| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Respiratory
Medicine, Ventilation
decreases at sleep onset. This change is initiated abruptly at
diaphragm; intercostals; genioglossus; tensor palatini; upper
airway resistance
VENTILATION ( However, there is some evidence to suggest that the fall in
If withdrawal of the wakefulness stimulus to breathe is responsible for
the sleep-related fall in To summarize, a hypothesis that may explain the reduced
Subjects
ABSTRACT
Top
Abstract
Introduction
Methods
Results
Discussion
References
-
electroencephalographic transitions. The aim of this study was to
determine the contributions of reduced activity in respiratory pump
muscles and upper airway dilator muscles to this change. Surface
electromyograms over the diaphragm (Di) and intercostal muscles and
fine-wire intramuscular electrodes in genioglossus (GG) and tensor
palatini (TP) muscles were recorded in nine healthy young men. It was
shown that phasic Di and both phasic and tonic TP activities were lower
during than during activity. Breath-by-breath analysis of the
changes at - transitions during the sleep-onset period showed a
number of changes. At - transitions, phasic activity of Di,
intercostal, and GG muscles fell and rose again, and phasic and tonic
activities of TP fell and remained at low levels during . With a
state transition from to , the phasic and tonic activities of
the Di, GG, and TP increased dramatically. It is now clear that the
fall in ventilation that occurs with sleep is related to a fall in
activities of both upper airway dilator muscles and respiratory pump
muscles.
INTRODUCTION
Top
Abstract
Introduction
Methods
Results
Discussion
References
) is lower in stable
sleep compared with wakefulness (10, 16). As arterial
PCO2 is higher in sleep than in
wakefulness (21), the reduced cannot simply be due to reduced CO2 production
associated with the reduced metabolic activity during sleep (5). Upper
airway resistance (UAR) is increased in stable sleep (16), and this
rise is thought to be due to narrowing of the upper airway (UA) as a
consequence of reduced tone in the UA dilator muscles, which allow the
negative pressure generated by diaphragm (Di) activation to collase the UA (10, 30). Inspiratory pump muscle activity is also higher in stable
sleep than in wakefulness (8, 22, 26), but as is
lower, compensation by the respiratory muscles for the increased UAR
can be considered to be incomplete (7). Because of the increased
inspiratory muscle activity in sleep, increased UAR, rather than
reduced drive to inspiratory muscles, has been thought to explain the
reduced in sleep (9).
with sleep is not simply due to elevated UAR. For
example, a correlation between the size of the change in UAR from
wakefulness to sleep and the change in would be
expected, but this has not been found (12). Also, an application of
nasal continuous positive airway pressure to eliminate the rise in
airway resistance in sleep does not eliminate the rise in end-tidal
PCO2 (PETCO2) in nonsnoring
subjects (16). In subjects with a permanent tracheostomy, UAR does not
rise with sleep, but PETCO2 is elevated and is lowered in non-rapid-eye-movement
sleep compared with wakefulness to the same degree as it is in normal age-matched subjects (17). Factors responsible for the fall in
during sleep could include an increased ventilatory
threshold to PCO2. In mechanically
ventilated subjects, it has been shown that the increase in
PCO2 with sleep is in part due to a
higher CO2 threshold for
recruitment of the Di; thus, for a particular level of
PCO2, there is reduced drive to the
respiratory muscles in sleep compared with wakefulness (21). This
altered response to CO2 can be
regarded as a manifestation of the wakefulness stimulus, but it is also
possible that the wakefulness exerts its influence by direct input to
motor neurons in the brain stem respiratory center. When 10 cmH2O of inspiratory positive
airway pressure were applied to spontaneously breathing and sleeping
subjects, PETCO2 remained
constant, indicating that chemical reflexes were dominant in
controlling , whereas in wakefulness
fell when inspiratory positive airway pressure was
added, presumably because of a wakefulness factor. This finding has
been regarded as indirect evidence of a wakefulness drive to breathe
(18).
