Peripheral chemoresponsiveness during exercise in male athletes with exercise‐induced arterial hypoxaemia

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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover><mml:mrow><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub><mml:mi>max</mml:mi></mml:mrow></mml:msub></mml:math> and ventilatory threshold (∼67% of <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover><mml:mrow><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub><mml:mi>max</mml:mi></mml:mrow></mml:msub></mml:math> )) in 12 males cyclists ( <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover><mml:mrow><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub><mml:mi>max</mml:mi></mml:mrow></mml:msub></mml:math> = 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, <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mi>S</mml:mi><mml:mrow><mml:mi>p</mml:mi><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:math> ): a normal oxyhaemoglobin saturation group (NOS, <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mi>S</mml:mi><mml:mrow><mml:mi>p</mml:mi><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:math> = 93.4 ± 0.4%, n = 5) and a low oxyhaemoglobin saturation group (LOS, <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mi>S</mml:mi><mml:mrow><mml:mi>p</mml:mi><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:math> = 89.9 ± 0.9%, n = 7). There was no difference in <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover><mml:mrow><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub><mml:mi>max</mml:mi></mml:mrow></mml:msub></mml:math> (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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mi>S</mml:mi><mml:mrow><mml:mi>p</mml:mi><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:math> (r = 0.75, P = 0.009) but not between the mean hyperoxic response and end-exercise <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:msub><mml:mi>S</mml:mi><mml:mrow><mml:mi>p</mml:mi><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:math> (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.