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Ventilatory Control during Thermoneu...

Sackett, James R.

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Ventilatory Control during Thermoneutral Head Out Water Immersion in Humans.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Ventilatory Control during Thermoneutral Head Out Water Immersion in Humans./
作者:	Sackett, James R.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	308 p.
附註:	Source: Dissertation Abstracts International, Volume: 80-02(E), Section: B.
Contained By:	Dissertation Abstracts International80-02B(E).
標題:	Kinesiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10844550
ISBN:	9780438455498

Ventilatory Control during Thermoneutral Head Out Water Immersion in Humans.
Sackett, James R.

Ventilatory Control during Thermoneutral Head Out Water Immersion in Humans. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 308 p.

Source: Dissertation Abstracts International, Volume: 80-02(E), Section: B.

Thesis (Ph.D.)--State University of New York at Buffalo, 2018.

Carbon dioxide (CO2) retention, or elevated arterial or end tidal partial pressure of CO2 (PCO2), occurs during underwater diving and appears to be a consequence of alveolar hypoventilation. Water immersion induces several hemodynamic, hormonal, and ventilatory alterations that may contribute to elevated arterial PCO2. Notably, the chemoreceptors (i.e., peripheral and central) are responsible for blood gas homeostasis during arterial hypercapnia and hypoxemia. However, the effect of water immersion on the chemical control of breathing is currently not known. Thus, there remain a few possible mechanisms that could contribute to elevated arterial PCO 2 during water immersion that have yet to be investigated. This dissertation project consisted of three investigations that aimed at determining the contribution of the chemical control of breathing to elevated arterial PCO2 during thermoneutral head out water immersion (HOWI) in humans.

ISBN: 9780438455498Subjects--Topical Terms:

517627
Kinesiology.

Ventilatory Control during Thermoneutral Head Out Water Immersion in Humans.
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300 $a 308 p.
500 $a Source: Dissertation Abstracts International, Volume: 80-02(E), Section: B.
500 $a Adviser: Blair D. Johnson.
502 $a Thesis (Ph.D.)--State University of New York at Buffalo, 2018.
520 $a Carbon dioxide (CO2) retention, or elevated arterial or end tidal partial pressure of CO2 (PCO2), occurs during underwater diving and appears to be a consequence of alveolar hypoventilation. Water immersion induces several hemodynamic, hormonal, and ventilatory alterations that may contribute to elevated arterial PCO2. Notably, the chemoreceptors (i.e., peripheral and central) are responsible for blood gas homeostasis during arterial hypercapnia and hypoxemia. However, the effect of water immersion on the chemical control of breathing is currently not known. Thus, there remain a few possible mechanisms that could contribute to elevated arterial PCO 2 during water immersion that have yet to be investigated. This dissertation project consisted of three investigations that aimed at determining the contribution of the chemical control of breathing to elevated arterial PCO2 during thermoneutral head out water immersion (HOWI) in humans.
520 $a The peripheral chemoreceptors sense arterial levels of CO2 and oxygen (O2) and contribute to blood gas homeostasis via cardiorespiratory adjustments. In this context, an altered peripheral chemosensitivity could contribute to elevated end tidal PCO2 during water immersion. Thus, our fist investigation tested the hypothesis that peripheral chemosensitivity to hypercapnia and hypoxia is blunted during two hours of thermoneutral HOWI in healthy adults. We assessed the ventilatory, heart rate, and blood pressure responses to acute hypercapnia and acute hypoxia at baseline, 10 minutes, 60 minutes, 120 minutes, and post HOWI (HOWI) and a time-control visit (Control). End tidal partial pressure of CO2 (PCO2) was greater during HOWI vs. Control at 10 minutes, 60 minutes, and 120 minutes, while minute ventilation was greater during HOWI vs. Control at post. The ventilatory, heart rate, and blood pressure responses to acute hypercapnia and acute hypoxia were not different during HOWI vs. Control at any time point. These data indicate that peripheral chemosensitivity is not altered during thermoneutral HOWI. We suggest that an unchanged peripheral chemosensitivity, in the presence of elevated end tidal PCO2, may contribute to augment end tidal PCO2.
520 $a The central chemoreceptors mediate the rise in minute ventilation during arterial hypercapnia via sensing changes in the pH (i.e., H+) of cerebrospinal fluid. To this end, a blunted central chemosensitivity could contribute to CO2 retention during water immersion. Thus, our second investigation tested the hypothesis that central chemosensitivity is blunted during two hours of thermoneutral HOWI in healthy adults. We assessed ventilatory sensitivity to CO2 (i.e., central chemosensitivity) at baseline, 10 minutes, 60 minutes, 90 minutes, 120 minutes, and post HOWI (HOWI) and a time-control visit (Control). The change in end tidal PCO2 was greater throughout HOWI vs. Control, while minute ventilation was not different during HOWI vs. Control. However, central chemosensitivity increased during HOWI and the change in central chemosensitivity was greater throughout HOWI vs. Control. These data indicate that end tidal PCO2 is elevated throughout HOWI despite an augmented central chemosensitivity. Therefore, changes in central chemosensitivity during HOWI likely do not contribute to enhance end tidal PCO2.
520 $a As previously mentioned, end tidal PCO2 and central chemosensitivity are augmented during water immersion. Furthermore, cerebral perfusion increases during thermoneutral water immersion. Our third investigation tested the hypothesis that minute ventilation, ventilatory sensitivity to CO2, cerebral perfusion, and cerebrovascular reactivity to CO2 are augmented during dry conditions while breathing a hypercapnic gas to match the elevated end tidal PCO2 that occurs during HOWI. A rebreathing test was conducted at baseline, 10 minutes, 30 minutes, 60 minutes, and post HOWI (HOWI) and a matched hypercapnia visit (Dry+CO2). End tidal PCO2 increased from baseline throughout HOWI and Dry+CO2 and was matched between conditions. Although minute ventilation was augmented during Dry+CO2 and not HOWI, ventilatory sensitivity to CO 2 was augmented during HOWI and not Dry+CO2. Middle cerebral artery blood velocity increased during HOWI, while it remained unchanged throughout Dry+CO2. However, cerebrovascular reactivity to CO2 was attenuated during both conditions. These data indicate that an augmented ventilatory sensitivity to CO2 and cerebral perfusion during HOWI do not appear to be related to the increases in end tidal PCO2. On the other hand, an attenuated cerebrovascular reactivity to CO2 appears to be modulated, in part, by elevated end tidal PCO2 during HOWI. (Abstract shortened by ProQuest.).
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