, then changes in
would be expected to coincide with shifts between
wakefulness and sleep. With the use of breath-by-breath analyses during
the sleep-onset period, it has been shown that falls
abruptly within one or two breaths of a change from to electroencephalographic (EEG) activity and rises abruptly with a change
from to (25). There is also a slight rise and fall in UAR at
to and to transitions, respectively (11, 12), but the
UAR rise in sleep does not correspond to the fall in
. If sleep becomes established after an to transition, falls only a little further before
stabilizing, but UAR continues to rise until slow-wave sleep is
established. Thus most of the fall in has occurred by the time non-rapid-eye-movement sleep is established, whereas the
rise in UAR progressively increases into slow-wave sleep (13).
in sleep is that there is a loss of drive to both
the respiratory pump muscles and UA dilator muscles at sleep onset,
resulting in an initial reduction in and rise in
UAR. This fall in activity can be regarded as a withdrawal of the
wakefulness stimulus to respiratory drive. Chemical and other reflexes
modify these changes as sleep progresses but not enough to return
and UAR to awake values. This study is designed to
assess the activities of two respiratory pump muscles, the Di and
external intercostals (ICs), and of two UA muscles, genioglossus (GG)
and tensor palatini (TP), at to and to transitions
during the sleep-onset period.
METHODS
Top
Abstract
Introduction
Methods
Results
Discussion
References
Laboratory Procedure
Subjects were asked not to consume alcohol or caffeine on the day of each study. They arrived in the sleep laboratory at 9:00 PM and, after having the monitoring equipment attached, went to bed at around 11:00 PM in a dark, quiet room. They maintained a supine posture throughout data collection. Initially, they were asked to remain awake for ~10 min before falling asleep so that baseline EEG activity could be
recorded. To obtain multiple sleep onsets, they were woken once stable
stage 2 sleep had been observed and then allowed to fall asleep again.
This was repeated until ~4 h of data had been collected.
Sleep, electromyographic (EMG), and respiratory measurements were
recorded with a 16-channel Grass polygraph (model 7D). Occipital EEG,
all EMGs, airflow, and pressure measurements were also recorded on an
IBM-compatible 486 personal computer. Central
(C3/A2)
and occipital
(O1/A2)
EEGs as well as an electrooculogram were recorded. For each subject,
the occipital EEG activity during each breath was assessed as being
predominantly or , as previously described (11). Briefly, for
each subject, 10 min of unambiguous and 10 min of unambiguous were identified visually. Automated period analysis, using peak-to-peak
analysis with an amplitude criterion of 5 µV to define a peak, was
used to calculate the ratio of each breath within these periods, and
the signal-detection measurement, the equal likelihood ratio, was used
to determine the value that best discriminated from breaths.
When this criterion ratio had been calculated for a particular subject,
that subject's occipital EEG was analyzed with the breath-by-breath
automated period analysis. For each breath, a ratio of EEG activity
>8 Hz () or 
8 Hz () was calculated. This ratio for each
breath was classified as or by comparison with the criterion
ratio for that subject.
In addition, the sleep period was classified into three phases. Phase 1 was defined as the period from lights out to the first appearance of
activity in which three of five consecutive breaths were classified
as . Phase 2 was defined as the period from the end of phase 1 to
the first occurrence of a sleep spindle or K complex. Phase 3 was
defined as the period from the end of phase 2 to the end of the onset.
The development of sleep was described in terms of these phases rather
than as stages of sleep, because the changes between phases can be
identified more precisely in time than changes between stages, which
are arbitrarily defined in terms of epochs extending over a period such
as 30 s. Each breath could then be identified as occurring during phase
1, 2, or 3, and breaths within phases 2 and 3 could be identified as occurring during or EEG activity.
