Viviana Shiffman’s MSc Thesis Defence – Oct 25

Title: Exercise-induced arterial hypoxaemia in female master athletes

Thesis Supervisor: Dr. Bill Sheel
Committee Members:  Dr. Michael Koehle, Dr. Don McKenzie, Dr. James McKinney
Dr. Karim Khan

Abstract: The pulmonary system can maintain arterial blood gas homeostasis during exercise in healthy, young adults. However, some endurance athletes demonstrate a significant reduction in arterial oxygenation during exercise, a phenomenon termed exercise-induced arterial hypoxemia (EIAH). EIAH has been previously observed in young adults, and male masters athletes but there are no reports of gas exchange impairment in female master athletes. It was hypothesized the majority of female master athletes will develop EIAH during submaximal, near maximal, and maximal treadmill exercise. Pulmonary function was assessed followed by an incremental exercise test to determine maximal O2 uptake (V̇O2max). Participants were instrumented with a radial arterial catheter, an esophageal balloon-tipped catheter, and temperature probe. Arterial samples were drawn while participants exercised at 60-70, 75, 90-95, and 100% V̇O2max for 2-4 minutes. Participants (n=6, 48-57 years) had an average V̇O2max of 47±2 ml/kg/min (range 40-55 ml/kg/min, 135-186% predicted). During submaximal, near maximal, and maximal exercise the arterial partial pressure of O2 (PaO2) decreased from rest by 14±2 mmHg (range 6-21), 13±4 (range -6-24), and 11±7 mmHg (range -7-21), respectively. There was a significant change in PaO2 from rest to 60 and 75% V̇O2max. The arterial partial pressure of CO2 (PaCO2) decreased from rest by 1.8±1 mmHg (range -2-6), 4±1 mmHg (range 0.3- 8), and 5±2 mmHg (range 2-5) at submaximal, near maximal, and maximal exercise, respectively with no significant changes between rest and exercise levels. There was a reduction in oxyhemoglobin saturation 2.5± 0.3% (range 1.9-3.4) and arterial O2 content 1.2± 0.2 mL O2/100 mL of blood (range 0.7-1.8) at all intensities. Participants with a a minimal change to PaCO2 tended to have a greater reduction in PaO2 (r = -0.85, R2 = 0.73, p< 0.05). The alveolar to arterial oxygen (A-aDO2) gradient increased during submaximal (range 7-34 mmHg), near maximal (range 7-47 mmHg) and maximal (range 7-48 mmHg) exercise. The decrease in PaO2 and increased A-aDO2 gradient indicates an inadequate ventilatory response to exercise. There was no relationship between V̇O2max and PaO2. These results suggest that female master athletes develop EIAH at submaximal and maximal exercise intensities and a high level of aerobic fitness is not requisite for the development of EIAH.