xvii, 174 p. : ill. A print copy of this thesis is available through the UO Libraries. Search the library catalog for the location and call number. / During acute altitude exposure, humans maintain higher skin temperature and lower core body temperature. However, the role of cutaneous vascular regulation in these thermoregulatory differences is unclear. Therefore, the purpose of these studies was to investigate the impact of altitude exposure on reflex control of skin blood flow and core temperature during cold exposure. In Chapter IV, the effects of hypoxia and hypocapnia on cutaneous vasoconstriction during mild cold exposure were investigated. We found that hypoxia stimulates cutaneous vasodilation in men whereas skin blood flow is unaltered in women. However, during whole body cooling skin blood flow is upward shifted in both sexes. The development of hypocapnia does not affect the vascular response to hypoxia in either sex, but reduces the magnitude of cutaneous vasoconstriction during cold exposure by 50% in women. In Chapter V, we studied the timecourse of α-adrenergic blockade by yohimbine in the cutaneous circulation and how the duration of cold exposure modulates cotransmitter-mediated vasoconstriction during cold stress. We found that yohimbine produces functional α-adrenergic blockade within 30 minutes of initial delivery and completely abolishes reflex cutaneous vasoconstriction during mild cold stress. This latter finding was surprising, and an additional protocol demonstrated that cotransmitter-mediated vasoconstriction only participates in the vascular response to cold stress when the exposure is more prolonged. In Chapter VI, the effects of hypoxia on cutaneous vasoconstrictor mechanisms and core cooling rate were tested during more prolonged and severe cold stress. In contrast to our findings during brief cold exposure, we showed that cutaneous vasoconstriction during prolonged cold stress is potentiated by hypoxia and abolishes hypoxic vasodilation. Moreover, increased cotransmitter-mediated vasoconstriction appears to account for this response. Hypoxia had no effect on core cooling rate during severe cold exposure. The selective potentiation of cotransmitter-mediated vasoconstriction observed during hypoxia in Chapter VI provided the basis for Chapter VII. This study was designed to test the effect of hypoxia on cutaneous vascular responsiveness to peripherally stimulated sympathetic vasoconstriction. The results demonstrated that α-adrenergic vasoconstrictor transduction is not affected by hypoxia, and that stimulation of adrenergic nerves with tyramine does not elicit cotransmitter-mediated vasoconstriction in skin. / Adviser: John R. Halliwill

