Thesis (M.S.)--University of Hawaii at Manoa, 2006. / Includes bibliographical references (leaves 41-47). / vii, 77 leaves, bound 29 cm

Thesis (M.S.)--University of Hawaii at Manoa, 2006. / Includes bibliographical references (leaves 101-105). / x, 105 leaves, bound ill. 29 cm

Thesis (M.S.)--University of Hawaii at Manoa, 2006. / Includes bibliographical references (leaves 26-28). / ix, 77 leaves, bound ill. 29 cm

Master of Science (Medicine) / Clinical studies have demonstrated an arousal deficit in infants suffering Obstructive Sleep Apnoea (OSA), and that treatment to alleviate the symptoms of OSA appears to reverse the deficit in arousability. Some sudden infant deaths are thought to be contingent upon such an arousal deficit. This research utilised young piglets during early postnatal development, and exposed them to intermittent hypercapnic hypoxia (IHH) as a model of clinical respiratory diseases. Arousal responses of control animals were compared to the animals exposed to IHH. Comparisons were also made between successive exposures on the first and the fourth consecutive days of IHH. Time to arouse after the onset of the respiratory stimulus, and frequency of arousals during recovery, demonstrated that arousal deficits arose after successive exposures and that these were further exacerbated on the fourth study day. After an overnight recovery period, the arousal deficit was apparently dormant, and only triggered by HH exposure. These studies confirm that both acute and chronic deficits can be induced on a background of otherwise normal postnatal development, suggesting that deficits observed in the clinical setting may be a secondary phenomenon.

Bibliography: leaves 246-280. / xxi, 280 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Identifies that exercise-induced hypoxemia occurs at a much lower exercise intensity than reported previously and that exercise mode changes the severity of the phenomonen. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1999

Master of Science (Medicine) / Clinical studies have demonstrated an arousal deficit in infants suffering Obstructive Sleep Apnoea (OSA), and that treatment to alleviate the symptoms of OSA appears to reverse the deficit in arousability. Some sudden infant deaths are thought to be contingent upon such an arousal deficit. This research utilised young piglets during early postnatal development, and exposed them to intermittent hypercapnic hypoxia (IHH) as a model of clinical respiratory diseases. Arousal responses of control animals were compared to the animals exposed to IHH. Comparisons were also made between successive exposures on the first and the fourth consecutive days of IHH. Time to arouse after the onset of the respiratory stimulus, and frequency of arousals during recovery, demonstrated that arousal deficits arose after successive exposures and that these were further exacerbated on the fourth study day. After an overnight recovery period, the arousal deficit was apparently dormant, and only triggered by HH exposure. These studies confirm that both acute and chronic deficits can be induced on a background of otherwise normal postnatal development, suggesting that deficits observed in the clinical setting may be a secondary phenomenon.

Abstract not available

The primary purpose of this doctoral dissertation was to investigate the effect of body temperature responses at physiologically relevant sites during an incremental exercise test on the phenomenon of exercise-induced hypoxemia (EIH). This phenomenon has been considered as an important limitation to physical performance with a prevalence of ~50 % in trained male athletes, but described in both sexes, across the range of both age and physical fitness in more recent literature. Previously this phenomenon has been described as a decrement in both arterial oxygen partial pressure (PaO₂) and oxy-haemoglobin saturation (SaO₂or SpO₂) with, particularly important for PaO₂, a lack of or inappropriate correction made for the change in body temperature during intense exercise. The initial study of this thesis determined the thermal response within the body at physiologically relevant sites measured simultaneously during an incremental exercise test. The results demonstrated the inadequacy of rectal temperature as an indicator of the acute temperature changes occurring during an incremental exercise test due to its slow response rate and relative thermal inertia. Radial arterial blood and oesophageal temperatures were shown to behave almost identically during the exercise test, albeit with an offset of approximately 1.3ºC, and were considered much more appropriate and relevant indicators of thermal changes during exercise. As an extension of the initial work active muscle temperature (vastus lateralis) was measured during the exercise test, demonstrating a significantly lower resting temperature than the oft-reported “core” temperatures (rectal and oesophageal) as well as a significantly greater increase in temperature in comparison to all other measurement sites. Overall, the results of this first study indicated that the physiologically relevant temperatures measured at the oesophageal and muscle sites differed markedly to the outdated rectal temperature measurement site and should be used as measures of thermal response when evaluating oxygen loading (oesophageal) or unloading (active muscle). Utilising the definition of EIH as a decrease in PaO₂ of ≥ 10 mmHg, the effect of temperature correcting PaO₂ was evaluated in the second study. Arterial blood gases measured simultaneously to the temperature measurements during the incremental exercise test were adjusted for the temperature changes at each site (every 1ºC increase in temperature will increase a PaO₂ value by ~5 mmHg). Whilst uncorrected PaO₂ values indicated an almost 100% prevalence of EIH in this group, oesophageal temperature corrected PaO₂ values decreased this prevalence to ~50% while muscle temperature corrections resolved all cases of EIH and demonstrated an HYPEROXAEMIA (i.e. the reverse of the well-established phenomenon) in the majority of subjects. Further investigation of arterial oxygen content during the exercise test indicates that there is no disruption in the delivery of oxygen to the active muscles and therefore any performance decrement should be attributed to another mechanism. Whilst the phenomenon of EIH is determined by the definition applied and the use of temperature corrections in the case of PaO₂, its reproducibility in a test-retest situation had not previously been determined. Utilising a subset of previously tested subjects, the reproducibility of both temperature and PaO₂ were determined with results indicating that the blood gas response was highly reproducible, especially the minimum PaO₂ value noted during each exercise test. However, comparing a more statistically relevant definition of a change in PaO₂ of ± 2 standard deviations from the mean resting PaO₂ to the previous delimiter of 10 mmHg indicated a lesser reproducibility of the prevalence of EIH. In summary, this thesis exposes the inadequacies of previous research into EIH with regard to the expected reproducibility of the phenomenon and the need to correctly adjust PaO₂ values for exercise-induce hyperthermia as well as demonstrating the difference in thermal responses to acute exercise in physiologically significant areas of the body. Furthermore, previously described correlations between the change in PaO₂ and VO₂ max were not evident in the subjects tested within this thesis, nor was there any indication of a diffusion limitation based on reduced pulmonary capillary transit time (by association with VO₂ max) or pulmonary oedema (rebuked by a rapid return of PaO₂ to above resting levels following exercise cessation). / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1320633 / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2008

