders) –age –gender –specificity of training

Cardiorespiratory training adaptations VO 2max  ~15% with training  ventilation? –training has no effect on ventilation capacity  O 2 delivery? –CO (  ~15%) –  plasma volume –  SV  O 2 utilization? –mitochondrial volume  >100%

1995 marathon training data (women)

Heart adaptations to training  sympathetic sensitivity  heart size, blood volume

Heart adaptations to training

Left ventricular adaptations depend on training type Endurance trained  preload (volume overload) Sedentary Resistance trained  afterload (pressure overload)  LV-EDV  myocardial thickness

Normalized data for VO 2max (ml  kg -1  min -1 ) Women Men

Which of the following would likely result in an increase of VO 2max ? A.breathing faster and deeper during maximal exercise B.faster HR at maximal exercise C.ability to deliver more O2 to muscles during maximal exercise D.more mitochondria

Which of the following does NOT occur following endurance training? A.  blood volume B.  HR max C.  SV max D.  CO max E.  mitochondrial volume F.  maximal ventilatory capacity

How would you evaluate a VO 2max of 28.9 mL/kg/min for a 22-year-old man? A.excellent B.above average C.average D.very low E.dead

Which of the following exercises would likely decrease TPR the LEAST? A.jogging B.fast walking C.shoveling snow D.cycling E.the above would decrease TPR similarly

What is the mechanism for the sudden increase in VE when the lactate threshold is reached during an incremental exercise test? A.greater muscle afferent input B.greater stimulation of peripheral baroreceptors C.greater stimulation of peripheral PCO 2 chemoreceptors D.greater stimulation of peripheral PO 2 chemoreceptors E.greater stimulation from motor cortex