Carotid chemoreflex activity restrains post‐exercise cardiac autonomic control in healthy humans and in patients with pulmonary arterial hypertension

Key points

Dysfunction of post‐exercise cardiac autonomic control is associated with increased mortality risk in healthy adults and in patients with cardiorespiratory diseases. The afferent mechanisms that regulate the post‐exercise cardiac autonomic control remain unclear. We found that afferent signals from carotid chemoreceptors restrain the post‐exercise cardiac autonomic control in healthy adults and patients with pulmonary arterial hypertension (PAH). Patients with PAH had higher carotid chemoreflex sensitivity, and the magnitude of carotid chemoreceptors restraint of autonomic control was greater in patients with PAH as compared to healthy adults. The results demonstrate that the carotid chemoreceptors contribute to the regulation of post‐exercise cardiac autonomic control, and suggest that the carotid chemoreceptors may be potential target to treat post‐exercise cardiac autonomic dysfunction in patients with PAH.

Abstract

Dysfunction of post‐exercise cardiac autonomic control predicts mortality, but its underling mechanisms remain unclear. We tested whether carotid chemoreflex activity restrains post‐exercise cardiac autonomic control in healthy adults (HA), and whether such restraint is greater in patients with pulmonary arterial hypertension (PAH) who may have both altered carotid chemoreflex and post‐exercise cardiac autonomic control. Twenty non‐hypoxemic patients with PAH and 13 age‐ and sex‐matched HA pedaled until 90% of peak work rate observed in a symptom‐limited ramp‐incremental exercise test. Recovery consisted of unloaded pedaling for 5 min followed by seated rest for 6 min. During recovery, subjects randomly inhaled either 100% O₂ (hyperoxia) to inhibit the carotid chemoreceptor activity, or 21% O₂ (normoxia) as control. Post‐exercise cardiac autonomic control was examined via heart rate (HR) recovery (HRR; HR change after 30, 60, 120 and 300 s of recovery, using linear and non‐linear regressions of HR decay) and HR variability (HRV; time and spectral domain analyses). As expected, the PAH group had higher carotid chemosensitivity and worse post‐exercise HRR and HRV than HA. Hyperoxia increased HRR at 30, 60 and 120 s and absolute spectral power HRV in both groups. Additionally, hyperoxia resulted in an accelerated linear HR decay and increased time domain HRV during active recovery only in the PAH group. In conclusion, the carotid chemoreceptors restrained recovery of cardiac autonomic control from exercise in HA and in patients with PAH, with the restraint greater for some autonomic indexes in patients with PAH.

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