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The global epidemic of obesity and the worldwide prevalence of obstructive sleep apnoea (OSA) are both increasing. Epidemiological studies reveal an association between obesity, weight gain and OSA. Metabolic or bariatric operations provide sustained weight loss and resolve or improve the symptoms of OSA in the majority of morbidly obese individuals. These operations also modulate the metabolic profile to improve glycaemic control, to decrease cardiovascular risk and obesityrelated mortality. The beneficial effects of metabolic operations on OSA include mechanical weight-dependent and metabolic weight-independent effects that are achieved through the BRAVE effects: (Bile flow alteration; Reduction of gastric size; Anatomical gut rearrangement and altered flow of nutrients; Vagal manipulation; and Enteric gut hormone modulation). These result in an improvement in insulin resistance, adipokines, cytokines and systemic inflammation. A literature analysis was performed with statistical pooling of available surgical and medical studies to determine whether the weighted mean decrease in body mass index and sleep apnoea severity (measured by the apnoea-hypopnoea index) are larger in metabolic surgical studies than in non-surgical weight loss studies (diet, exercise and medication). However, heterogeneity across available trials, poor follow-up measures and a deficiency in comparative studies between surgical and non-surgical therapy precludes definitive statements regarding the relative benefits of surgical therapy. Further research is required to quantify robustly the effects and mechanisms of sleep apnoea resolution by metabolic surgery, which may reveal novel non-surgical treatments or enhanced surgical strategies in the management of this multisystem sleep disorder.

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SUMMARY1. Three normal subjects performed rest-exercise transitions on a cycle ergometer, from rest to unloaded pedalling (0 W), 50, 100 and 150 W. Each experiment was performed in triplicate, with randomized work load order, in two sessions. Ventilation was obtained breath-to-breath by integration of a pneumotachygraph signal, and cardiac output beat-to-beat by a new development of the Doppler technique. Results were bin-averaged in 4 s bins over the first 20 s, and compared to resting values.2. Both ventilation and cardiac output increased significantly in the first 2 s. This initial rise in ventilation was due entirely to an increase in rate, the subsequent rise mainly to increase in tidal volume. Cardiac output increased predominantly through change in rate with smaller increases in stroke volume.3. A striking feature was a tendency for ventilation and cardiac output responses to be biphasic with an initial rise followed by a slight fall at the 14 s mark, and a subsequent rise, at all work loads. Overall correlation between ventilation and cardiac output was therefore high (r = 0 92).4. Six normal subjects hyperventilated for 45 s voluntarily, (a) at rate 24/min and normal tidal volume; (b) at normal rate and tidal volume of 1-5 1; (c) at rate 24/min and tidal volume of 1-5 1. Cardiac output, averaged over 10-45 s, rose by 0 4, 0 5, and 1-0 1 min-respectively, with falls in end-tidal PCO, of 4, 6, and 8 mmHg.5. Six normal subjects hyperventilated for 60 s with rate 24/min and tidal volume of 1-4 1, and end-tidal Pco, maintained at 38 + 2 mmHg. Cardiac output, averaged from 10-60 s, rose by 1-0 I min'.6. With increased rate and tidal volume, whether isocapnic or hypocapnic, cardiac output responses showed an overshoot with a peak value at about 30 s.7. The hypothesis of 'cardiodynamic hyperpnoea' considers a possible effect of increasing cardiac output on ventilation. The effects of ventilation on cardiac output must also be considered. We propose an extended hypothesis involving stable positive feed-back.