Background Several studies have shown a favorable effect of supervised exercise training on obstructive sleep apnea (OSA). This meta-analysis was conducted to analyze the data from these studies on the severity of OSA (primary outcome) in adults. Secondary outcomes of interest included body mass index (BMI), sleep efficiency, daytime sleepiness and cardiorespiratory fitness. Methods Two independent reviewers searched PubMed and Embase (from inception to March 6, 2013) to identify studies on the effects of supervised exercise training in adults with OSA. Pre- and postexercise training data on our primary and secondary outcomes were extracted. Results A total of 5 studies with 6 cohorts that enrolled a total of 129 study participants met the inclusion criteria. The pooled estimate of mean pre- to postintervention (exercise) reduction in AHI was −6.27 events/h (95 % confidence interval [CI] −8.54 to −3.99; p < 0.001). The pooled estimates of mean changes in BMI, sleep efficiency, Epworth sleepiness scale and VO2 peak were −1.37 (95 % CI −2.81 to 0.07; p = 0.06), 5.75 % (95 % CI 2.47–9.03; p = 0.001), −3.3 (95 % CI −5.57 to −1.02; p = 0.004), and 3.93 mL/kg/min (95 % CI 2.44–5.42; p < 0.001), respectively. Conclusions This meta-analysis shows a statistically significant effect of exercise in reducing the severity of sleep apnea in patients with OSA with minimal changes in body weight. Additionally, the significant effects of exercise on cardiorespiratory fitness, daytime sleepiness, and sleep efficiency indicate the potential value of exercise in the management of OSA.

Although the diagnostic test accuracy measures of transbronchial lung cryobiopsy lag behind those of VATS, with an acceptable safety profile and potential cost savings, the former could be considered as an alternative in the evaluation of patients with diffuse parenchymal lung diseases.

Objective To systematically analyze the studies that have examined the effect of continuous positive airway pressure (CPAP) on blood pressure (BP) in patients with resistant hypertension and obstructive sleep apnea (OSA). Methods Design – meta-analysis of observational studies and randomized controlled trials (RCTs) indexed in PubMed and Ovid (All Journals@Ovid). participants: individuals with resistant hypertension and OSA; interventions – CPAP treatment. Results A total of six studies met the inclusion criteria for preintervention to postintervention analyses. The pooled estimates of mean changes after CPAP treatment for the ambulatory (24-h) SBP and DBP from six studies were −7.21 mmHg [95% confidence interval (CI): −9.04 to −5.38; P <0.001; I2 58%) and −4.99 mmHg (95% CI: −6.01 to −3.96; P <0.001; I2 31%), respectively. The pooled estimate of the ambulatory SBP and DBP from the four RCTs showed a mean net change of −6.74 mmHg [95% CI: −9.98 to −3.49; P <0.001; I2 61%] and −5.94 mmHg (95% CI: −9.40 to −2.47; P =0.001; I2 76%), respectively, in favor of the CPAP group. Conclusion The pooled estimate shows a favorable reduction of BP with CPAP treatment in patients with resistant hypertension and OSA. The effects sizes are larger than those previously reported in patients with OSA without resistant hypertension.

Rationale: Several studies have reported that both short and long sleep durations are associated with the metabolic syndrome, but whether a dose-response relationship exists is unclear.Objectives: We performed a metaanalysis to study the magnitude of the association between the different durations of sleep and metabolic syndrome. Methods:We searched in the databases of PubMed, Web of Science, and Ovid (all Journals@Ovid) from inception to October 4, 2014 for cross-sectional studies where an association between metabolic syndrome and sleep duration was analyzed. Measurements and Main Results:Eighteen studies with 75,657 participants were included. Daily sleep duration of 7 to 8 hours was used as the reference group. The odds ratio (OR) of having metabolic syndrome for short (,7 h) sleep was 1.23 (95% CI, 1.11-1.37; P , 0.001; I 2 , 71%). The ORs for less than 5 hours, 5 to 6 hours, and 6 to 7 hours of sleep were 1.51 (95% CI, 1.10-2.08; P = 0.01), 1.28 (95% CI, 1.11-1.48; P , 0.001), and 1.16 (95% CI, 1.02-1.31; P = 0.02), respectively. The coefficient of sleep duration on log of ORs was 20.06 6 0.02 (P = 0.02). The OR for long sleep duration was 1.13 (95% CI, 0.97-1.32; P = 0.10; I 2 , 89%).Conclusions: A dose-response relationship exists between short sleep duration and metabolic syndrome. Those who report a sleep duration of less than 5 hours have a 1.5 higher odds of having metabolic syndrome. Our study does not support the notion that long sleep is associated with metabolic syndrome.

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Rationale: Obstructive sleep apnea (OSA) is an independent risk factor for the development of insulin resistance (IR). Treatment with continuous positive airway pressure (CPAP) for OSA has shown conflicting results on IR.Objectives: To conduct a meta-analysis of randomized controlled trials (RCTs) that have evaluated the effect of CPAP on a validated index of IR, the homeostasis model assessment of insulin resistance (HOMA-IR).Methods: PubMed and Embase were searched through August 10, 2012. Two independent reviewers screened citations to identify trials of the effect of CPAP on HOMA-IR. Data were extracted for postintervention HOMA-IR values. Measurements and Main Results:A total of five studies that enrolled 244 subjects (83% male) met the inclusion criteria. None of the subjects in the included studies had diabetes. The pooled estimate of the difference in means in HOMA-IR between the CPAP and sham CPAP/control groups was 20.44 (95% confidence interval, 20.82 to 20.06; P = 0.02). The funnel plot does not suggest the presence of any publication bias. The I-squared index for the data on difference in means in HOMA-IR between the CPAP and sham CPAP/control groups was 0.00 (P = 0.61). Conclusions:The pooled estimate of RCTs shows a favorable effect of CPAP on insulin resistance as measured by HOMA-IR in patients with OSA without diabetes. The effect size on HOMA-IR is modest, but not insignificant, when compared with the effects of thiazolidinedione in nondiabetic patients with metabolic syndrome. Further research and RCTs are warranted involving a larger number of patients and longer treatment periods to determine the beneficial effects of CPAP on IR.

The pooled estimate shows a favorable effect of OAs on SBP, MAP, and DBP. Most of the studies were observational. Therefore, more RCTs are warranted involving a larger number of patients and longer treatment periods to confirm the effects of OA on BP.