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On sait depuis longtemps que l’exposition à l’altitude est associée à une réduction de l’aptitude aérobie. Différentes hypothèses ont été posées pour expliquer cette limitation à l’effort en hypoxie (une limitation ventilatoire ou diaphragmatique, une altération de la diffusion pulmonaire et une disconcordance entre de la perfusion et la diffusion tissulaire, etc.) mais généralement, la limitation de l’effort aérobie en hypoxie est attribuée à une diminution du transport sanguin de l’O2 (TO2) parc convection vers les muscles. Le TO2 dépend du débit cardiaque (Q) et du contenu artériel en O2 (CaO2). <p>Le CaO2 est diminué en altitude à cause d’une diminution de la pression partielle inspirée en O2. Cependant, le chémoréflexe hypoxique tente de contrebalancer cet effet en élevant la ventilation et en diminuant la pression alvéolaire en CO2 afin de maintenir la pression alvéolaire en O2 constante. De plus, avec l’acclimatation, le rein produit de l’érythropoïétine permettant au taux d’hémoglobine d’augmenter. Ces deux principales adaptations à l’altitude ramènent le CaO2 à sa valeur de base du niveau de la mer en 2 à 3 semaines passées à 5000 m d’altitude mais sans amélioration de l’aptitude à l’effort aérobie.<p>L’exposition à l’altitude est aussi associée à une diminution du Q maximal. Les mécanismes à l’origine de cette limitation du Q maximal restent, à l’heure actuelle, incompris. Les principales explications évoquées sont, une diminution de la réserve chronotrope, une diminution de la commande nerveuse centrale vers le cœur ou une diminution de la demande périphérique. Récemment, des études sur des sujets sains en hypoxie suggérèrent qu’au moins une partie de la limitation du Q maximal à l’effort est liée à une élévation de la postcharge ventriculaire droite suite à l’hypertension pulmonaire induite par l’hypoxie. C’est cette hypothèse que nous avons voulu vérifier dans une première étude.<p>Nous avons étudié l’effet d’une inhibition de l’hypertension pulmonaire d’altitude par le sildénafil, un inhibiteur de la phosphodiestrérase-5, chez des sujets sains, en normoxie, en hypoxie aiguë et en hypoxie chronique. Les résultats de cette étude ont confirmé l’effet vasodilatateur pulmonaire du sildénafil et une augmentation de la VO2max en hypoxie aiguë. Cependant, la prise de ce dernier était couplée à une amélioration de l’oxygénation, si bien que l’élévation de la performance aérobie observée en hypoxie aiguë sous sildénafil ne pouvait être entièrement attribuée à une réduction de l’hypertension pulmonaire. <p>Nous conclurent que cette amélioration de la performance était probablement d’avantage liée à une amélioration de l'oxygénation qu’à un effet vasodilatateur pulmonaire.<p>Les résultats équivoques obtenus lors de cette première étude nous ont incité à tester les effets d’une amélioration de l’oxygénation sur la performance aérobie en haute altitude. Pour ce faire, quinze sujets sains ont été testés au niveau de la mer et après acclimatation à 4700 m d’altitude soit sous placebo, soit sous acétazolamide, un inhibiteur de l’anhydrase carbonique augmentant l’oxygénation par stimulation ventilatoire en réponse à une acidose métabolique. La prise d’acétazolamide n’eut aucun effet sur l’hémodynamique pulmonaire et sur la VO2max et la charge maximale. Nous avons toutefois observé qu’une amélioration de l’oxygénation durant l’effort retarde l’apparition du seuil ventilatoire améliorant ainsi la phase aérobie de l’effort. Cette étude confirme donc qu’une élévation du CaO2 permet une amélioration de l’aptitude aérobie. <p>Finalement, la dernière étude a pour but d’étudier les effets isolés d’une vasodilatation pulmonaire sur la performance aérobie en altitude. Les résultats d’une étude préliminaire montrent que l’inhibition de la vasoconstriction hypoxique par un agent pharmacologique antagoniste des récepteurs de l’endothéline ETA et ETB, le bosentan, permet une élévation de l’aptitude aérobie en hypoxie aiguë, sans effets sur l’oxygénation, confirmant ainsi notre hypothèse initiale qu’une postcharge ventriculaire droite augmentée en hypoxie peut contribuer à une limitation de l’aptitude à l’effort aérobie en hypoxie. <p><p>Conclusions :<p>L’ensemble de nos résultats suggère que l’aptitude aérobie en altitude est déterminée par le transport d’O2 qui peut être augmenté par manipulation pharmaceutique du débit ventriculaire droit maximal après inhibition de la vasoconstriction pulmonaire hypoxique (bosentan), amélioration de l’oxémie (acétazolamide) ou des deux (sildénafil).<p> / Agrégation de l'enseignement supérieur en kinésithérapie et réadaptation / info:eu-repo/semantics/nonPublished

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Orientador: Miguel de Arruda / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Educação Fisica / Made available in DSpace on 2018-08-03T23:56:04Z (GMT). No. of bitstreams: 1 CossioBolanos_MarcoAntonio_M.pdf: 1051790 bytes, checksum: 76555c654d14138b7c3f134813b01173 (MD5) Previous issue date: 2004 / Mestrado / Ciencia do Desporto / Mestre em Educação Física

