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Abstract Context In children, growth hormone (GH) pulses occur after sleep onset in association with slow-wave sleep (SWS). There have been no studies in children to quantify the effect of disrupted sleep on GH secretion. Objective This study aimed to investigate the effect of acute sleep disruption on GH secretion in pubertal children. Methods Fourteen healthy individuals (aged 11.3-14.1 years) were randomly assigned to 2 overnight polysomnographic studies, 1 with and 1 without SWS disruption via auditory stimuli, with frequent blood sampling to measure GH. Results Auditory stimuli delivered during the disrupted sleep night caused a 40.0 ± 7.8% decrease in SWS. On SWS-disrupted sleep nights, the rate of GH pulses during N2 sleep was significantly lower than during SWS (IRR = 0.56; 95% CI, 0.32-0.97). There were no differences in GH pulse rates during the various sleep stages or wakefulness in disrupted compared with undisrupted sleep nights. SWS disruption had no effect on GH pulse amplitude and frequency or basal GH secretion. Conclusion In pubertal children, GH pulses were temporally associated with episodes of SWS. Acute disruption of sleep via auditory tones during SWS did not alter GH secretion. These results indicate that SWS may not be a direct stimulus of GH secretion. 

Electrodermal activities (EDA) are any electrical phxenomena observed on the skin. Skin conductance (SC), a measure of EDA, shows fluctuations due to autonomic nervous system (ANS) activation induced sweat secretion. Since it can capture psychophysiological information, there is a significant rise in the research work for tracking mental and physiological health with EDA. However, the current state-of-the-art lacks a physiologically motivated approach for real-time inference of ANS activation from EDA. Therefore, firstly, we propose a comprehensive model for the SC dynamics. The proposed model is a 3D state-space representation of the direct secretion of sweat via pore opening and diffusion followed by corresponding evaporation and reabsorption. As the input to the model, we consider a sparse signal representing the ANS activation that causes the sweat glands to produce sweat. Secondly, we derive a scalable fixed-interval smoother-based sparse recovery approach utilizing the proposed comprehensive model to infer the ANS activation enabling edge computation. We incorporate a generalized-cross-validation to tune the sparsity level. Finally, we propose an Expectation-Maximization based deconvolution approach for learning the model parameters during the ANS activation inference. For evaluation, we utilize a dataset with 26 participants, and the results show that our comprehensive state-space model can successfully describe the SC variations with high scalability, showing the feasibility of real-time applications. Results validate that our physiology-motivated state-space model can comprehensively explain the EDA and outperforms all previous approaches. Our findings introduce a whole new perspective and have a broader impact on the standard practices of EDA analysis.