scholarly journals Arousal from Sleep Does Not Lead to Reduced Dilator Muscle Activity or Elevated Upper Airway Resistance on Return to Sleep in Healthy Individuals

SLEEP ◽  
2015 ◽  
Vol 38 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Amy S. Jordan ◽  
Jennifer M. Cori ◽  
Andrew Dawson ◽  
Christian L. Nicholas ◽  
Fergal J. O'Donoghue ◽  
...  
1998 ◽  
Vol 84 (3) ◽  
pp. 1055-1062 ◽  
Author(s):  
Rainer M. Popovic ◽  
David P. White

Obstructive sleep apnea is a disorder with a strong male predominance. One possible explanation could be an effect of female hormones on pharyngeal dilator muscle activity. Therefore, we determined the level of awake genioglossus electromyogram (EMGgg) and upper airway resistance in 12 pre- and 12 postmenopausal women under basal conditions and during the application of an inspiratory resistive load (25 cmH2O ⋅ l−1 ⋅ s). In addition, a subgroup of eight postmenopausal women were studied a second time after 2 wk of combined estrogen and progesterone replacement in standard doses. Peak phasic and tonic genioglossus activity, expressed as a percentage of maximum, were highest in the luteal phase of the menstrual cycle (phasic 23.9 ± 3.8%, tonic 10.2 ± 1.0%), followed by the follicular phase (phasic 15.5 ± 2.2%, tonic 7.3 ± 0.8%), and were lowest in the postmenopausal group (phasic 11.3 ± 1.6%, tonic of 5.0 ± 0.6), whereas upper airway resistance did not differ. There was a weak but significant positive correlation between progesterone levels and both peak phasic ( P < 0.05) and tonic ( P < 0.01) EMGgg. Finally, there was a significant increase in EMGgg in the postmenopausal group restudied after hormone therapy. In conclusion, female hormones (possibly progesterone) have a substantial impact on upper airway dilator muscle activity.


1998 ◽  
Vol 84 (2) ◽  
pp. 486-491 ◽  
Author(s):  
Kathe G. Henke

Henke, Kathe G. Upper airway muscle activity and upper airway resistance in young adults during sleep. J. Appl. Physiol. 84(2): 486–491, 1998.—To determine the relationship between upper airway muscle activity and upper airway resistance in nonsnoring and snoring young adults, 17 subjects were studied during sleep. Genioglossus and alae nasi electromyogram activity were recorded. Inspiratory and expiratory supraglottic resistance (Rinsp and Rexp, respectively) were measured at peak flow, and the coefficients of resistance ( K insp and K exp, respectively) were calculated. Data were recorded during control, with continuous positive airway pressure (CPAP), and on the breath immediately after termination of CPAP. Rinsp during control averaged 7 ± 1 and 10 ± 2 cmH2O ⋅ l−1 ⋅ s and K inspaveraged 26 ± 5 and 80 ± 27 cmH2O ⋅ l−1 ⋅ s−2in the nonsnorers and snorers, respectively ( P = not significant). On the breath immediately after CPAP, K insp did not increase over control in snorers (80 ± 27 for control vs. 46 ± 6 cmH2O ⋅ l−1 ⋅ s−2for the breath after CPAP) or nonsnorers (26 ± 5 vs. 29 ± 6 cmH2O ⋅ l−1 ⋅ s−2). These findings held true for Rinsp. K exp did not increase in either group on the breath immediately after termination of CPAP. Therefore, 1) increases in upper airway resistance do not occur, despite reductions in electromyogram activity in young snorers and nonsnorers, and 2) increases in Rexp and expiratory flow limitation are not observed in young snorers.


1987 ◽  
Vol 63 (2) ◽  
pp. 603-608 ◽  
Author(s):  
D. W. Hudgel ◽  
M. Mulholland ◽  
C. Hendricks

