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Background and objective: Peak oxygen consumption (pVO2), determined from CPET, provides a valuable indication of PAH severity and patient prognosis. However, CPET is often contraindicated in severe PAH and frequently terminated prior to achievement of a sufficient exercise effort. We sought to determine whether in PAH low‐intensity [i.e. freewheeling exercise (FW)] exercise reveals abnormal VE/VCO2 and PETCO2 responses that are associated with pVO2 and serve as indices of PAH risk stratification and mortality. Methods: Retrospective analysis of CPET from 97 PAH patients and 20 age‐matched controls was undertaken. FW VE/VCO2 and PETCO2 were correlated with pVO2% age‐predicted. Prognostication analysis was conducted using pVO2 > 65% age‐predicted, as known to represent a low mortality risk. Primary outcome was mortality from any cause. Results: FW PETCO2 was correlated with pVO2 (P < 0.0001; r = 0.52), while FW VE/VCO2 was not (P = 0.13; r = −0.16). ROC curve analyses showed that FW PETCO2 (AUC = 0.659), but not FW VE/VCO2 (AUC = 0.587), provided predictive information identifying pVO2 > 65% age‐predicted (best cut‐off value of 28 mm Hg). By Cox analysis, FW PETCO2 < 28 mm Hg remained a predictor of mortality after adjusting for age and PAH aetiology (HR: 2.360, 95% CI: 1.144–4.866, P = 0.020). Conclusion: Low PETCO2 during FW is associated with reduced pVO2 in PAH and provides predictive information for PAH risk stratification and prognostication. [ABSTRACT FROM AUTHOR]

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 chemoreceptor 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 a potential target to treat post‐exercise cardiac autonomic dysfunction in patients with PAH. Dysfunction of post‐exercise cardiac autonomic control predicts mortality, but its underlying 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 altered post‐exercise cardiac autonomic control. Twenty non‐hypoxaemic patients with PAH and 13 age‐ and sex‐matched HA pedalled until 90% of peak work rate observed in a symptom‐limited ramp‐incremental exercise test. Recovery consisted of unloaded pedalling 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. 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 chemoreceptor 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 a potential target to treat post‐exercise cardiac autonomic dysfunction in patients with PAH. [ABSTRACT FROM AUTHOR]

The advent of micro processed "metabolic carts" and rapidly incremental protocols greatly expanded the clinical applications of cardiopulmonary exercise testing (CPET). The response normalcy to CPET is more commonly appreciated at discrete time points, for example, at the estimated lactate threshold and at peak exercise. Analysis of the response profiles of cardiopulmonary responses at submaximal exercise and recovery, however, might show abnormal physiologic functioning which would not be otherwise unraveled. Although this approach has long been advocated as a key element of the investigational strategy, it remains largely neglected in practice. The purpose of this paper, therefore, is to highlight the usefulness of selected submaximal metabolic, ventilatory, and cardiovascular variables in different clinical scenarios and patient populations. Special care is taken to physiologically justify their use to answer pertinent clinical questions and to the technical aspects that should be observed to improve responses' reproducibility and reliability. The most recent evidence in favor of (and against) these variables for diagnosis, impairment evaluation, and prognosis in systemic diseases is also critically discussed. [ABSTRACT FROM AUTHOR]