oxygen transport systems
DESCRIPTION
Oxygen Transport Systems. Integration of Ventilation, Cardiac, and Circulatory Functions. Cardiovascular Function. transportation of O 2 and CO 2 transportation of nutrients/waste products distribution of hormones thermoregulation maintenance of blood pressure. - PowerPoint PPT PresentationTRANSCRIPT
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Oxygen Transport Systems
Integration of Ventilation, Cardiac, and Circulatory Functions
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Cardiovascular Function
transportation of O2 and CO2
transportation of nutrients/waste products distribution of hormones thermoregulation maintenance of blood pressure
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Long Refractory Period in Cardiac Muscle Prevents Tetany
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Cardiac Fibers Develop Graded Tension
Frank-Starling Law of the Heart
graded Ca2+ release from SR– dependent on
Ca2+ influx through DHP channels
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Autorhythmic cells depolarize spontaneously– leaky
membrane– SA and AV
node
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Central command input and output
Group III
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Cardiac output affected by:
1. preload – end diastolic pressure (amount of myocardial stretch)
affected by venous return
2. afterload – resistance blood encounters as it leaves ventricles
affected by arterial BP
3. contractility – strength of cardiac contraction
4. heart rate
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Mechanisms affecting HRVO2 = HR SV (a-v O2)
Sinoatrial node is pacemaker for heart– spontaneously depolarizes
• leakiness to Na+
– influenced by autonomic NS• training down-regulates ß-adrenergic system
causing bradycardia
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Cardiac Output Regulation
Extrinsic control autonomic nervous
system– sympathetic NS (1
control at HR >100 bpm)– parasympathetic NS (1
control at HR <100 bpm)– stimulates ß-adrenergic
receptors on myocardium hormonal
– EPI, NE
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Mechanisms affecting SV VO2 = [HR SV] (a-v O2)
amount of Ca2+ influx– APs open Ca2+ channels on t-
tubules– also stimulates Ca2+ release
from SR length-tension relationship
– [Ca2+]-tension relationship
ß1-adrenergic modulation– activates cAMP
phosphorylates L-type Ca2+, SR Ca2+ channels and pumps, troponin
Ca2+ influx and Ca2+ release from SR
training LV EDV
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Intrinsic control Frank-Starling
Principle Ca2+ influx w/
myocardial stretch– stretched fibers work
at optimal length-tension curve
Dotted lines indicate end-systole and end-diastole
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Cardiovascular Response to Exercise
Laughlin, M.H. Cardiovascular responses to exercise. Adv. Physiol. Educ. 22(1): S244-S259, 1999. [available on-line]
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Cardiovascular Response to Exercise
Fick principle
VO2 = Q (CaO2 – CvO2)
VO2 = [HR SV] (CaO2 – CvO2)
VO2 = [BP TPR] (CaO2 – CvO2)
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Exercise Effects on Cardiac Output
HR caused by sympathetic innervation parasympathetic innervation release of catecholamines
SV, caused by sympathetic innervation venous return
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Myocardial Mechanisms Influencing SV During Exercise
SV = EDV – ESV Factors that influence SV
– Heart size (LVV)– LV compliance during diastole
Progressive in ESV with graded exercise is from contractility– Attributed to sympathetic NS, length-tension
changes• Influx of Ca2+ through L-type Ca2+ channels stimulates
Ca2+ from SR release channels (Ca2+-induced Ca2+-release)
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Role of Ca2+ in Cardiac Function
influx of Ca2+ through L-type Ca2+ channels stimulates Ca2+ from SR release channels (Ca2+-induced Ca2+-release)
amount of Ca2+ released from SR dependent on sarcomere length
SERCA pumps return Ca2+ to sarcoplasmic reticulum sympathetic -adrenergic stimulation contractile
force and relaxation time– affects Ca2+ sensitivity through phosphorylation– increases length of diastole to filling time
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HR and Q responses to exercise intensity
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SV during graded running
Zhou et al., MSSE, 2001
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Effect of training and maximal exercise on VO2, Q, and a-v O2 difference
VO2 (L·min-1)
Q(L·min-1)
a-v O2
difference (ml O2·100 ml-1)
Untrained man
at rest 0.25 5.0 5.0
at maximal intensity 3.00 20.0 15.0
fold increase 12 4 3
Elite endurance male athlete
at rest 0.25 5.0 5.0
at maximal intensity 6.00 37.5 16.0
fold increase 24 7.5 3.2
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Effect of training and maximal exercise on VO2, Q, and a-v O2 difference
VO2 (L·min-1)
HR(bpm)
SV(ml·beat-1)
a-v O2
difference (ml O2·100 ml-1)
Untrained individual
at rest 0.25 72 70 5.0
at maximal intensity 3.00 200 100 15.0
fold increase 12 2.8 0.7 3.0
Elite endurance athlete
at rest 0.25 40 125 5.0
at maximal intensity 6.00 195 192 16.0
fold increase 24 4.9 1.5 3.2
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Effects of Exercise on Blood Pressure
BP = Q TPR
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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
capillary density 1 determinant of O2 diffusion
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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 BB
cardiac output
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0
5
10
15
20
25
0 50 100 150 200 250 300 350 400
Treadmill speed (m/min)
TP
R
Effects of Exercise Intensity on TPR
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Effects of Incremental Exercise on BP
0
25
50
75
100
125
150
175
200
225
250
0 50 100 150 200 250 300
Workload (W)
Blo
od
pre
ssu
re (
mm
Hg
)
Systolic BP
Diastolic BP
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Effects of Isometric Exercise on BP
0
25
50
75
100
125
150
175
200
225
0 30 60 90 120 150
Time (s)
Blo
od
pre
ssu
re (
mm
Hg
)
Systolic BP
Diastolic BP
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Control of Blood Flow
