ArticleSleep2015
Obstructive Sleep Apnea Impairs Postexercise Sympathovagal Balance in Patients with Metabolic Syndrome.
Article in Sleep, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Effect of Sleep-Disordered Breathing on Exercise Capacity after Myocardial Infarction - A Cross-Sectional Study.Reviews in cardiovascular medicine · 2023Article
- OSA and cardiorespiratory fitness: a review.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2022Review
- [Correlation of obstructive sleep apnea with components of metabolic syndrome and implications for long-term adverse cardiovascular risk in elderly patients].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Exaggerated Exercise Blood Pressure as a Marker of Baroreflex Dysfunction in Normotensive Metabolic Syndrome Patients.Frontiers in neuroscience · 2021Article
- Association of Metabolic Syndrome With Long-Term Cardiovascular Risks and All-Cause Mortality in Elderly Patients With Obstructive Sleep Apnea.Frontiers in cardiovascular medicine · 2021Article
- Identifying the risk of obstructive sleep apnea in metabolic syndrome patients: Diagnostic accuracy of the Berlin Questionnaire.PloS one · 2019Article
- The role of increased glucose on neurovascular dysfunction in patients with the metabolic syndrome.Journal of clinical hypertension (Greenwich, Conn.) · 2017Article
- The Role of Acute Intermittent Hypoxia in Neutrophil-Generated Superoxide, Sympathovagal Balance, and Vascular Function in Healthy Subjects.Frontiers in physiology · 2017Article
- Chronic obstructive pulmonary disease severity and its association with obstructive sleep apnea syndrome: impact on cardiac autonomic modulation and functional capacity.International journal of chronic obstructive pulmonary diseaseArticle
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
objectivesThe attenuation of heart rate recovery after maximal exercise (ΔHRR) is independently impaired by obstructive sleep apnea (OSA) and metabolic syndrome (MetS). Therefore, we tested the hypotheses: (1) MetS + OSA restrains ΔHRR; and (2) Sympathetic hyperactivation is involved in this impairment.
designCross-sectional study.
participantsWe studied 60 outpatients in whom MetS had been newly diagnosed (ATP III), divided according to apnea-hypopnea index (AHI) ≥ 15 events/h in MetS + OSA (n = 30, 49 ± 1.7 y) and AHI < 15 events/h in MetS - OSA (n = 30, 46 ± 1.4 y). Normal age-matched healthy control subjects (C) without MetS and OSA were also enrolled (n = 16, 46 ± 1.7 y).
interventionsPolysomnography, microneurography, cardiopulmonary exercise test. MEASUREMENTS AND
resultsWe evaluated OSA (AHI - polysomnography), muscle sympathetic nerve activity (MSNA - microneurography) and cardiac autonomic activity (LF = low frequency, HF = high frequency, LF/HF = sympathovagal balance) based on spectral analysis of heart rate (HR) variability. ΔHRR was calculated (peak HR minus HR at first, second, and fourth minute of recovery) after cardiopulmonary exercise test. MetS + OSA had higher MSNA and LF, and lower HF than MetS - OSA and C. Similar impairment occurred in MetS - OSA versus C (interaction, P < 0.01). MetS + OSA had attenuated ΔHRR at first, second, and at fourth minute than did C, and attenuated ΔHRR at fourth minute than did MetS - OSA (interaction, P < 0.001). Compared with C, MetS - OSA had attenuated ΔHRR at second and fourth min (interaction, P < 0.001). Further analysis showed association of the ΔHRR (first, second, and fourth minute) and AHI, MSNA, LF and HF components (P < 0.05 for all associations).
conclusionsThe attenuation of heart rate recovery after maximal exercise is impaired to a greater degree where metabolic syndrome (MetS) is associated with moderate to severe obstructive sleep apnea (OSA) than by MetS with no or mild or no OSA. This is at least partly explained by sympathetic hyperactivity.
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