EMG Recordings
Diaphragmatic EMG was recorded with gold-cupped surface electrodes placed anteriorly over the subcostal margin, and external IC EMG was recorded with surface electrodes placed laterally over the sixth intercostal space. Fine-wire intramuscular electrodes were used to record GG and TP EMGs. The wire was stainless steel 3/1,000-in. thick, with a 1/1,000-in. Teflon coating. The Teflon was stripped from the end of the wire for 1.5 mm, and a 1-mm hook was fashioned in the end of the wire. The wires were inserted into the muscles perorally with hypodermic needles. The sites of insertion were anesthetized with a small amount of 2% lidocaine gel. While the electrodes were being inserted the visual and auditory EMG signals were monitored to ensure that the electrodes were placed in muscle. To confirm that the electrodes were in the correct muscle, a series of maneuvers were performed that have previously been shown to elicit responses from GG and TP (14, 23). Jaw opening, jaw protrusion, blowing, sucking, swallowing, nasal breathing, and increased tidal volume produced increases in the EMG activity of TP. Tongue protrusion, the Muller maneuver, swallowing, and increased tidal volume produced increased EMG activity in GG.Sections of the recording containing movement and other artifacts were removed before analysis. Furthermore, 100- to 160-ms sections of the Di and IC surface EMGs containing QRS complexes were removed and replaced by the data points in the 50- to 80-ms periods before and after the QRS complex by using computer software. The raw EMG signals for all muscles were then integrated by using a 100-ms moving time average (MTA). For each muscle, several values were calculated on a breath-by-breath basis. 1) Tonic activity: for each breath, the preceding expiration was divided into 10 equal time periods, and the mean EMG amplitude from the period with the lowest mean amplitude was used as the tonic activity for that breath. 2) Phasic activity: the area under the inspiratory MTA curve above the tonic activity level identified in the previous expiratory phase. 3) Total inspiratory activity: the total area under the inspiratory MTA curve. It should be noted that because tonic activity was defined as the lowest level of activity during expiration, statistically, all muscles were identified as having phasic activity.
Measurement of
for each breath.
Measurement of UAR
Simultaneous recordings of mask pressure, epiglottic pressure, and airflow were used to calculate UAR. Mask pressure was recorded via a pressure transducer (Validyne DP45-28) and carrier demodulator (Validyne CD15). The other side of the pressure transducer was connected to an equal length of tubing left open to the atmosphere. Epiglottic pressure was measured with a transducer-tipped catheter (Millar model MPC-500) inserted through the nose and advanced until the tip was 1 cm below the base of the tongue. The nostril was premedicated with 0.05% oxymetazoline hydrochloride spray and 2% lidocaine gel. Computer software was used to calculate the pressure gradient across the UA from epiglottis to mask and to zero this pressure differential at the end of inspiration and at the end of expiration, the points of zero flow. Whereas a number of resistance measurements were generated by the software, the UAR reported was the resistance at peak airflow.Data Analysis
Overall mean values for each phase and state. The mean and UAR in phase
2, phase 2, phase 3 and phase 3 were calculated within
subjects by averaging all breaths of each type and then over subjects.
For each subject, the mean EMG activities of the four muscles for each
phase and state were expressed as a percentage of the average phase
1 activity for that subject. These data were then averaged across
the subjects.
Changes at to and to transitions. 1) Once
each breath had been classified as occurring during or EEG
activity, computer software was used to identify sets of consecutive
or breaths occurring on either side of to transitions
and of to transitions. Thus, for each transition, four to ten
breaths were identified, two to five consecutive breaths and two to five consecutive breaths. Each of these breaths then had an identifiable position within a transition from 
5 to +5. For each subject, the parameters of interest were averaged for each breath position. These parameters were , UAR at peak flow,
and the EMG activities of Di, IC, GG, and TP muscles expressed as
arbitrary units. Each subject had to have data from at least five
breaths at a particular breath position for those data to be included, so that an aberrant breath from one subject would not unduly bias the
group data.
2) As raw score EMG units are
arbitrary and depend on degrees of amplification, group data can be
excessively influenced by one subject, thus the EMG activity for each
posttransition breath was expressed as a percentage of the
pretransition baseline level. This baseline was defined as the average
of the breaths 5 to 2 for each type of transition, i.e.,
to in phase 2, to in phase 3, to in phase 2, and to in phase 3. Breath position 1 was not used to
determine the baseline, since a breath in the +1 or 1 position
may have the change in EEG activity occurring within it and so it may
not be purely or activity. It should be noted that because the
EEG state transition did not typically occur at the onset of the
inspiratory phase, there was a lack of precision in the classification
of breaths at transitions results in some smoothing of the data over
the transition, so that the impression is created that changes
occurring at a transition are commencing before the actual transiton
occurs.
