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The relationship between the hypoxic ventilatory response and arterial desaturation during heavy work Hopkins, Susan Roberta


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 Arterial samples for pH, PCO₂, PO₂, and SaO₂ were withdrawn via an indwelling arterial cannula at rest and every 15s throughout the exercise test.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.

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