DIFFERENTIAL MECHANISMS OF EXERCISE-INDUCED ARTERIAL HYPOXEMIA AT HIGH ALTITUDE IN MALES AND FEMALES

Author(s): MAIER, L., MACDONALD, T., JENKINS, E., HA, P., TSIOROS, S., STAPLETON, R., KILLICK, J., MACLEOD, D., BAYLIS, J., GASHO, C., ANHOLM, J., EVES, N., STACEY, B., SMITH, K., BAIN, A., GIBBONS, T., TYMKO, M., AINSLIE, P., Institution: UNIVERSITY OF BRITISH COLUMBIA - OKANAGAN, Country: CANADA, Abstract-ID: 1797

INTRODUCTION:
Females may be more susceptible to exercise-induced arterial hypoxemia (EIAH), in part due to sex differences in pulmonary structure and function which increase the likelihood of ventilatory and gas exchange limitations during exercise. These differences may be amplified at high-altitude, where changes in pulmonary diffusion capacity are known to occur.
METHODS:
To address this, 39 participants (16F; 26.1±4.7 years, 173.4±10.2 cm, 74.4±14.4 kg) performed an incremental maximal cycling test and 5-kilometer cycle time-trial at sea level (340m) and high-altitude (days 3-12; 3800m). Ventilation and pulmonary gas exchange were measured breath-by-breath during the incremental maximal cycling test and time-trial via metabolic cart. Arterial blood gases, corrected for changes in core-temperature, were collected at baseline and every kilometer during the time-trial via brachial artery catheter.
RESULTS:
Peak oxygen consumption (VO2peak) at sea level was 47.5±8.8 mL/min/kg in males and 41.3±9.1 mL/min/kg in females, which decreased by 18.0±10.4% and 19.1±5.8% at high-altitude in males and females, respectively. Throughout the time-trial, reductions in arterial oxygen saturation (SaO2) were similar between sexes at sea level (Females: -4.8±3.5% vs. Males: -4.5±2.4%; p=0.751) and high-altitude (Females: -14.4±5.7% vs. Males: -14.4±4.8%; p=0.346). A condition x altitude interaction (p<0.001) supports greater desaturation with continuing exercise at high-altitude in all participants. Considering participants’ fitness (VO2peak) as a covariate, a fitness x altitude x sex interaction (p=0.003) indicates females with higher VO2peak desaturated more at high-altitude compared to males and less fit females. The alveolar-arterial oxygen difference (A-aDO2) increased throughout the time-trial (p<0.001) and was lower at high-altitude compared to sea level throughout exercise (p=0.038) but was not different between sexes (p=0.214). However, at high-altitude, a greater widening of A-aDO2 contributed to worsened EIAH in males (p<0.001), whereas relative hypoventilation (indexed by an attenuated reduction in partial pressure of arterial carbon dioxide) contributed to EIAH in females (p<0.001 vs. males).
CONCLUSION:
Therefore, the aetiology of EIAH at high-altitude may differ between males and females. Relative fitness may contribute more to EIAH development at high-altitude in females than males. Further, females may experience a combination of diffusion limitation and relative hypoventilation (potentially mediated by expiratory flow limitation), compared to males who are driven mainly by diffusion limitation (i.e., a greater widening of A-aDO2). Thus, while males and females appear to experience EIAH similarly during a 5-kilometer time-trial at sea level and high-altitude, the contribution of relative fitness and underlying mechanisms may differ at high-altitude.