Contents I. Introduction
Sleep apnea syndrome is the second most common sleep disorder. It is one of a group of sleep disordered breathing syndromes that includes snoring and upper airway resistance syndrome. Sleep apnea syndromes are divided into central, obstructive, and mixed. The most common type, obstructive sleep apnea syndrome (OSAS), is characterized by sleep induced obstruction of the upper airways that results in cessation of airflow with preservation of respiratory effort, respiratory centre drive, and diaphragmatic contraction. Repeated obstruction of the upper airways results in blood oxygen desaturation and arousal from sleep. The majority of complications of OSAS are the results of long-term hypoxia, hypercapnia, and activation of the sympathetic nervous system. Severe or long-term untreated OSAS is a life-threatening condition [1], [2]. Pae et al. showed that short-term, exogenous electrical stimulation of genioglossus induces a phenotypic shift from the fast-twitch type II MHC isoform to the slow-twitch type I MHC isoform [3]. This might reflect a natural ability of muscles to adapt and thus compensate for congenital or acquired anatomical or functional disabilities of the upper airways. However, in patients with congenital disruption of the genes for particular MHC proteins, this natural ability is lost and they therefore lose their ability to compensate for such changes and develop OSAS.
