Emily A Granger1, Trevor K Cooper2, Susan R Hopkins3, Donald C McKenzie2, Paolo Dominelli1. 1. Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada. 2. School of Kinesiology and Division of Sports Medicine, University of British Columbia, Vancouver, British Columbia, Canada. 3. Departments of Medicine and Radiology, University of California, San Diego, CA, USA.
Abstract
NEW FINDINGS: What is the central question of this study? Do highly trained male endurance athletes who develop exercise-induced arterial hypoxaemia (EIAH) demonstrate reduced peripheral chemoresponsiveness during exercise? What is the main finding and its importance? Those with the lowest arterial saturation during exercise have a smaller ventilatory response to hypercapnia during exercise. There was no significant relationship between the hyperoxic ventilatory response and EIAH. The findings suggest that peripheral chemoresponsiveness to hypercapnia during exercise could play a role in the development of EIAH. The findings improve our understanding of the mechanisms that contribute to EIAH. ABSTRACT: Exercise-induced arterial hypoxaemia (EIAH) is characterized by a decrease in arterial oxygen tension and/or saturation during whole-body exercise, which may in part result from inadequate alveolar ventilation. However, the role of peripheral chemoresponsiveness in the development of EIAH is not well established. We hypothesized that those with the most severe EIAH would have an attenuated ventilatory response to hyperoxia and hypercapnia during exercise. To evaluate this, on separate days, we measured ventilatory sensitivity to hyperoxia and separately hypercapnia at rest and during three different exercise intensities (25, 50% of V ̇ O 2 max and ventilatory threshold (∼67% of V ̇ O 2 max )) in 12 males cyclists ( V ̇ O 2 max = 66.6 ± 4.7 ml kg-1 min-1 ). Subjects were divided into two groups based on their end-exercise arterial oxygen saturation (ear oximetry, S p O 2 ): a normal oxyhaemoglobin saturation group (NOS, S p O 2 = 93.4 ± 0.4%, n = 5) and a low oxyhaemoglobin saturation group (LOS, S p O 2 = 89.9 ± 0.9%, n = 7). There was no difference in V ̇ O 2 max (66.4 ± 2.9 vs. 66.8 ± 6.0 ml kg-1 min-1 , respectively, P = 0.9), peak ventilation during maximal exercise (182 ± 15 vs. 197 ± 32 l min-1 , respectively, P = 0.36) or ventilatory response to hyperoxia (P = 0.98) at any exercise intensity between NOS and LOS groups. However, those in the LOS group had a significantly lower ventilatory response to hypercapnia (P = 0.004, (η2 = 0.18). There was also a significant relationship between the mean hypercapnic response and end-exercise S p O 2 (r = 0.75, P = 0.009) but not between the mean hyperoxic response and end-exercise S p O 2 (r = 0.21, P = 0.51). A blunted hypercapnic ventilatory response may contribute to EIAH in highly trained men due to a failure to increase ventilation sufficiently to offset exercise-induced gas exchange impairments.
NEW FINDINGS: What is the central question of this study? Do highly trained male endurance athletes who develop exercise-induced arterial hypoxaemia (EIAH) demonstrate reduced peripheral chemoresponsiveness during exercise? What is the main finding and its importance? Those with the lowest arterial saturation during exercise have a smaller ventilatory response to hypercapnia during exercise. There was no significant relationship between the hyperoxic ventilatory response and EIAH. The findings suggest that peripheral chemoresponsiveness to hypercapnia during exercise could play a role in the development of EIAH. The findings improve our understanding of the mechanisms that contribute to EIAH. ABSTRACT: Exercise-induced arterial hypoxaemia (EIAH) is characterized by a decrease in arterial oxygen tension and/or saturation during whole-body exercise, which may in part result from inadequate alveolar ventilation. However, the role of peripheral chemoresponsiveness in the development of EIAH is not well established. We hypothesized that those with the most severe EIAH would have an attenuated ventilatory response to hyperoxia and hypercapnia during exercise. To evaluate this, on separate days, we measured ventilatory sensitivity to hyperoxia and separately hypercapnia at rest and during three different exercise intensities (25, 50% of V ̇ O 2 max and ventilatory threshold (∼67% of V ̇ O 2 max )) in 12 males cyclists ( V ̇ O 2 max = 66.6 ± 4.7 ml kg-1 min-1 ). Subjects were divided into two groups based on their end-exercise arterial oxygen saturation (ear oximetry, S p O 2 ): a normal oxyhaemoglobin saturation group (NOS, S p O 2 = 93.4 ± 0.4%, n = 5) and a low oxyhaemoglobin saturation group (LOS, S p O 2 = 89.9 ± 0.9%, n = 7). There was no difference in V ̇ O 2 max (66.4 ± 2.9 vs. 66.8 ± 6.0 ml kg-1 min-1 , respectively, P = 0.9), peak ventilation during maximal exercise (182 ± 15 vs. 197 ± 32 l min-1 , respectively, P = 0.36) or ventilatory response to hyperoxia (P = 0.98) at any exercise intensity between NOS and LOS groups. However, those in the LOS group had a significantly lower ventilatory response to hypercapnia (P = 0.004, (η2 = 0.18). There was also a significant relationship between the mean hypercapnic response and end-exercise S p O 2 (r = 0.75, P = 0.009) but not between the mean hyperoxic response and end-exercise S p O 2 (r = 0.21, P = 0.51). A blunted hypercapnic ventilatory response may contribute to EIAH in highly trained men due to a failure to increase ventilation sufficiently to offset exercise-induced gas exchange impairments.
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