Does Untreated OSA Really Influence Exercise Tolerance?

Daniel Okin, Ching-Ying Huang, George A. Alba, B. Taylor Thompson, Lisa M. Bebell,Peggy S. Lai

Chest(2023)

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In CHEST (January 2023), Elbehairy et al1Elbehairy A. Geneidy N. Mahmoud M. 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 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.1Elbehairy A. Geneidy N. Mahmoud M. 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 investigators used arterial blood gas analysis during CPET to help demonstrate ventilatory and gas exchange abnormalities during exercise in patients with untreated OSA. We believe there are a few important points worthy of mention. First is the issue of generalizability. Whether untreated OSA affects cardiovascular health remains unclear, though evolving research supports that the degree of nocturnal hypoxia more than the apnea-hypopnea index captures OSA severity and may drive the cardiovascular sequelae of this disease. Consequently, heterogeneity exists in how untreated OSA affects cardiovascular health, including CRF, influenced by the depth and duration of oxygen desaturation.2Dewan N. Nieto J. Somers V. Intermittent hypoxemia and OSA: implications for comorbidities.Chest. 2015; 147: 266-274Abstract Full Text Full Text PDF PubMed Scopus (382) Google Scholar In this study by Elbehairy et al,1Elbehairy A. Geneidy N. Mahmoud M. 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 hypoxia in the OSA group, as reflected by time with oxygen saturation (Spo2) less than 90%, Spo2 nadir, and the oxygen desaturation index is significant. This won’t be the case for every patient with an equivalent apnea-hypopnea index. Furthermore, subjects in the OSA group displayed evidence of pulmonary hypertension on echocardiography. This is not a universal finding in patients with OSA, although it has shown a correlation with significant nocturnal desaturation.3Atwood C. McCrory D. Garcia G. Abman S. Ahearn G. Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines.Chest. 2004; 126: 72S-77SAbstract Full Text Full Text PDF PubMed Scopus (155) Google Scholar Therefore, these results only apply to patients with OSA and more pronounced hypoxia. In comparison, we have previously demonstrated that military personnel with untreated OSA not associated with significant hypoxia maintain normal CRF.4Powell T.A. Mysliwiec V. Brock M.S. Morris M.J. OSA and cardiorespiratory fitness: a review.J Clin Sleep Med. 2022; 18: 279-288Crossref PubMed Scopus (1) Google Scholar Second, we caution against the assumption that increased dead space ventilation noted during exercise in OSA subjects in this study must be attributable to untreated OSA because a few notable baseline differences exist between groups. These differences include a higher percentage of patients who currently or actively smoke and lower resting FVC in the OSA group, which may be suggestive of underlying lung disease in this group. These confounders may have contributed to increased dyspnea experienced by subjects in the untreated OSA group, which limited exercise tolerance. Interestingly, subjective dyspnea was the predominant variable indicating maximal patient effort during CPET in this study. Other typically accepted variables include achieving a heart rate greater than 80% of predicted, achieving 80% of predicted maximum work rate, or obtaining a respiratory exchange ratio of greater than 1.15, none of which the subjects with OSA in the Elbehairy et al1Elbehairy A. Geneidy N. Mahmoud M. 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 study reached.5Ross R.M. ATS/ACCP statement on cardiopulmonary exercise testing.Am J Respir Crit Care Med. 2003; 167: 1451Crossref PubMed Scopus (183) Google Scholar None declared. Disclaimer: The views expressed herein are those of the authors and do not reflect the official policy or position of Brooke Army Medical Center, the U.S. Army Medical Department, the U.S. Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force and Department of Defense or the U.S. Government. 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 ResponseCHESTVol. 163Issue 6PreviewOSA 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.1 In this study,2 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. Full-Text PDF
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influence exercise tolerance,untreated osa
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