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Considering the five breathing cycles before and during TMS application, ventilation increased from 1.73 �� 0.64 to 2.07 �� 0.85 l min?1 (P selleckchem to prestimulation values after the second post-stimulation cycle (Fig. 4). During TMS sessions, maximal inspiratory flow and inspiratory volume increased significantly from the second breathing cycle and remained stable until the fifth. Analysis of the effects of applying consecutive TMS-induced twitches on flow regimen components of arousal-free respiratory cycles showed that the turbulent component decreased significantly from the third consecutive stimulated cycle and reached its lowest value at the fifth (r2 of all fits ranged from 0.93 to 0.99). Immediately after TMS cessation, the turbulent airflow component returned to the levels of the preceding non-stimulated breathing cycle (Fig. 5). In contrast, there was no difference in the laminar airflow component between non-stimulated and stimulated cycles. One hundred and fourteen series of consecutive TMS-induced twitches were applied, Montelukast Sodium and TMS-induced cortical and/or autonomic arousal was observed in 30.2% of them. In the presence of TMS-induced cortical arousal, the EEG power spectrum and its median frequency shifted towards higher frequencies (Fig. 3C and D). The occurrence of cortical and/or autonomic arousal was associated with marked changes in respiratory variables (Fig. 6) as well as in cardiac parameters (Table 1). In the presence of cortical and/or autonomic arousal, maximal inspiratory EPZ-6438 molecular weight flow and inspiratory volume increased by 91.5 �� 29.6 ml s?1 and 130.2 �� 32.2 ml, respectively, which is approximately 71 and 91% higher than the equivalent values obtained without arousing patients from sleep. This study shows that twitch recruitment of submental muscles by consecutive TMS without arousing OSA patients from sleep results in an increase airflow and inspiratory volume as well as a decrease in the turbulent component of airflow of flow-limited respiratory cycles. These results are consistent with a twitch-induced neuromechanical recruitment of upper airway dilator muscles altering the sleep-induced flow-limitation patterns. The rise of SUBMT during NREM sleep found in the present study is in line with the results of our previous study (Melo-Silva et al. 2013) and indicates a reduced excitability of the corticobulbar structures and hypoglossal motoneurons during sleep (Horner, 2008, 2011). These findings, together with those reported by Mehiri et al. (2006) showing a reduction of diaphragmatic responses to TMS, ratify the major effects of sleep on modulation of respiratory and upper airway muscle activation.