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

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 ${\dot{V}}_{O_2\max }$ and ventilatory threshold (∼67% of ${\dot{V}}_{O_2\max }$ )) in 12 males cyclists ( ${\dot{V}}_{O_2\max }$ = 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 ${\dot{V}}_{O_2\max }$ (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.

Keywords: carotid chemosensor; hypercapnia; hypoxia; ventilation.

FIGURE 1

Schematic representation of the chemosensitivity testing apparatus (a) along with a timeline for the hypercapnic (b) and hyperoxic (c) chemosensitivity trials. PT, pneumotachograph

FIGURE 2

Individual mean subject responses (a,c), and the group mean responses (b,d) for the hypercapnic and hyperoxic trials for rest and over the three exercise levels. Data in (a,c) are presented as the mean for each subject for each trial. There were no significant effects for the hyperoxic response. There was a main effect of saturation and exercise intensity for the hypercapnic response. There were no significant interactions for the hypercapnic response. LPO, low power output; MPO, moderate power output; VLPO, very low power output. *Significant main effect of saturation P < 0.05

FIGURE 3

The relationship between end exercise oxyhaemoglobin saturation and chemoresponsiveness. (a) The hyperoxic response trials; (b) the hypercapnic response trials. Data are the mean exercise response of each subject over the three exercise levels plotted against the subjects’ nadir oxyhaemoglobin saturation during the maximal exercise test. Nadir $S_{{\text{pO}}_2}$, lowest oxygen saturation of arterial haemoglobin