Transcript Cardiorespiratory control

Oxygen Transport Systems
Integration of Ventilation, Cardiac,
and Circulatory Functions
Cardiovascular Function
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



transportation of O2 and CO2
transportation of nutrients/waste products
distribution of hormones
thermoregulation
maintenance of blood pressure
Long Refractory Period in Cardiac Muscle Prevents Tetany
Cardiac Fibers Develop Graded Tension
 Frank-Starling
Law of the Heart
 graded Ca2+
release from SR
– dependent on
Ca2+ influx
through DHP
channels
 Autorhythmic
cells depolarize
spontaneously
– leaky
membrane
– SA and AV
node
Group III
Central command input and output
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
Mechanisms affecting HR
VO2 = 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
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
Mechanisms affecting SV
VO2 = [HR  SV]  (a-v O2)
 amount of Ca2+ influx
– APs open Ca2+ channels on ttubules
– 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
Intrinsic control
 Frank-Starling
Principle
Dotted lines indicate end-systole and
end-diastole
–  Ca2+ influx w/
myocardial stretch
– stretched fibers work
at optimal lengthtension curve
Cardiovascular Response to Exercise
Laughlin, M.H. Cardiovascular responses to exercise.
Adv. Physiol. Educ. 22(1): S244-S259, 1999.
[available on-line]
Cardiovascular Response to Exercise
Fick principle
VO2 = Q  (CaO2 – CvO2)
VO2 = [HR  SV]  (CaO2 – CvO2)
VO2 = [BP  TPR]  (CaO2 – CvO2)
Exercise Effects on Cardiac Output
  HR caused by
–  sympathetic innervation
–  parasympathetic innervation
–  release of catecholamines
  SV, caused by
–  sympathetic innervation
–  venous return
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)
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
HR and Q responses to exercise intensity
SV during
graded running
Zhou et al., MSSE, 2001
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)
at rest
0.25
5.0
5.0
at maximal intensity
3.00
20.0
15.0
12
4
3
at rest
0.25
5.0
5.0
at maximal intensity
6.00
37.5
16.0
24
7.5
3.2
Untrained man
fold increase
Elite endurance male athlete
fold increase
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)
at rest
0.25
72
70
5.0
at maximal intensity
3.00
200
100
15.0
12
2.8
0.7
3.0
at rest
0.25
40
125
5.0
at maximal intensity
6.00
195
192
16.0
24
4.9
1.5
3.2
Untrained individual
fold increase
Elite endurance athlete
fold increase
Effects of Exercise on
Blood Pressure
BP = Q  TPR
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
Regulation of Blood Flow and
Pressure
Blood flow and pressure determined by:
A. Vessel resistance
(e.g. diameter) to
blood flow
B. Pressure difference
between two ends
A
cardiac
output
A
B
arterioles
B
Effects of Exercise Intensity on TPR
25
TPR
20
15
10
5
0
0
50
100
150
200
250
300
Treadmill speed (m/min)
350
400
Effects of Incremental Exercise on BP
250
Blood pressure (mm Hg)
225
200
175
150
125
100
75
Systolic BP
Diastolic BP
50
25
0
0
50
100
150
200
Workload (W)
250
300
Effects of Isometric Exercise on BP
Blood pressure (mm Hg)
225
200
175
150
125
100
75
Systolic BP
Diastolic BP
50
25
0
0
30
60
90
Time (s)
120
150
Control of Blood Flow
Blood flow to working muscle
increases linearly with muscle
VO2
Blood
Distribution
During Rest
Blood Flow Redistribution During Exercise
Effect of exercising muscle
mass on blood flow
(1-adrenergic
receptor blocker)
30 s
Onset of exercise
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
Adenosine metabolism in myocytes
and endothelial cells
ATP  ADP  AMP  adenosine
Adenosine is released in response to hypoxia,
ischemia, or increased metabolic work
Single layer of endothelial cells line
innermost portion of arterioles that
releases nitric oxide (NO) causing
vasodilation
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)
CO2 transport
Factors affecting Oxygen Extraction
Fick principle
VO2 = Q  (CaO2 – CvO2)
O2 extraction during
graded exercise
Sympathetic stimulation
causes spleen to constrict
releasing RBC into blood,
thus increasing O2-carrying
capacity
Bohr effect on
oxyhemoglobin
dissociation
 PO2, pH and 
PCO2, temperature,
and 2,3 DPG shift
curve to left causing
greater O2 release
Cardiovascular Adaptations to
Training
HR and Q responses to exercise intensity
SV during
graded running
Zhou et al., MSSE, 2001
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 crosssectional)
• longitudinal growth doesn’t affect sarcomere length
 contractility (systolic function) and relaxation
(diastolic function)
– Ca2+ sensitivity
– Ca2+ removal
Left ventricular adaptations depend
on training type
myocardial
thickness
LV-EDV
Endurance
trained
 preload
(volume overload)
Sedentary
Resistance
trained
 afterload
(pressure overload)
Ventilation
PO2 and PCO2 in
lungs and blood
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-
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
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
O2 and CO2
exchange in
alveolar capillaries
PO2 = 40
PCO2 = 46
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-
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)
Bohr effect on
oxyhemoglobin
dissociation
CO2 transport
Ventilatory Control of Blood pH
Ventilatory Regulation of AcidBase 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
Minute Ventilation
Minute Ventilation (L/min)
200.0
180.0
160.0
140.0
120.0
100.0
80.0
60.0
40.0
20.0
0.0
2
3
4
5
6
7
8
9
10 11 12 13 14 15
Treadmill Speed (mph)
VE and VO2
Response to
Incremental Exercise
Blood pH
7.45
7.40
7.35
pH
7.30
7.25
7.20
7.15
7.10
7.05
4
5
6
7
8
9
10
11
12
Treadmill Speed (mph)
13
14
15
CO2 Production
90
VCO2 (ml/kg/min)
80
70
60
50
40
30
20
10
0
2
3
4
5
6
7
8
9
10 11 12 13 14 15
Treadmill Speed (mph)
Respiratory Exchange Ratio
1.3
RER
1.2
1.1
1.0
0.9
0.8
4
5
6
7
8
9
10
11
12
Treadmill Speed (mph)
13
14
15
35
VE/VO2
30
25
20
15
100 125 150 175 200 225 250 275 300 325 350 375
Treadmill Speed (m/min)
Ventilatory equivalents for VO2 (dark blue) and VCO2
(yellow). Arrow indicates occurrence of ventilatory threshold.