Response

OSA is a complex disorder that requires careful phenotyping. We agree that the apnea-hypopnea index does not consider the magnitude of oxygen desaturation or the distribution of nocturnal events throughout the sleep stages and assumes that apnea and hypopnea are equal in their biological effects.1Borsini E. Nogueira F. Nigro C. Apnea-hypopnea index in sleep studies and the risk of over-simplification.Sleep Sci. 2018; 11: 45-48Crossref PubMed Scopus (15) Google Scholar In this study,2Elbehairy A.F. Geneidy N.M. Elhoshy M.S. et al.Exercise intolerance in untreated OSA: role of pulmonary gas exchange and systemic vascular abnormalities.Chest. 2023; 163: 226-238Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar the degree of nocturnal hypoxemia (as assessed by oxygen desaturation index, minimal oxygen saturation [Spo2] during sleep, and time with Spo2 < 90%) was significant and correlated with increased peripheral arterial stiffness. We also acknowledge that the presence of nocturnal hypoxemia (regardless of it being related to apneas and hypopneas) is associated with impaired cardiovascular function, including increased pulmonary artery pressure.3Rafanan A.L. Golish J.A. Dinner D.S. Hague L.K. Arroliga A.C. Nocturnal hypoxemia is common in primary pulmonary hypertension.Chest. 2001; 120: 894-899Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar,4Maiolino G. Bisogni V. Maggi M. et al.Nocturnal hypoxia indexes are associated with left ventricular remodeling and diastolic dysfunction in obstructive sleep apnea patients.Sleep Med. 2023; 103: 180-186Crossref PubMed Scopus (1) Google Scholar Given that intermittent nocturnal hypoxemia is a core underlying factor of OSA-associated cardiovascular impairments, we agree with Powell et al that results may not be generalized to those with less severe nocturnal hypoxemia. As noted in that article,2Elbehairy A.F. Geneidy N.M. Elhoshy M.S. et al.Exercise intolerance in untreated OSA: role of pulmonary gas exchange and systemic vascular abnormalities.Chest. 2023; 163: 226-238Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar the results also may not be generalized to patients with milder OSA severity or patients with higher BMI; these factors are expected to affect resting and exertional physiological and cardiovascular functional measurements. In this regard, the cross-relationship between the pathophysiological and clinical phenotypes of OSA plays an important role in diagnosis, prognosis, and treatment selection in patients with OSA, rather than relying solely on apnea-hypopnea index. In this study,2Elbehairy A.F. Geneidy N.M. Elhoshy M.S. et al.Exercise intolerance in untreated OSA: role of pulmonary gas exchange and systemic vascular abnormalities.Chest. 2023; 163: 226-238Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar most participants (57%) in the OSA group had never smoked, and those who smoked had an insignificant smoking history. We acknowledge that FVC was lower in the OSA group than in the asymptomatic control participants, but it was still within the normal range, and there was no clinical evidence of any restrictive disease. During exercise, patients were able to expand their tidal volume similarly to control participants. Thus, it is unlikely that these factors were the main contributors to increased dead space ventilation and dyspnea intensity during exercise in this cohort.2Elbehairy A.F. Geneidy N.M. Elhoshy M.S. et al.Exercise intolerance in untreated OSA: role of pulmonary gas exchange and systemic vascular abnormalities.Chest. 2023; 163: 226-238Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar Nevertheless, we concede that increased dead space ventilation might be related to OSA itself or impaired left ventricular diastolic function, a known sequela of untreated OSA.5Van Iterson E.H. Johnson B.D. Borlaug B.A. Olson T.P. Physiological dead space and arterial carbon dioxide contributions to exercise ventilatory inefficiency in patients with reduced or preserved ejection fraction heart failure.Eur J Heart Fail. 2017; 19: 1675-1685Crossref PubMed Scopus (48) Google Scholar Lastly, in that article,2Elbehairy A.F. Geneidy N.M. Elhoshy M.S. et al.Exercise intolerance in untreated OSA: role of pulmonary gas exchange and systemic vascular abnormalities.Chest. 2023; 163: 226-238Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar we noted that deliberately choosing a slow ramp exercise protocol (because of poor fitness level of most of the participants) may have affected measurements at the peak of exercise but allowed running comparisons between parameters of interest (eg, ventilatory and gas exchange parameters, including dead space ventilation and exertional dyspnea) at several submaximal workloads rather than being limited to a couple of time points in faster protocols. See earlier cited article for author conflicts of interest. Does Untreated OSA Really Influence Exercise Tolerance?CHESTVol. 163Issue 6PreviewIn CHEST (January 2023), Elbehairy et al1 present a cross-sectional observational study evaluating cardiorespiratory fitness (CRF) via cardiopulmonary exercise testing (CPET) in patients with untreated OSA compared with matched control subjects.1 The investigators used arterial blood gas analysis during CPET to help demonstrate ventilatory and gas exchange abnormalities during exercise in patients with untreated OSA. Full-Text PDF Exercise Intolerance in Untreated OSA: Role of Pulmonary Gas Exchange and Systemic Vascular AbnormalitiesCHESTVol. 163Issue 1PreviewPatients with OSAHS showed evidence of pulmonary gas exchange abnormalities during exercise (in the form of increased dead space) and resting systemic vascular dysfunction that may explain reduced exercise capacity and increased exertional dyspnea intensity. Full-Text PDF