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Pulmonary diffusion limitation, V̇ /Q̇ mismatch and pulmonary transit time in highly trained athletes during maximal exercise Hopkins, Susan R.

Abstract

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.

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