copyright © 2007 lippincott williams & wilkins.mcardle, katch, and katch: exercise physiology:...

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

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

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 alkalosisH2O + 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.

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