Extended transition data. Initially,
only five breaths on either side of a transition were used so that a
reasonable numbers of breaths and subjects were represented at each
breath position. However, to see whether there were further changes in
the EMG activities beyond the 5th posttransition breath, the to transitions were extended to 20 posttransition breaths. In this
analysis, there only had to be one breath from each subject at each
breath position for the data to be included, and the EMG activities
were again expressed as a percentage of the mean activity of the
5 to 2 breaths. Data from phases 2 and 3 were combined.
Statistics
Overall mean data for each phase and state. A 2 × 2 ANOVA with repeated measures on each factor was used to assess the effect of phase and state on, UAR, and EMG activities expressed as a percentage
of phase 1 activity. In addition, one-sample
t-tests were used to compare EMG
activity in phase 2 and phase 3 with activity in phase 1.
Changes at transitions. For each
transition type, single-sample t-tests
were performed, comparing data at each posttransition breath position
expressed as a percentage of the mean of the 5 to 2 data
with a reference value of 100%.
Extended transitions. Single-sample
t-tests were again performed,
comparing data at each posttransition breath position expressed as a
percentage of the mean of the 5 to 2 data with a
reference value of 100%.
A P value <0.05 was considered to be significant for all statistical analyses.
| |
RESULTS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
The data from one subject were discarded because the computer file was
corrupted and the data could not be analyzed, and the data from another
were discarded because he had frequent apneas. Thus the data from nine
subjects, each completing 2 nights, were analyzed. An example of the
raw data is shown in Fig. 1. It shows changes in the EEG activity from to and then from to , and the associated falls and rises in and EMG
activities of Di, IC, GG, and TP. The ECG signal can be seen in the raw
Di and IC EMG tracings. Note that the changes in the EMG activities
coincide very closely with the change in the EEG.
|
Overall Mean Values for Each Phase and State
The group mean data as a function of state ( and ) and phase (2 and 3) for all breaths for , UAR at peak flow, and
the activities of the muscles expressed as a percentage of phase 1 activity are shown in Table 1.
was significantly lower in than in in both
phases 2 and 3. UAR was greater in than in in both phases 2 and
3 (Table 1). Di total inspiratory activity and phasic activity were
lower in sleep () compared with wakefulness (), but there was no
difference in tonic activity. IC and GG total inspiratory, phasic, and
tonic activities were not significantly different between sleep and
wakefulness. TP total inspiratory, phasic, and tonic activities were
greater in wakefulness than in sleep. With respect to phase, Di and GG
total inspiratory activities and phasic activities were higher in phase
3 than in phase 2. There were no differences in their tonic activities
between the phases. IC and TP total inspiratory, phasic, and tonic
activities were not significantly different between phases 2 and 3. There were no significant state-by-phase interactions.
|
A comparison of values in phases 1, 2, and 3, expressed as a
percentage of phase 1 activity, indicated that Di total inspiratory and phasic activities and GG total inspiratory and phasic activities were all significantly greater in phase 3 than in phase 1. There were
no other significant differences between phase 3 and phase 1
activities. There were no significant differences between phase 2
and phase 1 activities for any of the muscles.
Changes at Transitions
To examine the state changes in more detail, the group data for each of the five breaths on either side of transitions were plotted. There was an average of seven sleep onsets per night (range 3-13). The mean number of transitions per subject were 55.0 to transitions in
phase 2 (range 20-84), 68.4 to transitions in phase 3 (range 0-180), 43.6 to transitions in phase 2 (range
13-93), and 58.0 to transitions in phase 3 (range
0-146). The data for total inspiratory EMG activity are illustrated in Figs. 2 and
3, for phasic activity in Figs.
4 and 5, and
for tonic activity in Figs. 6 and
7. Significant effects have been indicated
on the graphs.
|
|
|
|
|
|
fell and UAR increased at to transitions and
rose again and UAR fell at to transitions.
The changes were greater in phase 3 than in phase 2.
Di total inspiratory activity fell at to transitions, with a
greater fall in phase 3. Phasic activity also fell, but there was no
significant change in tonic activity. At to transitions, Di
total inspiratory and phasic activities increased, more so in phase 3 than in phase 2.
