Pulmonary Ventilation and Respiration

Dynamics of Pulmonary Ventilation

• Pulmonary ventilation involves the movement of air into and out of the lungs
• Minute ventilation (VE) is measured in liters per minute (L/min)

Anatomy of the Respiratory System

• The respiratory system has a conducting zone and a respiratory zone
• Airflow through the conducting zone has elements that include cartilaginous rings, smooth muscle walls, sympathetic nervous system stimulation (beta receptors), and inflammation/allergens
• The conducting zone provides protection via mucus secretion, phagocyte activity, warming, humidifying air and phonation through the larynx and vocal cords
• Type I epithelial cells are thin, flat, and facilitate gas exchange, while Type II epithelial cells secrete pulmonary surfactant
• Pulmonary capillaries completely surround each alveolus
• Interstitial space provides diffusion distance for O2 and CO2

Respiration and Gas Exchange

• Gas exchange in tissues occurs both internally and externally
• Respiration gains energy by reacting glucose and O2, which results in H2O and CO2

Pulmonary Ventilation

• Air movement occurs in response to pressure changes
• Boyle’s Law indicates that there is an inverse relationship between volume and pressure
• Gas/air moves from areas of high to low pressure
• During inspiration, the diaphragm lowers, which reduces pressure and increases volume, which results in air rushing into the lungs
• During expiration, the diaphragm recoils and the rib cage falls, which increases pressure and reduces volume, which results in air rushing out of the lungs

Inspiratory and Expiratory Muscles

• Inspiratory Muscles: Increase volume and decrease pressure
  • Diaphragm: principle muscle inspiration
  • External and internal intercostal muscles
  • Pectoralis minor
  • Scalenes, sternocleidomastoid muscles
  • Maximal exercise: trapezium
• Expiratory Muscles: Decrease volume and increase pressure
  • Relaxation of diaphragm
  • Abdominal muscles
  • Internal intercostal muscles & obliques

The Cost of Breathing

• Oxygen is required for respiratory muscles to operate
• The diaphragm is a good endurance muscle
• Oxygen cost per liter of ventilation (VE) more than doubles from low to high exercise intensity
• Low-intensity exercise lung uses 3-6% of total VO2
• High-intensity exercise lung uses 10-15% of total VO2

Energy Cost of Breathing

• The oxygen requirement of breathing at rest and during light-to-moderate exercise is low
• In exercise where VE ≥100 L/min, O2 cost = 1.5 to 2.0 mL O2/L air breathed per min, or 3 to 5% of total VO2 in moderate exercise, and 8 to 11% for VE at VO2max
• For highly trained endurance athletes with VE ≥ 150 L/min, the energy cost of exercise hyperpnea equals or exceeds 15% of total VO2

Energy Cost of Breathing: Respiratory Disease and Smoking

• Chronic obstructive pulmonary disease (COPD) results in 3x the normal cost of breathing at rest
• COPD severely limits the exercise capacity of individuals
• Smokers have lower dynamic lung function, which can result in into COPD
• Chronic smoking obstructs airways and slows normal lung development in adolescents
• Children who smoke have higher rates of asthma and reduced dynamic lung function
• Airway resistance at rest increases 3x in chronic smokers and nonsmokers following 15 puffs

Regulation of Pulmonary Ventilation

• Complex mechanisms adjust breathing rate and depth
• Intricate neural circuits relay information from higher brain centers, the lungs, and other bodily sensors to coordinate ventilatory control
• The gaseous and chemical states of the blood that surrounds the medulla and aortic and carotid artery chemoreceptors also mediate alveolar ventilation, maintaining relatively constant alveolar gas pressures during exercise

Control of Ventilation

• Peripheral chemoreceptors are acted upon, but decreases in PO2 depress central chemoreceptors
• The peripheral chemoreceptors are relatively insensitive unless potentiated by increased PCO2
• Chemoreceptors respond to PO2, not O2 content (e.g., not to anemia or CO poisoning)
  • Central and peripheral chemoreceptors are responsive to increased PCO2
    • The central chemoreceptors are the most important regulators, acting through increased [H+] (decreased pH)
  • Increased PCO2 acts via decreased pH
    • Decreased pH also comes from other sources (e.g., metabolism)

Increased Ventilation and Exercise

• Exercise increases respiration, but levels of CO2, O2, and pH do not change
• Lungs inflate from the inherent activity of inspiratory neurons with cell bodies in the medulla
• Inspiratory neurons cease firing because of self-limitations and the inhibitory influence of expiratory neurons
• During exercise, ventilatory adjustments occur from ascending neural signals

Humoral Factors

• The blood’s chemical state exerts the greatest control on pulmonary ventilation at rest
• Variations in arterial Po2, Pco2, pH, and temperature activate sensitive neural units
• These neural units are in the medulla (central chemoreceptors) and arterial system (peripheral chemoreceptors) and adjust ventilation to maintain blood chemistry

Plasma O2 and Peripheral Chemoreceptors

• Peripheral chemoreceptors control sensitivity to reduced O2 pressure
• Carotid bodies monitor the state of arterial blood before it perfuses brain tissues
• Decreased arterial Po2 increases alveolar ventilation through aortic and carotid chemoreceptor stimulation These receptors protect against reduced oxygen pressure in inspired air
• Bearing in mind that Po2 is rarely influencing ventilation during exercise
• May be impactful in cases of high-altitude or lung disease
• Peripheral chemoreceptors stimulate ventilation during exercise by increases in temperature, acidity (H+), CO2, and K+ concentrations

