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Ventilatory Control
Dynamics of Pulmonary
Ventilation
Figure 14.1
Neural Factors
• Medulla (respiratory center), pons, subcortical
region & motor cortex
• Inspiratory neurons activate diaphragm and
intercostals
a) Limited by influence of expiratory neurons
9Stretch receptors
• Neural center in the hypothalamus integrates
input from ascending & descending neurons:
a) Influences duration and intensity of respiratory
cycle
Plasma PCO2 & H+ Concentrations
• PCO2 in arterial blood provides the most
important respiratory stimulus at rest
a) Ventilation increases to decrease PCO2
Humoral Factors
• Peripheral chemoreceptors located in:
a) Aorta and carotid arteries
9Stimulated by ↓ PO2
9Stimulated also by exercise
• During exercise:
a) ↑ PCO2
b) ↑ Temperature
c) ↑ acidity
d) ↑ potassium concentrations
Ventilation During Exercise
• Chemical Control:
a) Combination of factors
9 Fluctuations in PO2, PCO2
• ↓ blood pH reflects CO2 retention or lactate
accumulation (exercise)
• Hyperventilation & breath-holding
a) Sport-specific application: swimming & divers
Figure
14.3
9 Metabolic production of CO2 & H+
1
Ventilation During Exercise
• Nonchemical Control:
a) Neurogenic Factors – responsible for rapid response
to increase ventilation
1. Cortical influence – activated in anticipation
2. Peripheral influence – sensory input from limbs
b) Temperature has little influence on respiratory rate
during exercise
9 Ventilation fluctuation to rapid to reflect changes in core
temperature
Integrated Regulation During Exercise
• Phase I (beginning of exercise): neurogenic
stimuli from cortex increases respiration
• Phase II: after about 20 seconds VE rises
exponentially to reach steady state
a) Central command
b) Peripheral chemoreceptors
• Phase III: fine tuning of steady-state ventilation
through peripheral sensory feedback mechanisms
In Recovery
• An abrupt decline in ventilation reflects removal
of central command and input from receptors in
active muscle
• Slower recovery phase from gradual metabolic,
chemical and thermal adjustments
Figure 14.4
Pulmonary Ventilation During Exercise
1. Ventilation (VE) in Steady-State Exercise:
a) During light to moderate exercise:
9 Ventilation increases linearly with O2 consumption and
CO2 production
9 At lower intensities, ventilation ↑ primarily due to ↑
TV
9 At higher intensities, primarily ↑ breathing rate
Ventilatory Threshold (VT)
• The point at which pulmonary ventilation ↑
disproportionately with O2 consumption during
exercise
a) pulmonary ventilation no longer tightly associated
with O2 demand at the cellular level
• Excess ventilation results from:
a) CO2 increased output from buffering of lactate
2. Ventilation in Non-Steady-State Exercise:
a) VE rises sharply and the ventilatory equivalent rises
as high as 35–40
Lactate + NaHCO3
Na lactate + H2CO3
H2O + CO2
b) ↑ nonmetabolic CO2 stimulates ventilation
2
Relationship to Lactate Threshold
Figure 14.6
Figure 14.5
Other factors affecting ventilation
• Energy Cost of
Breathing:
• Ventilation in healthy
individuals is not the
limiting factor in
exercise
a) 3 to 5% of total O2
consumption during
light to moderate
exercise
b) 8 to 15% during
maximal exercise
c) Respiratory muscles
at max ~ 15% of total
blood flow
a) Breathing reserve
even at maximal
exercise
Figure 14.9
Figure 14.11
Exception…Exercise induced arterial hypoxemia
No difference
in Time
100
x^
SaO2
95
80
75
x
Acid-Base Regulation
• General terms:
max = 92.7%±1.1
90
85
Does VE Limit Aerobic Power & Endurance?
x^
a) Acids: dissociate H+ in solution
b) Bases: accept H+ to form OH- ions
c) Buffering: minimize changes in pH or [H+]
^
Sea Level
1500m
3000m
*
max = 84.9%±1.6
max = 80.0%±2.0*
70
0.0 1.5 3.0 4.5 6.0 7.5 9.0 10.5 12.0 13.5 15.0
• The term pH designates a quantitative measure of
acidity or alkalinity
a) Concentration of H+
Time (min)
x = LT2
^ = VT
* = significantly different from sea level
3
Regulation of internal pH
• Chemical buffers:
H+ + Buffer
H-Buffer
a) Sodium bicarbonate, phosphate, certain proteins
• Ventilatory buffer:
a) Direct stimulation of respiratory centers &
expiration of excess CO2
• Renal buffer:
a) Long-term maintenance
Blood pH & Blood lactate relationship
Figure 14.13
4