Blood flow to working muscle increases linearly with muscle VO2
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Blood Distribution During Rest
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Blood Flow Redistribution During Exercise
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Effect of exercising muscle mass on blood flow
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Onset of exercise
(1-adrenergic receptor blocker)
30 s
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Local Control of Microcirculation
metabolic factors that cause local vasodilation PO2
PCO2
H+
– adenosine endothelial factors that cause local vasodilation
– nitric oxide (NO)• released with shear stress and EPI• redistributed from Hb—greater O2 release from Hb induces
NO release as well
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Adenosine metabolism in myocytes and endothelial cells
ATP ADP AMP adenosine
Adenosine is released in response to hypoxia, ischemia, or increased metabolic work
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Single layer of endothelial cells line innermost portion of arterioles that releases nitric oxide (NO) causing
vasodilation
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Hemoglobin
consists of four O2-binding heme (iron containing) molecules
combines reversible w/ O2 (oxy-hemoglobin)
Bohr Effect – O2 binding affected by
– PO2
– PCO2
– pH
– temperature
– 2,3-DPG (diphosphoglycerate)
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CO2 transport
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Factors affecting Oxygen Extraction
Fick principle
VO2 = Q (CaO2 – CvO2)
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O2 extraction during graded exercise
Sympathetic stimulation causes spleen to constrict releasing RBC into blood,
thus increasing O2-carrying capacity
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Bohr effect on oxyhemoglobin
dissociation
PO2, pH and PCO2, temperature,
and 2,3 DPG shift curve to left causing
greater O2 release
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Cardiovascular Adaptations to Training
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HR and Q responses to exercise intensity
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SV during graded running
Zhou et al., MSSE, 2001
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Cardiovascular Adaptations to Endurance Training
VO2max = HRmax SVmax (a-v O2 diff)max
~50% of VO2max is because of SVmax
1 mechanism is from LV-EDV compliance (ability to stretch) myocardial growth (longitudinal and cross-
sectional)• longitudinal growth doesn’t affect sarcomere length
contractility (systolic function) and relaxation (diastolic function) Ca2+ sensitivity Ca2+ removal
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Left ventricular adaptations depend on training type
Endurance trained preload
(volume overload)
SedentaryResistance
trained afterload
(pressure overload)
LV-EDV myocardial thickness
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Ventilation
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PO2 and PCO2 in lungs and blood
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Humoral Chemoreceptors
PAO2
– not normally involved in control
PACO2
– central PACO2 chemoreceptors are 1º control factor at rest
H+
– peripheral H+ chemoreceptors are important factor during high-intensity exercise
– CO2 + H2O H2CO3 H+ + HCO3-
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Matching of Ventilation and Perfusion
100% of cardiac output flows through lungs– low resistance to flow
pulmonary capillaries cover 70-80% of alveolar walls
upper alveoli not opened during rest
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Pulmonary Gas Exchange
alveolar thickness is ~ 0.1 µm total alveolar surface area is ~70 m2
at rest, RBCs remain in pulmonary capillaries for 0.75 s (capillary transit time)– 0.4-0.5 s at maximal exercise
• adequate to release CO2; marginal to take up O2
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O2 and CO2 exchange in alveolar capillaries
PO2 = 40PCO2 = 46
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Gas Exchange and Transport
Oxygen Transport ~98% of O2 transported bound to
hemoglobin
Carbon Dioxide Transport dissolved in plasma (~7%) bound to hemoglobin (~20%) as a bicarbonate ion (~75%)
CO2 + H2O H2CO3 H+ + HCO3-
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Hemoglobin
consists of four O2-binding heme (iron containing) molecules
combines reversible w/ O2 (oxy-hemoglobin)
Bohr Effect – O2 binding affected by– temperature
– pH
– PO2
– PCO2
– 2,3-DPG (diphosphoglycerate)
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Bohr effect on oxyhemoglobin
dissociation
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CO2 transport
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Ventilatory Control of Blood pH
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Ventilatory Regulation of Acid-Base Balance
CO2 + H2O H2CO3 H+ + HCO3-
source of these expired carbons is from bicarbonate ions (HCO3
-), NOT substrates at low-intensity exercise, source of CO2 is
entirely from substrates at high-intensity exercise, bicarbonate ions
also contribute to VCO2
Can RER every exceed 1.0? When? Explain
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Minute Ventilation
0.0
20.0
40.0
60.0
80.0
100.0
120.0
140.0
160.0
180.0
200.0
2 3 4 5 6 7 8 9 10 11 12 13 14 15
Treadmill Speed (mph)
Min
ute
Ven
tila
tio
n (
L/m
in)
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VE and VO2 Response to
Incremental Exercise
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Blood pH
7.05
7.10
7.15
7.20
7.25
7.30
7.35
7.40
7.45
4 5 6 7 8 9 10 11 12 13 14 15
Treadmill Speed (mph)
pH
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CO2 Production
0
10
20
30
40
50
60
70
80
90
2 3 4 5 6 7 8 9 10 11 12 13 14 15
Treadmill Speed (mph)
VC
O2
(m
l/k
g/m
in)
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Respiratory Exchange Ratio
0.8
0.9
1.0
1.1
1.2
1.3
4 5 6 7 8 9 10 11 12 13 14 15
Treadmill Speed (mph)
RE
R
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Ventilatory equivalents for VO2 (dark blue) and VCO2 (yellow). Arrow indicates occurrence of ventilatory threshold.
15
20
25
30
35
100 125 150 175 200 225 250 275 300 325 350 375
Treadmill Speed (m/min)
VE
/VO
2