AbstractRecently, endurance athletes and high altitude climbers have gained access to commercially available, portable normobaric hypoxic chambers. Intermittent exposures to hypoxia in these chambers may elicit adaptations similar to those observed during acclimatization to altitude. Manufactures of these systems purport that intermittent exposures may elicit adaptations similar to those observed in response to the hypoxia of high altitude, however there have been no reports in the scientific literature that ventilatory acclimatization or alterations in cerebrovascular dynamics occur following repeated episodes in the portable chambers.
The goal of this dissertation is to provide a detailed investigation into the physiologic and symptomatic responses following an intervention of discontinuous normobaric hypoxia, which employs portable chambers. To accomplish this, an intermittent protocol was developed which cycled between 8 hrs of nocturnal hypoxia at a simulated altitude of 4300m, followed by 16 hrs of normoxia, for five consecutive days. Specifically, it is not currently known if cerebrovascular and ventilatory sensitivities to acute hypoxia are altered, or if altitude-like symptoms develop, in response to such an intermittent hypoxic protocol.
The studies within the thesis are separated into four distinct phases, which were conducted sequentially. This sequential construction of the thesis was necessary because the results of each phase helped to finalize the research protocol for each subsequent investigation. The following summary outlines the progression and key findings related to the series of experiments. A critical comparison between the non-invasive measurements of oxygen saturation with direct blood measurements revealed that pulse oximetry is a reliable method to monitor levels of hypoxemia during mild to moderate exposures of normobaric hypoxia. Subsequently, in order to establish a method for the quantification of cerebrovascular and ventilatory responses to acute variations in O2 and CO2 a sophisticated protocol was designed utilizing the technique of end-tidal forcing. This protocol was successful in replicating measurements in control subjects overtime, and therefore was deemed capable of quantifying alterations in cerebrovascular and ventilatory sensitivities arising from chronic or intermittent hypoxic exposures. An intervention consisting of five consecutive overnight normobaric hypoxic exposures was then implemented, and the protocol was used to determine the extent and time frame for the development and reversibility of physiological and symptomatic modifications.
From the studies described above, the main conclusions are that an intermittent normobaric hypoxic
intervention, consisting of five consecutive overnight exposures to a simulated altitude of 4300m, elicits
perturbations in the acute cerebrovascular and ventilatory responses to both hypoxia and hypercapnia,
which are similar to changes following chronic altitude exposure. Individual variability to intermittent
hypoxia may have an impact on the rate at which the process of acclimatization proceeds. The extent of
physiological and symptomatic responses to intermittent hypoxia are likely to be associated with the
severity of hypoxia as well as the length and number of recurrent episodes of hypoxia.