IC total inspiratory and phasic activity had inconsistent changes at
to transitions, and tonic activities did not change. At to
transitions, there were no significant changes.
GG total inspiratory and phasic inspiratory activity fell at to transitions for one to three breaths but then returned to the baseline
level. Tonic GG activity did not show a consistent fall. At to transitions, GG total inspiratory, phasic, and tonic activities
significantly increased on the first or second breath in phase 3, but not in phase 2.
TP total inspiratory, phasic, and tonic activities decreased in phase
2. The decreases in phase 3 were not significant because of
one subject's data. In phase 3, the subject's TP EMG activity fell to
very low levels when there was a long period of , rose with activity, and fell again when was resumed, consistent with other
subjects' data, but took a while to fall to the very low
levels. When an to transition was spanned by a breath that
was classified as occurring during activity, some of the very low TP EMG activity in the period of preceding the
transition was incorporated into the breath, so that the average
TP activity for that breath was artificially low, distorting the
pattern of change. When these data were excluded, the changes in phase
3 were significant. At to transitions, TP total inspiratory and
phasic activities increased, but there was no significant increase in
tonic activity.
In summary, at transitions from to , there were decreases in the
EMG activities of Di, IC, GG, and TP, although there were differences
in duration over which activity was decreased. At transitions from to , there were increases in the activities of Di, GG, and TP.
Extended Transitions
The to transition data for total inspiratory EMG activity were
extended to 20 posttransition breaths; phases 2 and 3 were combined
(Fig. 8). There was a significant fall in
Di activty, although by the 17th posttransition breath its activity was
no longer significantly below baseline. There was no significant change
from baseline in IC. GG activity had an initial significant fall below
baseline, although by the 4th posttransition breath it was no longer
significantly below baseline and by the 15th breath it was
significantly above baseline. TP activity fell below baseline
immediately after the transition and was still significantly below
baseline by the 20th posttransition breath.
|
| |
DISCUSSION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
This study illustrates several findings with respect to the activities
of respiratory pump and UA muscles at sleep onset. The first was that
both phasic Di activity and phasic and tonic TP activities were reduced
in sleep compared with wakefulness. This conclusion only applies to the
sleep-onset period during which our subjects were studied. Because the
subjects were woken once stable sleep had become established, the
results could not be applied to differences between stable sleep and
wakefulness. The discrepancy between our study and others
that have found Di activity to be higher, or the same, in sleep than in
wakefulness (8, 22) is likely to be due to recruitment of the Di if
sleep is allowed to progress undisturbed after the initial fall in Di activity at the transition from to . The TP findings are
consistent with those of Wheatley et al. (27) and Tangel et al. (24), who found that TP activity was lower in stable sleep than in
wakefulness. Other studies have shown that overall GG activity is the
same in stable sleep as in stable wakefulness (23, 24, 30), which is
consistent with our data.
The second and more important finding of this study relates to the
detailed examination of the changes in respiratory muscles. This has
shown that the phasic activities of all muscles decreased within a few
breaths of a change from to EEG activity and that the tonic
activity of TP also decreased. Not only did GG activity fall abruptly
but it had recruitment that occurred within five breaths of the
transition, so that the level of GG activity in was the same as in
. This is consistent with the idea that GG activity is important for
maintaining a patent UA in sleep (24); if GG was not recruited during
sleep, then UAR would rise further and the UA would be subject to
collapse and, possibly, closure. We do not have data to explain the
mechanism of recruitment of GG following its initial fall but,
consistently with others, we speculate that GG is
recruited in response to increasing negative UA pressure and/or
rising CO2. The response of GG to
negative UA pressure is delayed in sleep and is variable between
studies and between subjects within studies (26). An increase in
activity in response to CO2 has
been shown in GG in humans (1), in GG in rabbits (2), and in the
hypoglossal nerve in cats (3). In contrast to GG, TP activity did not
recover over 20 breaths following a transition.
At to transitions, there were abrupt increases in the
activities of Di, GG, and TP, particularly in phase 3. As these changes
occurred within a few breaths of a change from to and from to , it is likely that state had a direct influence on the
activities of these muscles. This supports the notion of the
wakefulness stimulus having a direct influence on the activities of
respiratory muscles (both pump and UA) during wakefulness, so that,
when it is withdrawn in sleep, respiratory muscle activity falls.