The purposes of this study were 1) to characterize the immediate inspiratory muscle and ventilation responses to inspiratory resistive loading during sleep in humans and 2) to determine whether upper airway caliber was compromised in the presence of a resistive load. Ventilation variables, chest wall, and upper airway inspiratory muscle electromyograms (EMG), and upper airway resistance were measured for two breaths immediately preceding and immediately following six applications of an inspiratory resistive load of 15 cmH2O.l–1 X s during wakefulness and stage 2 sleep. During wakefulness, chest wall inspiratory peak EMG activity increased 40 +/- 15% (SE), and inspiratory time increased 20 +/- 5%. Therefore, the rate of rise of chest wall EMG increased 14 +/- 10.9% (NS). Upper airway inspiratory muscle activity changed in an inconsistent fashion with application of the load. Tidal volume decreased 16 +/- 6%, and upper airway resistance increased 141 +/- 23% above pre-load levels. During sleep, there was no significant chest wall or upper airway inspiratory muscle or timing responses to loading. Tidal volume decreased 40 +/- 7% and upper airway resistance increased 188 +/- 52%, changes greater than those observed during wakefulness. We conclude that 1) the immediate inspiratory muscle and timing responses observed during inspiratory resistive loading in wakefulness were absent during sleep, 2) there was inadequate activation of upper airway inspiratory muscle activity to compensate for the increased upper airway inspiratory subatmospheric pressure present during loading, and 3) the alteration in upper airway mechanics during resistive loading was greater during sleep than wakefulness.


1990 ◽  
Vol 69 (4) ◽  
pp. 1252-1261 ◽  
Author(s):  
D. A. Wiegand ◽  
B. Latz ◽  
C. W. Zwillich ◽  
L. Wiegand

Sleep-related reduction in geniohyoid muscular support may lead to increased airway resistance in normal subjects. To test this hypothesis, we studied seven normal men throughout a single night of sleep. We recorded inspiratory supraglottic airway resistance, geniohyoid muscle electromyographic (EMGgh) activity, sleep staging, and ventilatory parameters in these subjects during supine nasal breathing. Mean inspiratory upper airway resistance was significantly (P less than 0.01) increased in these subjects during all stages of sleep compared with wakefulness, reaching highest levels during non-rapid-eye-movement (NREM) sleep [awake 2.5 +/- 0.6 (SE) cmH2O.l-1.s, stage 2 NREM sleep 24.1 +/- 11.1, stage 3/4 NREM sleep 30.2 +/- 12.3, rapid-eye-movement (REM) sleep 13.0 +/- 6.7]. Breath-by-breath linear correlation analyses of upper airway resistance and time-averaged EMGgh amplitude demonstrated a significant (P less than 0.05) negative correlation (r = -0.44 to -0.55) between these parameters in five of seven subjects when data from all states (wakefulness and sleep) were combined. However, we found no clear relationship between normalized upper airway resistance and EMGgh activity during individual states (wakefulness, stage 2 NREM sleep, stage 3/4 NREM sleep, and REM sleep) when data from all subjects were combined. The timing of EMGgh onset relative to the onset of inspiratory airflow did not change significantly during wakefulness, NREM sleep, and REM sleep. Inspiratory augmentation of geniohyoid activity generally preceded the start of inspiratory airflow. The time from onset of inspiratory airflow to peak inspiratory EMGgh activity was significantly increased during sleep compared with wakefulness (awake 0.81 +/- 0.04 s, NREM sleep 1.01 +/- 0.04, REM sleep 1.04 +/- 0.05; P less than 0.05). These data indicate that sleep-related changes in geniohyoid muscle activity may influence upper airway resistance in some subjects. However, the relationship between geniohyoid muscle activity and upper airway resistance was complex and varied among subjects, suggesting that other factors must also be considered to explain sleep influences on upper airway patency.


1985 ◽  
Vol 58 (5) ◽  
pp. 1489-1495 ◽  
Author(s):  
J. P. Farber

The suckling opossum exhibits an expiration-phased discharge in abdominal muscles during positive-pressure breathing (PPB); the response becomes apparent, however, only after the 3rd-5th wk of postnatal life. The purpose of this study was to determine whether the early lack of activation represented a deficiency of segmental outflow to abdominal muscles or whether comparable effects were observed in cranial outflows to muscles of the upper airways due to immaturity of afferent and/or supraspinal pathways. Anesthetized suckling opossums between 15 and 50 days of age were exposed to PPB; electromyogram (EMG) responses in diaphragm and abdominal muscles were measured, along with EMG of larynx dilator muscles and/or upper airway resistance. In animals older than approximately 30 days of age, the onset of PPB was associated with a prolonged expiration-phased EMG activation of larynx dilator muscles and/or decreased upper airway resistance, along with expiratory recruitment of the abdominal muscle EMG. These effects persisted as long as the load was maintained. Younger animals showed only those responses related to the upper airway; in fact, activation of upper airway muscles during PPB could be associated with suppression of the abdominal motor outflow. After unilateral vagotomy, abdominal and upper airway motor responses to PPB were reduced. The balance between PPB-induced excitatory and inhibitory or disfacilitory influences from the supraspinal level on abdominal motoneurons and/or spinal processing of information from higher centers may shift toward net excitation as the opossum matures.


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