Open Collections

Pulmonary diffusing capacity and exercise-induced hypoxemia in highly trained athletes

University of British Columbia

The purpose of this study was to determine whether a reduced post-exercise pulmonary diffusing capacity (DL) had a physiological effect on subsequent exercise. Thirteen endurance-trained male athletes (age = 27 ± 3 yrs; ht = 179.6 ± 5.0 cm; mass = 71.8 ± 6.9 kg; VChmax = 67.0 ± 3.6 ml‧kg⁻¹‧min⁻¹) performed two consecutive V02max exercise tests, separated by 60 min of recovery. Testing was on an electronicallybraked cycle ergometer (Quinton, Excalibur) using a ramp protocol (30 W-min"1). Arterial oxygen saturation (%SaO₂) was measured via ear oximetry (Ohmeda Biox 3740 pulse oximeter), and resting DL was measured by a single-breath carbon monoxide diffusing capacity test (Collins Survey Tach Pulmonary Function Testing Unit), prior to exercise and 60 min following each exercise bout. In order to partition the membrane diffusing capacity (DM) and pulmonary capillary volume (Vc) from DL, two test gases were used (21% O₂ and 90% O₂ with 0.3% CO). Athletes that exhibited a decrease in %SaO₂ ≤ 91 during exercise were grouped as desaturaters (D) all others were grouped as nondesaturaters (ND). There was a significant difference in %SaO₂ between D and N D (p = 0.0001); however, all other measures between the two groups were not significantly different. There were no significant differences in VO₂max or %SaO₂min between exercise bouts. A 1.7% decrease (p = 0.003) in peak power output occurred during the second exercise test (Ex2). Significant decreases occurred in DL (p< 0.0001), DM (p = 0.02) and Vc (p < 0.0001) post-exercise, as compared to pre-exercise. DL decreased 11% following the initial exercise bout (p < 0.05) and a further 6% (p < 0.05) from post-exercise 1 (Exl) to post-Ex2. Similarly, Vc showed an overall decrease of 20% with a 10% decrease (p < 0.05) between exercise bouts. DM showed a significant (p < 0.05) 11% decrease from pre-exercise to post-Exl and a further 2% decrease (p > 0.05) between post-Ex 1 and post-Ex2. A strong positive linear relationship existed in D between changes in %SaO₂ and changes in D L (r = 0.87, p = 0.03), and between changes in %SaO₂ and changes in DM (r = 0.85, p = 0.03) consequent to Exl. No linear relationship existed for changes in D during Ex2 or during either exercise bout for ND. Rapid shallow breathing (RSB) was observed during recovery (R) following both exercise bouts. No significant differences in breathing pattern existed between Exl - Rl and Ex2 - R2, or between D and ND. The development of RSB and decreases in DM following exercise support the presence of pulmonary edema. Because no further changes were observed following the second exercise bout and no differences existed between D and ND, alternate mechanisms in addition to diffusion limitations, must contribute to the final decrease in %SaO₂.

Thesis/Dissertation

application/pdf

2009-02-06

For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.

http://hdl.handle.net/2429/4249

Human Kinetics

University of British Columbia

UBCV

DSpace