Because the wakefulness stimulus returns with activity, the
activities of these muscles increase. It is not possible in this study
to determine how the wakefulness stimulus exerts its influence on the
respiratory muscles, but as discussed below it could be by altering the
ventilatory sensitivity and/or set point to
CO2.
Mezzanotte et al. (15) is the only other group to study respiratory
muscle changes at sleep onset. They found that in the first two breaths
after the EEG changed to the GG EMG fell to 89.7 and 87.4% of the
baseline activity, and TP EMG fell to 94.5 and 98.8%. These are
comparable to the changes we found, although by analyzing 20 posttransition breaths we found that GG increased again after this
fall and that TP activity continued to fall so that it was 75% of its
pretransition level by the 5th posttransition breath, and 61% by the
20th breath. Our study also looked at to transitions and showed
brisk rises in Di, IC, GG, and TP activities with a return to activity. We simultaneously measured , UAR, and the
EMG activities of Di and IC, demonstrating a fall in
and Di activity and rise in UAR at to transitions. When a
distinction is made between the phasic and tonic components of the
respiratory muscles, it can be seen that at to transitions phasic activity of Di and GG fell with little change in tonic activity.
In contrast, TP had little change in phasic activity but a clear fall
in tonic activity. This is consistent with White's proposition that GG
is predominantly a phasic muscle and TP is predominantly a tonic muscle
(29).
These data support the hypothesis that the reduced
seen at sleep onset is at least in part
due to a fall in Di activity and is not solely a consequence of raised
UAR. The data also indicate that the increase in UAR, which is
initiated early in sleep onset, is a consequence of the fall in
activity of the UA dilator muscles. It is likely that as sleep
progresses phasic respiratory muscles such as Di are recruited (8, 22,
24), probably via chemical and UA reflexes. Phasic UA muscles such as
GG are also recruited after an initial fall, but tonic UA muscles such
as TP are not, and so UAR remains above awake levels. It is not well
understood how the various UA muscles interact to maintain UA patency.
However, it is quite likely that TP helps to maintain UA patency by
decreasing UA collapsibility, even though in isolation it may not be an
active UA dilator. Thus falls at sleep onset for two
reasons: first, because of reduced activity of respiratory muscles,
either because of a direct reduction in activation of these muscles or
because of reduced sensitivity of chemoreflexes during sleep; and
second, because of an increase in UAR, both because of reduced TP
activity and because UA reflexes are diminished during sleep,
contributing to the elevated UAR.
If the levels of muscle activity were simply switching up and down in
association with changes in EEG activity between and , the
changes in EMG activities at to transitions would be expected
to be of the same magnitude as the changes at to transitions.
However, the increase in EMG activity at to transitions is
greater than the fall at to transitions, suggesting that other
mechanisms are playing a role at to transitions. One possibility is that there is an additional component specifically associated with arousal that occurs in association with a shift from
to , and this produces an increase in activity beyond that just
due to a state change. Another contributing factor may be a difference
in the response to chemical stimuli at to and to transitions. It is known that there is a reduced ventilatory response to CO2 during sleep (28) and that
respiratory effort occurs at a higher
CO2 threshold in sleep than in
wakefulness (21). At to transitions, there is a fall in
chemoreceptor sensitivity in association with a relatively lower
chemical drive in the period of wakefulness preceding the transition.
At to transitions, there is an increase in chemoreceptor
sensitvity, but this is associated with a greater chemical drive
because of the increased PCO2 and
decreased PO2 during sleep.
Therefore, at to transitions, the increase in chemoreceptor sensitivity produces a greater change in because the
baseline drive is higher, whereas the same degree of chemoreceptor
drive change at to transitions has a smaller effect as the
baseline level of drive is lower. Either of these explanations or a
combination of the two can explain the greater Di activity in phase
3 compared with phase 1.
The third finding of this study was that changes of pump muscle (Di and
IC) activity differed between phases 2 and 3. The two phases were
analyzed separately because previous work (10) has shown that
and UAR have greater changes between and in
phase 3 than in phase 2. There is a number of explanations for this.
