Sleep disordered breathing (SDB) is commonly treated with continuous positive airway pressure (CPAP) therapy. This first-line medical treatment modality is highly efficacious in reducing apneic/hypopneic events during sleep, improving nocturnal oxygenation, and reducing cortical arousals during sleep.1 Yet the overall effectiveness of CPAP for SDB is significantly limited by adherence. Across numerous studies and various applied adherence definitions over the past three decades, rates of adherence to CPAP are approximately 50%, with an additional 8% to 15% refusing CPAP after initial exposure.2 Further, adherence rates have remained largely stable since CPAP was first introduced in 1981, and intervention trials to promote CPAP adherence have not been highly successful.3 In order to address this clinical and scientific quandary, exploration of alternative SDB treatment approaches may present significant opportunities to improve the overall health and functional outcomes of the SDB population.
A physically active lifestyle is known to be associated with an array of health benefits, including reduced mortality from all causes.4,5 Although the physiologic adaptations that occur in response to physical activity and exercise are well described, one often overlooked benefit is the potential to improve sleep quality. As Kline and colleagues note in this issue of SLEEP,6 several epidemiologic studies have shown that physically active individuals have better sleep quality, with exercise training reported to improve the apnea hypopnea index (AHI) in persons with underlying obstructive sleep apnea (OSA). Unfortunately, though, according to the Centers for Disease Control and Prevention (CDC), only 35% of adults engage in regular leisure-time physical activity in spite of clear messages about the benefits.
Building on this evidence, Kline et al.6 randomized a sample of 43 sedentary and overweight or obese adults with untreated OSA to exercise training or stretching (control group) for a 12-week study. The exercise group met 4 times each week and performed 150 min each week of moderate-intensity aerobic activity followed by resistance training twice weekly. The control group met twice weekly for 12 weeks to perform low-intensity stretching. Compared with stretching, exercise resulted in a significant (24%) reduction in AHI. Major strengths of the study6 include randomization stratified by sex and AHI in a 3:2 ratio, in-laboratory PSG testing at 3 intervals, blinding, and intention-to-treat analysis. A run-in period was used to minimize drop-out and likely mechanisms of effect (body composition, pulmonary function, and respiratory muscle strength changes) were assessed. The study was not, however, without limitations.
The sample used by Kline et al.6 largely consisted of moderate severity OSA participants, as defined by an AHI ≥ 15 without representation of severe OSA (AHI > 30 events/hour), which may have limited the observed intervention effects. Further, the study-defined SDB oxygenation parameters (i.e., minimum saturation, oxygen desaturation index [ODI], and total sleep time with SpO2 < 90%) fail to robustly capture significant variation in SDB severity. The effect size of the intervention on SDB oxygenation variables was small, with the exception of ODI. Future studies of the efficacy of exercise training on OSA will need to include not only larger samples, but greater heterogeneity in SDB severity across disease indices that address both upper airway events and oxygenation.
An important aspect of the Kline et al.6 study was a test of weight loss as the mechanism of effect. OSA is associated with obesity,7 and it is commonly accepted that weight loss can improve SDB. One of the seminal findings in the study by Kline et al.6 is that 12 weeks of exercise training reduced the AHI in obese subjects without significantly altering body mass or body composition. Thus, these data importantly suggest that weight-independent factors are involved in the improved SDB and sleep quality profiles in obese subjects. They also showed no changes in pulmonary function or respiratory muscle strength following training, suggesting that the pulmonary system also is not the mechanism of effect.
A variety of cardiac, vascular, and neurohumoral mechanisms may explain the beneficial effects of exercise on SDB.8 These improvements include (1) reduced sympathetic overdrive,9,10 (2) improved endothelial function,11,12 and/or (3) improved cardiac function.10 These hypotheses are rooted in the heart failure literature, which shows that heart failure patients, like obese subjects, often have SDB.13 Moreover, both obese persons and those with heart failure exhibit sympathetic overdrive, which can impair endothelial and cardiac function. These cardiovascular impairments may make those with SDB less able to regulate overnight fluid shifts. That is, in the supine position, positive pressure in the lower body induces fluid displacement from the legs into the neck, which increases neck circumference, pharyngeal collapsibility, and the AHI.14 Exercise training is known to reduce sympathetic activity in heart failure,9,10 thereby improving both endothelial and cardiac function.9,11,12 Attenuation in sympathetic overdrive with exercise may improve both vascular endothelial and cardiac function, thereby reducing systemic resistance, blood pressure, and fluid accumulation in the neck. Two recent studies have shown that exercise can improve the AHI in patients with systolic heart failure and SDB.10,15 In addition, exercise offers additional benefits such as control of the comorbid diseases (e.g., diabetes, cardiovascular disease) commonly associated with SDB.
In conclusion, exercise is not yet ready for prime time as a treatment choice for SDB, although the results of Kline and colleagues6 are encouraging. Many patients choose not to use CPAP, and although they may not like exercise any better, at least they would have a choice. Exercise training may induce favorable, as yet unelucidated, phenotypical shifts that improve sleep and OSA, and necessitate further research.
DISCLOSURE STATEMENT
The authors have indicated no financial conflicts of interest.
ABBREVIATIONS
- SDB
Sleep disordered breathing
- CPAP
continuous positive airway pressure
- OSA
obstructive sleep apnea
- CDC
Centers for Disease Control and Prevention
- AHI
apnea hypopnea index
- ODI
oxygen desaturation index
CITATION
Riegel B; Sawyer AM; Libonati J. The lesser of two evils. SLEEP 2011;34(12):1621-1622.
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