Response

We and others1Elbehairy 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 (2) Google Scholar, 2Mendelson M. Bailly S. Marillier M. et al.Obstructive sleep apnea syndrome, objectively measured physical activity and exercise training interventions: a systematic review and meta-analysis.Front Neurol. 2018; 9: 73Crossref PubMed Scopus (65) Google Scholar, 3Hargens T.A. Guill S.G. Aron A. et al.Altered ventilatory responses to exercise testing in young adult men with obstructive sleep apnea.Respir Med. 2009; 103: 1063-1069Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar reported reduced exercise capacity and impaired ventilatory efficiency in patients with OSA. As we noted in that article,1Elbehairy 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 (2) Google Scholar OSA is a complex multisystem disorder, and associated comorbidities may contribute to these abnormalities. Some of these comorbidities are, in fact, sequelae of untreated intermittent nocturnal hypoxemia; this inevitably makes it difficult to conclude whether some of our findings are related to the primary disease or its closely related complications. Also considering that this was an observational study, direct causality cannot be asserted confidently. We acknowledge the lack of polysomnography in the control group,1Elbehairy 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 (2) Google Scholar but we included only participants who were asymptomatic and deliberately identified them as “asymptomatic control participants.” Apart from one participant with controlled diabetes mellitus, none of these participants had other relevant comorbidities that could affect exercise responses. Because untreated OSA is related strongly to increased arterial stiffness and impaired cardiovascular function,4Usui Y. Takata Y. Inoue Y. et al.Severe obstructive sleep apnea impairs left ventricular diastolic function in non-obese men.Sleep Med. 2013; 14: 155-159Crossref PubMed Scopus (34) Google Scholar these parameters were (as expected) significantly different between groups and were likely to contribute to impaired exercise responses. Severe OSA may contribute directly to left ventricular diastolic dysfunction, irrespective of left ventricular geometry, arterial stiffness, obesity, and its associated cardiovascular risk factors;4Usui Y. Takata Y. Inoue Y. et al.Severe obstructive sleep apnea impairs left ventricular diastolic function in non-obese men.Sleep Med. 2013; 14: 155-159Crossref PubMed Scopus (34) Google Scholar left ventricular dysfunction is also amenable to improvement when OSA is treated with CPAP.5Shim C.Y. Kim D. Park S. et al.Effects of continuous positive airway pressure therapy on left ventricular diastolic function: a randomised, sham-controlled clinical trial.Eur Respir J. 2018; 511701774Crossref PubMed Scopus (25) Google Scholar Thus, distinguishing whether the elevated VD/VT and V.E-V. CO2, that we identified,1Elbehairy 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 (2) Google Scholar were caused directly by OSA or by one of its sequelae (ie, left ventricular diastolic dysfunction) can be difficult. It is worth noting that exertional (and not resting) VD/VT and V.E-V. CO2 were different between groups, which suggests impairments in exercise-related adaptations. We noted the lower FVC in the OSA group, but values were still within the normal range, and there was no clinical evidence of any restrictive disease. Patients were also able to expand their tidal volume during exercise like the control participants, with no plateau noted towards end exercise. Impaired respiratory mechanics is thus less likely to contribute to reduced exercise capacity in our sample. Finally, we deliberately chose a slow ramp protocol given the sedentary lifestyle and poor fitness level of most participants; this protocol may have affected peak exercise measurements but allowed running comparisons at several submaximal workloads.1Elbehairy 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 (2) Google Scholar The anaerobic threshold was identified with the use of two methods by two independent researchers. In summary, our findings support the idea that exercise intolerance (and exertional dyspnea) in OSA is multifactorial and could be related to OSA and/or its complications. This observational study sets the stage for future studies to confirm direct causality, and we agree with Zeba et al that a well-conducted and controlled cross-over study would help advance understanding. See earlier cited article for author conflicts of interest. Challenges in Studying Exercise PhysiologyCHESTVol. 163Issue 5PreviewWe read with interest the article in CHEST (January 2023) by Elbehairy et al1 on exercise tolerance in untreated sleep apnea. The study found that, during exercise at an equivalent work rate, patients with untreated OSA had decreased ventilatory efficiency with increased dead space to tidal volume ratio than control subjects. The authors argue these findings could be due to a reduction in pulmonary vessel recruitment with increased cardiac output during exercise. Although this hypothesis is attractive, we wonder if some features of the study should reduce confidence in the conclusion that the observed differences between groups are, in fact, caused by 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