1) If the wakefulness stimulus is
having a direct influence on respiratory motoneurons and if its
withdrawl is incomplete during phase 2 and complete in phase 3,
then the changes in muscle activity between and would be
greater in phase 3 than in phase 2. 2) The difference in response to
chemoreceptor drive between and is greater in phase 3 than in
phase 2 (4), again, producing greater muscle changes in phase 3 than in
phase 2. 3) The difference in
chemoreceptor drive itself may be greater. 4) If there is an arousal complex
producing greater muscle activity with shifts from to , this
arousal response may have a greater influence in phase 3. 5) There is also a
methodological explanation. The periods of between periods of tended to be longer in phase 2 than in phase 3, in which a period of
may only last for two or three breaths. Also, the periods of were generally briefer in phase 2 than in phase 3. This means that the
five breaths preceding an to transition in phase 2 represented a more stable , whereas the breaths before an to
transition in phase 3 may have been the same or arousal breaths
that form part of the to transition. Thus the pretransition
activity was higher in phase 3 than in phase 2, at least in part
explaining the trend to greater falls in Di activity at to transitions in phase 3 than in phase 2.
Mezzanotte et al. (15) did not observe phasic TP activity in any of their eight normal subjects, whereas phasic TP activity was observed visually in all of our subjects in established sleep. One reason for the discrepancy with our study is the periods in which phasic activity is sought. Our subjects only showed evidence of phasic activity in TP after sleep had become established and the level of tonic activity had fallen considerably. We postulate that there is a low level of underlying phasic activity in TP, which is masked by the tonic activity during wakefulness and early sleep but which becomes apparent when the level of tonic activity falls to very low levels as sleep becomes established. Mezzanotte et al. (15) did not report data from their subjects in stable sleep so they did not have the same opportunity to observe phasic TP activity as we had.
It is not possible to draw any conclusions about the relative changes
of the muscles at sleep onset because it is not possible to determine
whether the neural input to each muscle is the same or whether the
baseline EMG activities of different muscles are the same. Also, it is
not possible to relate changes in EMGs with changes in UAR or
, as the relationship between EMG activities and the
force generated by the muscles is not known. What was of importance was
that the muscles change in the same direction as each other in
association with changes in state.
The level of resting in our subjects was high, most
likely because of stimulation of oral and nasal mucosa by the Millar catheter (20). The differences in that we observed
were similar to those reported by others (6, 11-13, 19, 22, 25,
28, 30) and so are not simply explained by voluntary hyperventilation in our subjects. A fall in with sleep has also been
demonstrated with impedance plethysmography (32) and magnetomters (7,
27), and so it was not specifically related to the instrumentation we
used. Also, the changes at the transitions that we observed were too
abrupt to be explained by changes in
CO2 levels.
There are two other technical points.
1) It is possible that the surface
Di electrodes were not recording pure Di activity; however, we believed
that the main aim of the study could not justify the use of
intramuscular or esophageal Di electrodes, since we were interested in
the Di as a representative pump muscle rather than as a discrete muscle
by itself. 2) We chose to record from the external ICs rather than from the parasternal ICs because, as
the external IC muscles are less active than the parasternal ICs during
quiet respiration, if there was an increase in activity at to transitions, it would be more likely to be observed.
In summary, we have shown that during the sleep-onset period phasic
activity of Di, IC, and GG and phasic and tonic activities of TP fell within a few breaths of a change from to
and that there was recruitment of GG after the initial fall but no
recruitment of TP for at least 20 breaths. With changes from to
, the phasic and tonic activities of Di, GG, and TP increased. It
was concluded that the fall in at sleep onset is a
direct consequence of both the reduction in activities of the
respiratory pump and UA muscles with sleep.
| |
ACKNOWLEDGEMENTS |
|---|
This work was supported by a grant from the Department of Veterans' Affairs, Australia. C. J. Worsnop is a National Health and Medical Research Council of Australia Postgraduate Medical Scholar.
| |
FOOTNOTES |
|---|
Address for correspondence: J. Trinder, School of Behavioural Science, The Univ. of Melbourne, Parkville, Victoria 3052, Australia.
