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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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Fig 10.13

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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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Fig 10.14

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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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Fig 10.17

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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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Fig 10.18

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Fig 10.19

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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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Fig 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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Fig 10.24

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Fig 10.25

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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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Fig 10.26

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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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Fig 10.27

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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