Critical diaphragm failure in sudden infant death syndrome 119 SIDS deaths worldwide between 40% (Argentina) and 83% (Ireland) (2). SIDS can occur in the supine resting position, but any hypothesis regarding the etiology of SIDS must convincingly explain why the prone sleeping position is such a signiﬁcant risk factor. The effects of the prone sleeping position on diaphragm function have been considered previously (82). The hypothesis that the prone sleeping position signiﬁcantly increases the work-load of the dia- phragm was tested by Rehan and co-workers in a study with 16 healthy infants (83). The study showed that in the prone position the diaphragm is signiﬁ- cantly thicker and, therefore, shorter at the end of both expiratory (EEV) and inspiratory lung volumes (EIV). The shortening of any muscle produces a marked fall in the maximal tension it can develop (19), indicating that the inspiratory muscle force of the diaphragm decreases as it shortens. Indeed, Rehan and colleagues note that ‘this degree of dia- phragm shortening is similar to that seen with an increase in lung volume of 15%–30% of vital capacity’. Such increases in EEV can signiﬁcantly impair diaphragm performance, and, as Rehan and colleagues conclude, ‘in adults, diaphragm strength and endurance as well as the efﬁciency of breathing are reduced by 40%–50% with this magnitude of increase in lung volume’. Greenough and colleagues have reported similar results in several clinical studies with premature infants and observe that respiratory muscle strength is signiﬁcantly reduced in the prone compared to the supine position in (106–108). Interestingly, an earlier study that measured infant breathing did not ﬁnd signiﬁcant differences in ven- tilatory performance as a function of sleep position (84). However, the study reported a signiﬁcant increase (+66%) in rib-cage motion in the prone compared with the supine position. Others have observed that due to the high rib-cage compliance in young infants, the thorax motion increases either during deep inspiratory effort or when the intercostals are inactivated (31). As both the sleep position studies were conducted during non-REM (NREM) sleep when the intercostals are active, it is possible that the signiﬁcantly increased thoracic motion in the prone position was due to increased diaphragm work needed to maintain ventilation pressure at the same level as in the supine position. Indeed, in another study with healthy infants sleeping in the prone position, chest wall distortion during REM sleep led to the reduction of the tidal volume, but ventilation was upheld by signiﬁcantly (P < 0.01) increasing the work-load of the diaphragm (85). We suggest that healthy infants with normal diaphragms can easily tolerate the added mechanical strain that the prone position imposes on the diaphragm. How- ever, for some infants the prone sleeping position combined with an infectious episode can increase the risk of CDF. Why is SIDS associated with sleep? SIDS deaths often take place between midnight and 6 a.m. (5,86), and there is a close temporal relation- ship between SIDS and sleep (87). The original name for SIDS, ‘cot death’, reﬂects this basic observation. The reason for the preponderance of SIDS deaths during sleep is unclear, and while we should remem- ber that newborns sleep up to 20 hours per day, there seems to be a causal link between sleep and SIDS. A premature infant spends up to 80% and a 3-month- old approximately 38% of his sleep in the REM phase (19). It is well known that the intercostals muscles show both phasic and tonic inhibition during REM sleep that renders them largely or totally inactive, and that this has a signiﬁcant effect on respiratory function (31,88–90). The intercostals play a central role in stabilizing the thorax, and, as Davis and Bureau note, ‘chest wall muscles are critical for ventilation in the infant with a pliable chest wall’ (66). Others have suggested that the inactivation of the intercostals during REM sleep may be a contributing factor in SIDS (82). We argue that the inactivation of the intercostal muscles in combination with other factors can increase the risk of CDF. The internal and external intercostal muscles are activated to attenuate diaphragm fatigue (19,91,92). In a study with preterm infants, diaphragm fatigue was followed either by a 50%–150% increase in inter- costal activity or apnea that lasted 10–30 s and often required stimulation (93). In full-term infants, dia- phragm fatigue provokes similar responses: the inter- costal muscles are activated to support the respiratory effort or apnea lasting 5–20 s ensues (followed by intercostal muscle activation) (91). In another study, the diaphragmatic work-load in the young infant increased by over 150% (P < 0.001) during REM sleep (29). Diaphragmatic fatigue patterns were observed only in REM sleep together with marked reductions in intercostal activity and rib-cage retrac- tion. In the young infant intercostal muscle support is even more important than in the adult because their rib-cage is mostly cartilaginous and signiﬁcantly more compliant compared to adults. If the intercostals do not stabilize the rib-cage during inspiration, a signif- icant portion of the power generated by the diaphragm will be wasted sucking in the ribs rather than fresh air (94), and to maintain the same tidal volume the work of the diaphragm has to increase substantially (88).