Includes list of publications arising from this thesis / Erratum attached to inside back cover. / "25/03/2004." / Includes bibliographical references (leaves 185-257) / xii, 257 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine and Royal Adelaide Hospital, Rheumatology Unit, 2004

The primary purpose of this doctoral dissertation was to investigate the effect of body temperature responses at physiologically relevant sites during an incremental exercise test on the phenomenon of exercise-induced hypoxemia (EIH). This phenomenon has been considered as an important limitation to physical performance with a prevalence of ~50 % in trained male athletes, but described in both sexes, across the range of both age and physical fitness in more recent literature. Previously this phenomenon has been described as a decrement in both arterial oxygen partial pressure (PaO₂) and oxy-haemoglobin saturation (SaO₂or SpO₂) with, particularly important for PaO₂, a lack of or inappropriate correction made for the change in body temperature during intense exercise. The initial study of this thesis determined the thermal response within the body at physiologically relevant sites measured simultaneously during an incremental exercise test. The results demonstrated the inadequacy of rectal temperature as an indicator of the acute temperature changes occurring during an incremental exercise test due to its slow response rate and relative thermal inertia. Radial arterial blood and oesophageal temperatures were shown to behave almost identically during the exercise test, albeit with an offset of approximately 1.3ºC, and were considered much more appropriate and relevant indicators of thermal changes during exercise. As an extension of the initial work active muscle temperature (vastus lateralis) was measured during the exercise test, demonstrating a significantly lower resting temperature than the oft-reported “core” temperatures (rectal and oesophageal) as well as a significantly greater increase in temperature in comparison to all other measurement sites. Overall, the results of this first study indicated that the physiologically relevant temperatures measured at the oesophageal and muscle sites differed markedly to the outdated rectal temperature measurement site and should be used as measures of thermal response when evaluating oxygen loading (oesophageal) or unloading (active muscle). Utilising the definition of EIH as a decrease in PaO₂ of ≥ 10 mmHg, the effect of temperature correcting PaO₂ was evaluated in the second study. Arterial blood gases measured simultaneously to the temperature measurements during the incremental exercise test were adjusted for the temperature changes at each site (every 1ºC increase in temperature will increase a PaO₂ value by ~5 mmHg). Whilst uncorrected PaO₂ values indicated an almost 100% prevalence of EIH in this group, oesophageal temperature corrected PaO₂ values decreased this prevalence to ~50% while muscle temperature corrections resolved all cases of EIH and demonstrated an HYPEROXAEMIA (i.e. the reverse of the well-established phenomenon) in the majority of subjects. Further investigation of arterial oxygen content during the exercise test indicates that there is no disruption in the delivery of oxygen to the active muscles and therefore any performance decrement should be attributed to another mechanism. Whilst the phenomenon of EIH is determined by the definition applied and the use of temperature corrections in the case of PaO₂, its reproducibility in a test-retest situation had not previously been determined. Utilising a subset of previously tested subjects, the reproducibility of both temperature and PaO₂ were determined with results indicating that the blood gas response was highly reproducible, especially the minimum PaO₂ value noted during each exercise test. However, comparing a more statistically relevant definition of a change in PaO₂ of ± 2 standard deviations from the mean resting PaO₂ to the previous delimiter of 10 mmHg indicated a lesser reproducibility of the prevalence of EIH. In summary, this thesis exposes the inadequacies of previous research into EIH with regard to the expected reproducibility of the phenomenon and the need to correctly adjust PaO₂ values for exercise-induce hyperthermia as well as demonstrating the difference in thermal responses to acute exercise in physiologically significant areas of the body. Furthermore, previously described correlations between the change in PaO₂ and VO₂ max were not evident in the subjects tested within this thesis, nor was there any indication of a diffusion limitation based on reduced pulmonary capillary transit time (by association with VO₂ max) or pulmonary oedema (rebuked by a rapid return of PaO₂ to above resting levels following exercise cessation). / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1320633 / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2008