Plasma CO2 and H+ Concentration

• At rest, Pco2 in arterial plasma provides an important respiratory stimulus
• Small increases in Pco2 in inspired air cause larger increases in minute ventilation (e.g., 1 mm Hg rise in Pco2 results in a 2 L/m increase in VE)
• Plasma acidity, which varies with the blood's CO2 content, exerts a strong command over ventilation
• A fall in blood pH signals acidosis
• Signifies that there is CO2 retention and carbonic acid formation

Hyperventilation and Breath Holding

• After breath-hold, it takes ~40s for the urge to breathe to predominate
  • Comes from increased arterial Pco2 and H+ concentration
  • The breakpoint for breath holding = 50 mm Hg Pco2
• Hyperventilating before breath holding lowers alveolar Pco2 to 15 mm Hg
  • This decreases arterial Pco2, extending breath-holding duration until arterial Pco2 and/or H+ concentration rise to cause urge to breathe

Regulation of Ventilation During Physical Activity

• As exercise intensity increases, alveolar Po2 does not decrease to an extent that increases ventilation through chemoreceptor stimulation
• Large ventilatory volumes result
• During intense exercise alveolar Po2 rises, hastening oxygenation of blood in alveolar capillaries
• Pulmonary ventilation during light and moderate exercise closely couples with metabolism and increases proportional to VO2 and VCO2
• Neurogenic factors for ventilatory control include cortical and peripheral influences Cortical influence: Neural outflow stimulates respiratory neurons
  • Impulses from motor cortex and cortical activation in anticipation of exercise stimulates in the medulla, beginning abrupt increase in exercise ventilation Peripheral influence: Sensory input from joints, tendons and muscles throughout exercise adjusts ventilation
• Except for extreme hyperthermia, an increase in core temperature exerts little effect on ventilatory regulation during exercise

Integrated Regulation of Ventilation During Physical Activity

• There are three phases during exercise and recovery:
  • Phase I: Neurogenic stimuli from cerebral cortex and feedback from active limbs stimulate the medulla to abruptly increase ventilation
  • Phase II: After a brief plateau, ventilation rises exponentially to achieve a steady rate related to metabolic gas exchange demands
  • Phase III: Fine-tuning of steady-rate ventilation through peripheral sensory feedback mechanisms
• There are two factors that impact the abrupt decline in ventilation when exercise ceases:
  • Removal of central command drive
  • Decreased sensory input from previously active muscles
• Slower recovery phase results from two factors
  • Gradual diminution of short-term potentiation of respiratory center Re-establishment of body's normal metabolic, thermal, and chemical milieu
• With exercise, O2 diffuses from alveoli into venous blood as it returns to lungs, with CO2 moving from blood into alveoli
• Increased alveolar ventilation maintains the proper gas concentrations to facilitate rapid gas exchange
• Physical activity has the most profound effect on VE, VO2, and VCO2 dynamics

Ventilation in Steady-Rate Physical Activity

• During light-to-moderate exercise, VE increases linearly with VO2 and VCO2
• The average ventilation is 20 to 25L, with of ventilation for each litre of oxygen consumed
• Alveolar Po2 and Pco2 remain near resting levels because of the adjustments

Ventilatory Equivalent

• The ventilatory equivalent is symbolised by VE/VO2
• During submaximal exercise, VE/VO2 = 25L for healthy young adults up to ~55% VO2max
  • Higher VE/VO2 values occur in children and average 32L
  • Exercise mode affects VE/VO2
  • Training reduces VE/VO2 during submaximal exercise

Ventilation in Non-Steady-Rate Physical Activity

• At intense submaximal exercise, VE increases upward to increase disproportionately in relation to VO2
• VE/VO2 can attain values of 35 or 40L air breathed per L VO2 in exhaustive exercise

Ventilatory Threshold (Tvent)

• Ventilatory Threshold marks the point where pulmonary VE increases disproportionately to VO2 during graded exercise
• Terms for this: expiratory compensation threshold; anaerobic threshold, onset of blood lactate accumulation; aerobic-anaerobic threshold;
• Other terms: onset of plasma lactate accumulation; individual anaerobic threshold; point of metabolic acidosis
• Stimulating effects of CO2 released buffers accumulating lactate and H+ resulting in excess ventilation
• Excess CO2 causes RER ≥ 1.0

Onset of Blood Lactate Accumulation (OBLA)

• Lactate threshold (LT) describes highest VO2 or exercise intensity before a 1.0 mM increase in blood lactate concentration
• OBLA signifies when blood lactate concentration systematically increases to 4.0 mM

Factors that Impact Lactate Threshold

• Imbalance between rate of glycolysis and mitochondrial respiration
• Decreased redox potential (increased NADH relative to NAD+)
• Lowered blood O2 content
• Lowered blood flow to muscle

Lactate Threshold Measurement

• Lactate Threshold measurement is a sensitive indicator of aerobic training status
• It predicts endurance performance, often with greater accuracy than VO2max
• It establishes effective training intensity geared to active muscles' aerobic metabolic dynamics