Thesis (Ph. D.)--University of Hong Kong, 1991.

Thesis (M.S.)--Springfield College, 2004. / Includes bibliographical references. Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis (M.S.)--Springfield College, 2004. / Includes bibliographical references.

Arterial desaturation in fit athletes, during exercise at an intensity greater than or equal to 90% of VO₂ max has been reported by a number of authors yet the etiology of these changes remain obscure. Inadequate pulmonary ventilation due to a blunted respiratory drive, or lung mechanics has been implicated as a factor in the etiology of this phenomenon. It was the purpose of this experiment to investigate the relationship between arterial desaturation and ventilatory response to hypoxia (HVR). Twelve healthy male subjects ( age = 23.8 ± 3.6 yrs., height = 181.6 ±₋₁ 5.6 cms., Weight = 73.7 ± 6.2 kg., VO₂ max = 63.2 ± 2.2 ml .kg . -1 2 .min⁻¹) performed a five minute exercise test on a treadmill at 100% of VO₂ max. Arterial samples for pH, PCO₂, PO₂, and SaO₂ were withdrawn via an indwelling arterial cannula at rest and every 15s throughout the exercise test. The blood gas samples were analyzed with an Instrument Laboratories 1306 blood gas analyzer. Ventilation and VO₂ were measured by a Beckman metabolic measurement cart. On a separate occasion the ventilatory response to hypoxia (HVR) was determined by recording VE as progressive hypoxia was induced by adding N₂ to a mixing chamber. SaO₂ was measured using a Hewlett-Packard ear oximeter; to maintain isocapnia small ammounts of CO₂ were added to the open circuit system. ANOVA for repeated measured was used to evaluate changes in blood gases, ventilation, and VO₂. Simple linear regression and multiple linear regression was used to evaluate the relationship between the changes in SaO₂ and HVR and the descriptive variables. Subjects showed a significant decline in arterial saturation and PO₂ over the course of the test (p < 0.01,and p < 0.01). Four subjects (Mild) exhibited modest decreases in SaO₂ to (94.6 ± 1.9%), three (Moderate) showed an intermediate response (SaO₂ 91.6 ± 0.1%) and five (Marked) demonstrated a marked decrease in arterial saturation (SaO₂ = 90.0 + 1.2%). The differences in PO₂ and SaO₂ between Mild and Marked groups were significant ( p < 0.05, and p < 0.01); there were no significant differences between groups in VE, VO₂, pH or PCO . There was no significant correlation between the lowest SaO₂ reached and HVR, or any of the descriptive variables. Nine subjects did not reach maximal VE (as determined by the VO₂ max test) on the exercise test, two subjects 2 exhibited similar ventilation, and the remaining subject exceeded maximal VE, but fell into the Mild group with respect to desaturation. Oxygen uptake exceeded that recorded for the VO₂ max determination for four of the five subjects in the Marked group; the remaining subjects demonstrated lower or similar values. It was concluded that arterial desaturation was not related to blunted hypoxic drive. / Education, Faculty of / Curriculum and Pedagogy (EDCP), Department of / Graduate

No description available.

No description available.

published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

To investigate the relationship between pulmonary diffusion limitation, ventilation-perfusion (VA/Q) mismatch, pulmonary transit times (PTT) and pulmonary gas exchange during exercise, 10 highly trained male athletes (age=26.4±4.4 years, Height=185.5±5.3cms, Weight=78.2±8.6 kg, V 02max=5.15±0.521-min-1) under went exercise testing at rest (R) and 150W, 300W and maximal exercise (372±22W), corresponding to an oxygen consumption (V0₂) of 0.41±0.09, 2.16±0.17, 4.32±0.35 and 5.13±0.50 1-min-1respectively, while trace amounts of six inert gases were infused via a peripheral vein. Arterial blood samples, mixed expired gas samples and metabolic data were obtained. Observed alveolar arterial difference ([A-a]D0₂(0)was calculated according to the alveolar gas equation. Indices of VA/Q mismatch: LogSDi and Log SDa and predicted [A-a]D0₂([A-a]DO₂(p)) were derived from 50 compartment model analysis of retentions and excretions of the inert gases. Additional indices of '/A/I,) mismatch: DISPR*, DISPE and DISPR*_E and inert gas alveolar difference ([A-a]D, R(A-a)D and E(A-a)D) were obtained directly from the inert gas data. One to two weeks later, the subjects underwent first pass radionuclide angiography using a Siemens ZLC wide field of view gamma camera. Following in vitro labeling with 99mTechnecium, 5-10 ml of the subject's blood, containing 10-20 mCi of activity, were injected at rest. First pass and post-static data were obtained on an ADAC 3003 computer and cardiac output was calculated using the Stewart Hamilton equation. PTT was determined using deconvolution and centroid methods. Gated radionuclide angiography was then performed at rest, 150, and 300W. On a separate occasion, first pass cardiac outputs and pulmonary transit times were obtained at maximal exercise. Mean arterial partial pressure of 0₂ (Pa0₂) decreased significantly from rest to 150W , and from 150 to 300W to a low value of 86±9 torn, before increasing to near resting values at maximal exercise. [A-a]D0₂(3) increased across each exercise levels however only the increase from 150 to 300 W was significant. The overall and perfusion-related indices of VA/Q mismatch showed a significant increase with exercise, mainly as a result of increasing perfusion of areas of high VA/Q [A-a]D0₂(0 was greater than predicted, becoming significant during heavy exercise, indicating diffusion limitation. Cardiac output increased from 6.9±0.9 1-min-1 (R) to 25.2±2.5 1-min-1 at 300W and 33.3±3.7 1-min-1 at maximal exercise. End diastolic volume increased from R to heavy exercise (p < 0.001), accompanied by a decrease in end systolic volume (p =0.05). Stroke volume and ejection fraction also increased significantly from R to 300W (p <0.001). Deconvolution PTT decreased from 9.32±1.41 s at rest to 2.91±0.30 s during max exercise and was highly correlated with centroid PTT both at rest (r=0.99, p<0.001) and during maximal exercise (r=0.96, p<0.001). PTT during maximal exercise was significantly correlated with Pa0₂ (1=0.65, p<0.05) and [A-a]D0₂(0)_[A-a]D0₂(p) (r=-0.60, p<0.05). Calculated pulmonary blood volume increased during maximal exercise by 57% over resting values to over 25% of total blood volume and when corrected for body surface area correlated significantly with Pa0₂ (r=0.69, p<0.05). There was a significant correlation between (A-a)D, PTT, the ventilatory equivalent for CO₂ and Pa0₂ during maximal exercise (r=0.94, p<0.01) allowing prediction of over 80% of the variance in Pa0₂ between subjects. These data indicate that highly trained athletes develop VA/Q mismatch accompanied by diffusion limitation during maximal exercise. Observed decrease in Pa0₂2 during high intensity exercise is the result of a complex interaction between VA/Q mismatch, hypoventilation and diffusion limitation secondary to shortened pulmonary transit.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 1995. / Vita. Abstract. Includes bibliographical references. Also available via the Internet.

Thesis (M.Sc.) - Carleton University, 2001. / Includes bibliographical references (p. 94-112). Also available in electronic format on the Internet.