Chapter14 Dynamics of Pulmonary Ventilation (2).ppt

Copyright © 2007 Lippincott Williams & Wilkins. McArdle, Katch, and Katch: Exercise Physiology: Energy,
Nutrition, and Human Performance, Sixth Edition
Chapter 14
Dynamics of Pulmonary Ventilation

Ventilatory Control
• Complex mechanisms adjust rate and depth
of breathing in response to metabolic
needs.
• Neural circuits relay information.
• Receptors in various tissues monitor pH,
PCO2, PO2, and temperature.

Neural Factors
• Medulla contains respiratory center
• Neurons activate diaphragm and intercostals
• Neural center in the hypothalamus integrates
input from descending neurons to influence
the duration and intensity of respiratory
cycle

Humoral Factors
• At rest, chemical state of blood exerts the
greatest control of pulmonary ventilation

Plasma PO2 and Peripheral
Chemoreceptors
• Peripheral chemoreceptors are located in
aorta and carotid arteries
• Monitor PO2
• During exercise
– PCO2 increases
– Temperature increases
– Decreased pH stimulates peripheral
chemoreceptors

Hyperventilation & Breath Holding
• Hyperventilation decreases alveolar PCO2 to
near ambient levels.
• This increases breath-holding time.

Regulation of Ventilation
During Exercise
• Chemical control
– Does not entirely account for increased
ventilation during exercise

Nonchemical Control
• Neurogenic factors
– Cortical influence
– Peripheral influence
• Temperature has little influence on
respiratory rate during exercise.

Integrated Regulation During
Exercise
• Phase I (beginning of exercise): Neurogenic
stimuli from cortex increase respiration.
• Phase II: After about 20 seconds, VE rises
exponentially to reach steady state.
– Central command
– 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

Ventilation and Energy
Demands
• Exercise places the most profound
physiologic stress on the respiratory
system.

Ventilation in Steady-Rate
Exercise
• During light to moderate exercise
– Ventilation increases linearly with O2
consumption and CO2 production

Ventilatory Equivalent
• TVE / O2
• Normal values ~ 25 in adults
– 25 L air breathed / LO2 consumed
• Normal values ~ 32 in children
V


Ventilation in Non–Steady-Rate
Exercise
• VE rises sharply and the ventilatory
equivalent rises as high as 35 – 40 L of air
per liter of oxygen.

Ventilatory Threshold VT
• The point at which pulmonary vent increases
disproportionately with O2 consumption during
exercise
• Sodium bicarbonate in the blood buffers almost all
of the lactate generated via glycolysis.
• As lactate is buffered, CO2 is regenerated from the
bicarbonate, stimulating ventilation.

Onset of Blood Lactation
Accumulation
• Lactate threshold
– Describes highest O2 consumption of exercise
intensity with less than a 1-mM per liter increase
in blood lactate above resting level
• OBLA signifies when blood lactate shows a
systemic increase equal to 4.0 mM.

Specificity of OBLA
• OBLA differs with exercise mode due to
muscle mass being activated.
• OBLA occurs at lower exercise levels during
cycling of arm-crank exercise.

Some Independence Between OBLA
and O2max
• Factors influencing ability to sustain a
percentage of aerobic capacity without
lactate accumulation
– Muscle fiber type
– Capillary density
– Mitochondria size and number
– Enzyme concentration
V


Energy Cost of Breathing
• At rest and during light exercise, the O2 cost
of breathing is small.
• During maximal exercise, the respiratory
muscles require a significant portion of total
blood flow (up to 15%).

Respiratory Disease
• COPD may triple the O2 cost of breathing
at rest.
• This severely limits exercise capacity in
COPD patients.

Cigarette Smoking
• Increased airway resistance
• Increased rates of asthma and related
symptoms
• Smoking increases reliance on CHO during
exercise.
• Smoking blunts HR response to exercise.

Does Ventilation Limit Aerobic
Power and Endurance?
• Healthy individuals overbreathe at higher
levels of O2 consumption.
• At max exercise, there usually is a breathing
reserve.
• Ventilation in healthy individuals is not the
limiting factor in exercise.

An Important Exception
• Exercise-induced arterial hypoxemia may
occur in elite endurance athletes.
• Potential mechanisms include
– V/Q inequalities
– Shunting of blood flow bypassing alveolar
capillaries
– Failure to achieve end-capillary PO2
equilibrium

Acid–Base Regulation
• Buffering
– Acids dissociate in solution and release H+.
– Bases accept H+ to form OH− ions.
– Buffers minimize changes in pH.

Acid–Base Regulation
• Alkalosis increases pH.
• Acidosis decreases pH.
• Three mechanisms help regulate internal
pH.
– Chemical buffers
– Pulmonary ventilation
– Renal function

Chemical Buffers
• Chemical buffers consist of a weak acid
and the salt of that acid.
• Bicarbonate buffers = weak acid, carbonic
acid, salt of the acid, and sodium
bicarbonate

Bicarbonate Buffers
• Result of acidosis
H2O + CO2  H2CO3  H+ + HCO3
−
• Result of alkalosis
H2O + CO2  H2CO3  H+ + HCO3
−

Phosphate Buffer
• Phosphoric acid and sodium phosphate
• Exerts effects in renal tubules and
intracellular fluids

Protein Buffer
• Intracellular proteins possess free radicals
that, when dissociated, form OH−, which
reacts with H+ to form H2O.
• Hemoglobin is the most important protein
buffer.

Physiologic Buffers
• Ventilatory buffer
– Increase in free H+ stimulates ventilation
– Increase ventilation, decrease PCO2
• Lower plasma PCO2 accelerates
recombination of H+ + HCO3
−, lowering H+
concentration

Renal Buffer
• Kidneys regulate acidity by secreting
ammonia and H+ into urine and reabsorbing
chloride and bicarbonate.

Effects of Intense Exercise
• During exercise, pH decreases as CO2 and
lactate production increase.
• Low levels of pH are not well tolerated and
need to be quickly buffered.

Chapter14 Dynamics of Pulmonary Ventilation (2).ppt

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Chapter14 Dynamics of Pulmonary Ventilation (2).ppt