Non-rapid eye movement sleep activation occurs during NREM that is comparable to the type that occurs during REM. It is this sub-cortical activation that results in dreaming during the NREM stage during the morning hours. During non-REM sleep, the tonic drive to most respiratory muscles of the upper airway is inhibited. This has two consequences: However, because the diaphragm is largely driven by the autonomous system, it is relatively spared of non-REM inhibition. As such, the suction pressures it generates stay the same. This narrows the upper airway during sleep, increasing resistance and making airflow through the upper airway turbulent and noisy. For example,
Rapid eye movement sleep circulation which do not occur in any other modes of sleeping or waking. The body abruptly loses muscle tone, a state known as REM atonia. Professor Nathaniel Kleitman and his student Eugene Aserinsky defined rapid eye movement and linked it to dreams in 1953. REM sleep was further described by researchers including William Dement and Michel Jouvet. Many experiments have involved awakening test subjects whenever they begin to enter the REM phase, thereby producing a state known as REM deprivation. Subjects allowed to sleep normally again usually experience a modest REM rebound. Techniques of neurosurgery, chemical injection, electroencephalography, positron emission