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Lecture 5

Ve-Lecture 5.docx

3 Pages
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Department
Kinesiology
Course Code
Kinesiology 2230A/B
Professor
Glen Belfry

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The Bends - Returning to the surface nitrogen gas will bubble within the body Last day - Arterial blood and muscle pH - Ventilatory control o Neural – respiratory centres  Peripheral input  Cerb  Voluntarily change resp rate (hyperventilate)  Decrease in resp rate originates in medulla  Receives information to dictate to increase or decrease resp rate Respiratory Neurons - Inherent activity of inspiratory neurons in medial portion of the medulla - Theses neurons activate diaphragm and intercostals - Inhibitory influence of expiratory neurons Neural control - Resp rate will increase as soon as exercise begins - Receiving info from stretch receptors from lung, can override these to increase tidal volume - Insp/exp centres act upon external intercostals and diaphragm - Exp Ventilatory Control - Chemical - H - PCO2, PO2, K - - K associated with changes of K, increase in vent increase in K - - changes in temperature Chemical Control - Aortic arch: changes of pressure (systemic circle) - Exits heart, aorta bodies monitor changes in pressure - Peripheral chemoreceptors monitor changes in pH, PCO2 and PO2 - Central chemoreceptors measure changes in pH and PCO2 - At rest most important stimulus is PCO2 in arterial plasma - Central chemoreceptors are not sensitive to changes in PO2 of cerebral blood or CSF Graph - Ve increases if PO2 falls below 60mmHg - Significant drops in PP does not change response % in “buffer zone” - Hit around 75, response % increases drastically - Blunting of ventilation when looking at PP changes of O2 o In comparison to changes of PCO2 - A - Ventilator responses to hypoxia at three different levels of arterial PCO2 and PO2 - 38 torr (mmhg): big changes in ventilation at 60mmhg (normal conditions) - 45 torr: high PO2, ventilation has increased ( doubled), response in vent change occurs much sooner o Added rel
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