Derived from the present study: 1) repeated testing of "failed" newborns in the maternity hospital and before discharge leads to an acceptable referral rate of 2%; 2) the 1-month follow-up of "failed" newborns further limits the false positive results but leads to high rate of newborns lost to follow-up; 3) a dedicated secretariat system should be implemented to follow-up each "failed" newborn and remind parents about their follow-up appointments; and 4) additional measures such as detailed educational material and parental friendly approach should also be implemented.
Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists (V O 2 max : 70.0 ± 1.6 ml kg -1 min -1 ; mean ± S.E.M.) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O 2 saturation (S a,O 2 ): 92 ± 1%) and one hyperoxic (F I,O 2 : 0.5% O 2 ; S a,O 2 : 97 ± 1%) 5 min exercise test at intensities equal to 80 ± 3 and 90 ± 3% of maximal work rate (WR max ), respectively, producing the same tidal volume (V T ) and breathing frequency (f ) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure (P di,tw ) during recovery. Hyperoxic exercise at 90% WR max induced significantly (P = 0.022) greater post-exercise reduction in P di,tw (15 ± 2%) than did normoxic exercise at 80% WR max (9 ± 2%), despite the similar mean ventilation (123 ± 8 and 119 ± 8 l min -1 , respectively), breathing pattern (V T : 2.53 ± 0.05 and 2.61 ± 0.05 l, f : 49 ± 2 and 46 ± 2 breaths min -1 , respectively), mean changes in P di during exercise (37.1 ± 2.4 and 38.2 ± 2.8 cmH 2 O, respectively) and end-exercise arterial lactate (12.1 ± 1.4 and 10.8 ± 1.1 mmol l -1 , respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S a,O 2 tested. Rather, this result leads us to hypothesize that blood flow competition with the legs is an important contributor to diaphragmatic fatigue in heavy exercise, assuming that higher leg work required greater leg blood flow.
The results of this study imply an increase in the stiffness of the middle ear, which has not been detected by conventional tympanometry. This represents the first concrete documentation of minor alterations in the conductive properties of the middle ear and seems to support the various hypotheses on the middle-ear origin of aural complaints in patients with TMJ disorders. Further studies are needed before a clear insight on the presumably multifactorial pathophysiology of these complaints can finally be reached.