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Intermittent hypoxia : cardiorespiratory and cerebrovascular consequences to acute hypoxia and submaximal exercise

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Title: Intermittent hypoxia : cardiorespiratory and cerebrovascular consequences to acute hypoxia and submaximal exercise
Author: Querido, Jordan S
Degree Master of Science - MSc
Program Human Kinetics
Copyright Date: 2007
Abstract: Intermittent hypoxia (IH) is broadly defined as repeatedly breathing decreased amounts of oxygen (hypoxia) interspersed with periods of room air breathing (normoxia). In animal, human diseased, and healthy human models, research has shown IH to negatively affect cerebrovascular vessel dilation. We have previously shown poikilocapnic (uncontrolled carbon dioxide (CO₂)) IH to blunt the vasodilatory response of a cerebral vessel during acute hypoxia. The purpose of this study was to measure the ventilatory, cardiovascular and cerebrovascular responses to: I) acute hypoxia and; II) to submaximal exercise following an isocapnic (controlled CO₂) IH protocol. Healthy males (n = 9) with normal pulmonary function underwent 10 consecutive days of isocapnic IH (oxyhaemoglobin saturation (SaO₂) = 80%, 1 hr/day). Ventilatory, cardiovascular, and cerebrovascular (transcranial Doppler) responses to acute isocapnic hypoxia (SaO₂ = 80%, 5 minutes) were measured before (PRE-IH) and after (POST-IH) IH. Also, ventilatory, cardiovascular, and cerebrovascular parameters were measured during a submaximal cycle exercise test (50, 100, 150 watts) PRE-IH and POST-IH. To further investigate cerebrovascular regulation during exercise, 5% CO₂ was added for two minutes of each exercise stage. Over the 10 days of IH, there was a significant increase in minute ventilation (VE) during the IH bouts (p<0.05). IH did not significantly alter the ventilatory, cardiovascular, and cerebrovascular responses to acute hypoxia. However, there was a significant association (r = 0.86, p<0.05) between the change in the mean arterial blood pressure (MAP) and mean middle cerebral arterial blood flow velocity (MCAVm) responses to acute hypoxia. Exercise caused significant increases in VE , MCAVm, and MAP (p<0.05), but there were no differences in measured variables between PRE-IH and POST-IH exercise trials (p>0.05). Similarly, hypercapnia caused significant increases in VE and MCAVm (p<0.05), although the magnitude of the response did not change following IH. Our results suggest that the effect of IH on ventilatory, cardiovascular, and cerebrovascular regulation during acute hypoxia is individualistic, and changes in the MAP response may strongly influence the changes in cerebral blood flow (CBF). Also, our results suggest that IH does not alter ventilatory, cardiovascular, or cerebrovascular regulation during submaximal exercise or responsiveness to hypercapnia.
URI: http://hdl.handle.net/2429/32125
Series/Report no. UBC Retrospective Theses Digitization Project [http://www.library.ubc.ca/archives/retro_theses/]
Scholarly Level: Graduate

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