The original work presented in this thesis investigates some of the mechanisms that may be responsible for the aetiology of altitude-related cough. Particular attention is paid to its relationship to the long recognised, but poorly understood, changes in lung volumes that occur on ascent to altitude. The literature relevant to this thesis is reviewed in Chapter 1.<p><p>Widespread reports have long existed of a debilitating cough affecting visitors to high altitude that can incapacitate the sufferer and, on occasions, be severe enough to cause rib fractures (22, 34, 35). The prevalence of cough at altitude has been estimated to be between 22 and 42% at between 4200 and 4900 m in the Everest region of Nepal (10, 29). Traditionally the cough was attributed to the inspiration of the cold, dry air characteristic of the high altitude environment (37) but no attempts were made to confirm this aetiology. In the first formal study of cough at high altitude, nocturnal cough frequency was found to increase with increasing altitude during a trek to Everest Base Camp (5300 m) and massively so in 3 climbers on whom recordings were made up to 7000 m on Everest (8). After 9 days at 5300 m the citric acid cough threshold, a measure of the sensitivity of the cough reflex arc, was significantly reduced compared with both sea level and arrival at 5300 m.<p><p>During Operation Everest II, a simulated climb of Mount Everest in a hypobaric chamber, the majority of the subjects were troubled above 7000 m by pain and dryness in the throat and an irritating cough despite the chamber being maintained at a relative humidity of between 72 and 82% and a temperature of 23ºC (18). This argued against the widely held view that altitude-related cough was due to the inspiration of cold, dry air. <p><p>In the next major hypobaric chamber study, Operation Everest III, nocturnal cough frequency and citric acid cough threshold were measured on the 8 subjects in the study. The chamber temperature was maintained between 18 and 24ºC and relative humidity between 30 and 60% (24). This work is presented in Chapter 2 and, demonstrated an increase in nocturnal cough frequency with increasing altitude which immediately returned to control values on descent to sea level. Citric acid cough threshold was reduced at 8000 m compared to both sea level and 5000 m values. Changes in citric acid cough threshold at lower altitudes may not have been detected because of the constraints on subject numbers in the chamber. The study still however demonstrated an increase in clinical cough and a reduction in the citric acid cough threshold at extreme altitude, despite controlled environmental conditions, and thus refuted the long held belief that altitude-related cough is solely due to the inspiration of cold, dry air. <p><p>If altitude-related cough is not simply due to the inspiration of cold, dry air, other possible aetiologies are:<p>•\ / Doctorat en Sciences médicales / info:eu-repo/semantics/nonPublished

Southern Africa is characterised by an unpredictable environment with daily and seasonal temperature fluctuations. As a local or non-migratory endothermic species occurring over an altitudinal gradient from the Drakensberg to the coast of KwaZulu- Natal in southern Africa, Amethyst Sunbirds (Chalcomitra amethystina) experience challenging thermal conditions and increased energetic stress as a result of ambient temperature variation. Flexibility of metabolic rates within a species allows for the colonization of different habitats along an altitudinal and thus temperature gradient. It was predicted that over this altitudinal gradient Amethyst Sunbirds would exhibit variation in metabolic rates, particularly basal metabolic rates, pre- and postacclimation, as well as variation in hematocrit levels in winter and summer trials. It was also predicted that Amethyst Sunbirds would exhibit seasonal variation in metabolic parameters. Sunbirds were caught in a winter and summer season (2006-2007) using mist nets in three locations; Underberg (1553 m), Howick (1075 m) and Oribi Gorge (541 m). Upon capture, metabolic rate was measured indirectly by quantifying oxygen consumption (VO2) using flow through respirometry, at 5 and 25°C. Birds were then acclimated at 25°C for 6 weeks on a 12L:12D cycle. VO2 was measured postacclimation at 8 different temperatures (15, 5, 10, 20, 30, 28, 25 and 33°C). Hematocrit levels were taken pre-acclimation and pre-release. Winter and summer data were compared. In the winter trials it was found that there was little variation in VO2 between individuals from the same locality, whereas significant variation was observed at the same temperatures between localities and thus between altitudes. The subpopulation from the highest altitudinal site had the highest basal metabolic rate (BMR). Summer trials showed that metabolic rates did not differ significantly between altitudinal subpopulations of Amethyst Sunbirds, however, BMR was observed to decrease as altitude decreased. The comparison of seasonal data showed that Amethyst Sunbird subpopulations from Underberg and Howick showed higher post-acclimation VO2 values per temperature in winter than in summer trials. Post-acclimation resting metabolic rate (RMR) values for Howick subpopulations were generally higher in winter than in summer, Underberg Amethyst Sunbirds showed a significant difference between summer and winter RMR at 5 and 10°C and Howick sunbirds showed a significant difference in RMR between seasons at 5°C. The Oribi Gorge subpopulation, however, showed no significant differences in metabolic rate between any temperatures when comparing a summer and a winter season. Thermal neutral zones of all of the subpopulations of Amethyst Sunbirds shifted between the winter and summer trial period. This study thus emphasized the need to understand plasticity in metabolic rates and acknowledge altitudinal and seasonal differences within a species, in order to make accurate predictions about a species thermal physiology and responses to changes in ambient temperatures. In particular, the variation in BMR, which is usually used as a species specific value, should be acknowledged in comparative studies of avian metabolic rates or in climate change models. / Thesis (M.Sc.) - University of KwaZulu-Natal, Pietermaritzburg, 2007.

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