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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