This thesis is concerned with the chemical control of breathing during exercise in humans. Chapter 1 reviews some of the relevant studies in animals and humans. Chapter 2 describes the experimental apparatus and the technique of dynamic end-tidal forcing performed using a computer-controlled gas-mixing system. Chapter 3 describes a study of the effects of sustained hypoxia on ventilation during steady exercise. The acute ventilatory response to hypoxia (AHR) was increased during exercise as compared with rest, but the magnitude of the subsequent decline in ventilation (HVD), expressed as a fraction of the AHR, was reduced. A simple model of the hypoxic peripheral chemoreflex is proposed, in which the mechanisms underlying AHR and HVD are functionally separate and can be independently modulated by external factors. Chapter 4 assesses changes in peripheral chemoreflex sensitivity to hypoxia in terms of the degree of decline in AHR measured in the resting periods shortly after prior conditioning periods of hypoxia and/or exercise. At rest, a second AHR measured 6 min after a period of sustained hypoxia had declined by 30% as compared with the initial AHR. In contrast, the AHR measured in the resting period after a period of sustained hypoxic exercise was only 11% smaller in magnitude than the AHR measured after a period of euoxic exercise. The results suggest that the degree to which hypoxic sensitivity declines during sustained hypoxia is genuinely attenuated, rather than masked, by exercise. Chapter 5 describes the changes in respiration during prolonged exercise breathing air with and without added CO₂. During prolonged poikilocapnic exercise, ventilation remained constant, but metabolic CO₂ production, respiratory quotient and end-tidal P_CO2 declined; a result which suggests that in man, ventilation can be dissociated from the CO₂ flux. During hypercapnic exercise, ventilation progressively increased; this was interpreted as being due to a correction by end-tidal forcing of the natural tendency for end-tidal CO₂ to decline, together with an independent effect of CO₂ per se on the ventilation. Chapter 6. Electrical muscle stimulation was used as means of inducing non-volitional exercise. Electrically-induced exercise increased the AHR as compared with rest, and with voluntary exercise at matched external work rate. The AHRs during electrical stimulation and voluntary exercise matched to the internal work rate were similar. Chapter 7. Electrical muscle stimulation was used in paraplegic subjects in whom there would be no neural control of exercise. Electrically-induced exercise increased the AHR as compared with rest. When compared with the data from Chapter 6, the results suggest that the observed increase in AHR during normal voluntary exercise can be wholly accounted for by the increase in metabolic CO₂ production, or closely related factors. Chapter 8 presents a brief summary of the findings in this thesis.

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The investigation and management of patients with life threatening haemoptysis is a common clinical problem in South African Hospitals. Establishing the aetiology and origin of the haemorrhage and treating these patients is both difficult and expensive in terms of human and financial resources. The purpose of this study was to identify common local aetiologies for severe haemoptysis, review the investigation and treatment of these patients at Wentworth Hospital, Durban and to formulate a plan of management. Retrospective and prospective studies of consecutive patients treated at Wentworth Hospital were performed. In the prospective study a new embolic material gelatin linked acryl microspheres (embospheres) was used for bronchial artery embolization (BAE). The study demonstrated a change in the spectrum of aetiologies of haemoptysis, from bronchiectasis following tuberculosis to destructive pneumonias. The chest radiograph was always the initial imaging investigation but was found to be inaccurate in detecting the origin of the bleeding. High resolution computed tomography of the lungs (HRCT) was the single best investigation to detect the cause and origin of the haemoptysis. HRCT detected focal bronchiectasis and intracavitatory aspergillomas that were undetected on the chest radiograph. Pleural thickening detected on CT was a good indicator of the presence of transpleural collaterals. The major limitation with HRCT was that it could not be performed if the patient was too dyspnoeic to cooperate during the scan. The role of bronchoscopy appears limited in patients with severe haemoptysis to those patients who are potential surgical candidates. I found that bronchoscopy was not accurate in detecting the source of bleeding in the few patients in which it was performed. Bronchial arteriography remains the gold standard in the detecting the source of haemorrhage. Bleeding sites were detected on angiography in the presence of focal hypervascularity, neovascularity and the presence of broncho-pulmonary shunts. Bronchial arteries were hypertrophied in bronchiectasis but were normal in size in some patients who had acute pneumonias. Bronchial artery embolization was the treatment of choice for severe haemoptysis in the patients studied. The use of gelatin cross linked micro spheres has significantly improved the initial success rate following the procedure with less complications compared to the use of polyvinyl alcohol particles (PVA). It is important to identify systemic transpleural collaterals at arteriography and to embolize them to reduce recurrent haemoptysis. Patients with aspergillomas responded well to embolization. Recurrent haemoptysis remains the major limitation of BAE but is reduced with the use of micro spheres as embolic agents and thorough embolization of systemic collaterals on the affected side. Surgical resection was an option for a limited number of patients with focal disease in one lung and good respiratory reserve. The major limitation of the study was the absence of long term follow up to detect those patients with late recurrent haemoptysis. / Thesis (D. Med.)-University of Natal, Durban, 2003.

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Bibliography: leaves 181-201 / 201, [ca. 75] leaves ; 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, 1987

Thesis (M. Phil.)--University of Hong Kong, 2007. / Also available in print.

Thesis (M. Sc.)--University of Adelaide, Dept. of Physiology, 1989. / Typescript (Photocopy). Includes bibliographical references (leaves 42-52).