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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