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8/8/2019 EP edit new
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Explain the principle physiological functionof the pulmonary system
Outline the major anatomical componentsof the respiratory system
List major muscles involved in inspiration &expiration at rest & during exercise
Discuss the importance of matching bloodflow to alveolar ventilation in the lung
Explain how gases are transported acrossthe blood-gas interface in the lung
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Discuss the major transportation modes
of O2 & CO2 in the blood
Discuss the effects of o temp, q pH, & olevels of 2,3 DPG on the oxygen-
hemoglobin dissociation curve
Describe the ventilatory response to
constant load, steady-state exercise
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Ventilation/perfusion ratio¾ Indicates matching of blood flow to
ventilation¾ Ideal: ~1.0
Base¾ Overperfused (ratio <1.0)
Apex¾ Underperfused (ratio >1.0)
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Approximately 99% of O2 is
transported in the blood bound to
hemoglobin (Hb)¾ Oxyhemoglobin: O2 bound to Hb
¾ Deoxyhemoglobin: O2 not bound to Hb
Amount of O2 that can be transported
per unit volume of blood independent on the concentration of
hemoglobin
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Blood pH declinesduring heavy
exercise Results in a
´rightwardµ shift ofthe curve
¾ Bohr effect
¾ Favors ´offloadingµof O2 to the tissues
Fig 10.15
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Increased bloodtemperature
results in aweaker Hb-O2
bond
Rightward shift
of curve¾ Easier ´offloadingµ ofO2 at tissues
Fig 10.16
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RBC must rely on anaerobic glycolysis tomeet the cell·s energy demands
Aby-product is 2-3 DPG, which cancombine with hemoglobin and reduce
hemoglobin·s affinity of O2
2-3 DPG increase during exposure toaltitude
At sea level, right shift of of curve not tochanges in 2-3 DPG, but to degree ofacidosis and blood tempurature
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Myoglobin (Mb) shuttles O2 from the cell
membrane to the mitochondria
Higher affinity for O2 than hemoglobin¾ Even at low PO2
¾ Allows Mb to store O2
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Dissolved in plasma (10%)
Bound to Hb (20%)
Bicarbonate (70%)
¾ CO2 + H2Om H2CO3m H+ + HCO3-
¾ Also important for buffering H+
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Initially,ventilation
increasesrapidly
¾ Then, a slower rise towardsteady-state
PO2 and PCO2
are maintained
Fig 10.20
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During prolongedsubmaximal
exercise:¾ Ventilation tends
to drift upward
¾ Little change inPCO2
¾ Higher ventilationnot due toincreased PCO2
Fig 10.21
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Linear increase in ventilation
¾ Up to ~50-75% VO2max
Exponential increase beyond this point
Ventilatory threshold (Tvent)
¾ Inflection point where VE increases
exponentially
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In the trained runner
¾
Decrease in arterial PO2 near exhaustion¾ pH maintained at a higher work rate
¾ Tvent occurs at a higher work rateFig 10.22
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1980·s: 40-50% of elite male enduranceathletes were capable of developing
1990·s: 25-51% of elite female enduranceathletes were also capable ofdeveloping
Causes:
¾ Ventilation-perfusion mismatch¾ Diffusion limitations due to reduce time of
RBC in pulmonary capillaries due to highcardiac outputs
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Respiratorycontrol center ¾
Receives neuraland humoral input
x Feedback frommuscles
x CO2 level in the
blood¾ Regulates
respiratory rate
Fig 10.23
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Humoral chemoreceptors¾ Central chemoreceptors
x Located in the medulla
x PCO2 and H+
concentration in cerebrospinalfluid
¾ Peripheral chemoreceptors
x Aortic and carotid bodies
x PO2, PCO
2, H+, and K+ in blood
Neural input¾ From motor cortex or skeletal muscle
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Submaximal exercise
¾ Linear increase due to:
x Central commandx Humoral chemoreceptors
x Neural feedback
Heavy exercise
¾ Exponential rise above Tvent
x Increasing blood H+
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Ventilation is lower at same work rate
following training
¾ May be due to lower blood lactic acid levels¾ Results in less feedback to stimulate
breathing
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Low-to-moderate intensity exercise
¾ Pulmonary system not seen as a limitation
Maximal exercise¾ Not thought to be a limitation in healthy
individuals at sea level
¾ May be limiting in elite endurance athletes
¾ New evidence that respiratory musclefatigue does occur during high intensityexercise