Received 9 June 1997; accepted in final form 27 April 1998.
| |
REFERENCES |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
1.
Badr, M. S.,
J. B. Skatrud,
P. M. Simon,
and
J. A. Dempsey.
Effect of hypercapnia on total pulmonary resistance during wakefulness and during NREM sleep.
Am. Rev. Respir. Dis.
144:
406-414,
1991[Medline].
2.
Brouillette, R. T.,
and
B. T. Thach.
Control of genioglossus muscle inspiratory activity.
J. Appl. Physiol.
49:
801-808,
1980
3.
Bruce, E. N.,
J. Mitra,
and
N. S. Cherniak.
Central and peripheral chemoreceptor inputs to phrenic and hypoglossal motoneurons.
J. Appl. Physiol.
53:
1504-1511,
1982
4.
Dunai, J.,
M. Wilkinson,
and
J. Trinder.
Interaction of chemical and state effects on ventilation during sleep onset.
J. Appl. Physiol.
81:
2235-2243,
1996
5.
Fraser, G.,
J. Trinder,
I. M. Colrain,
and
I. Montgomery.
The effect of sleep and circadian cycle on sleep period energy expenditure.
J. Appl. Physiol.
66:
830-836,
1989
6.
Gothe, B.,
M. D. Altose,
M. D. Goldman,
and
N. S. Cherniak.
Effect of quiet sleep on resting and CO2-stimulated breathing in humans.
J. Appl. Physiol.
50:
724-730,
1981
7.
Henke, K. G.,
M. S. Badr,
J. B. Skatrud,
and
J. A. Dempsey.
Load compensation and respiratory muscle function during sleep.
J. Appl. Physiol.
72:
1221-1234,
1992
8.
Henke, K. G.,
J. A. Dempsey,
J. M. Kowitz,
S. Badr,
and
J. B. Skatrud.
Effects of sleep-induced increases in upper airway resistance on respiratory muscle activity.
J. Appl. Physiol.
70:
158-168,
1991
9.
Henke, K. G.,
J. A. Dempsey,
J. M. Kowitz,
and
J. B. Skatrud.
Effects of sleep-induced increases in upper airway resistance on ventilation.
J. Appl. Physiol.
69:
617-624,
1990
10.
Hudgel, D. W.,
R. J. Martin,
B. Johnson,
and
P. Hill.
Mechanics of the respiratory system and breathing pattern during sleep in normal humans.
J. Appl. Physiol.
56:
133-137,
1984
11.
Kay, A.,
J. Trinder,
G. Bowes,
and
Y. Kim.
Changes in airway resistance during sleep onset.
J. Appl. Physiol.
76:
1600-1607,
1994
12.
Kay, A.,
J. Trinder,
and
Y. Kim.
Individual differences in relationship between upper airway resistance and ventilation during sleep onset.
J. Appl. Physiol.
79:
411-419,
1995
13.
Kay, A.,
J. Trinder,
and
Y. Kim.
Progressive changes in airway resistance during sleep.
J. Appl. Physiol.
81:
282-296,
1996
14.
Mezzanotte, W. S.,
D. J. Tangel,
and
D. P. White.
Waking genioglossus EMG in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism).
J. Clin. Invest.
89:
1571-1579,
1992.
15.
Mezzanotte, W. S.,
D. J. Tangel,
and
D. P. White.
Influence of sleep onset on upper airway muscle activity in apnea patients versus normal controls.
Am. J. Respir. Crit. Care Med.
153:
1880-1887,
1996[Abstract].
16.
Morrell, M. J.,
H. R. Harty,
L. Adams,
and
A. Guz.
Changes in total pulmonary resistance and PCO2 between wakefulness and sleep in normal human subjects.
J. Appl. Physiol.
78:
1339-1349,
1995
17.
Morrell, M. J.,
H. R. Harty,
L. Adams,
and
A. Guz.
Breathing during wakefulness and NREM sleep in humans without an upper airway.
J. Appl. Physiol.
81:
274-281,
1996
18.
Morrell, M. J.,
S. A. Shea,
L. Adams,
and
A. Guz.
Effects of inspiratory support upon breathing in humans during wakefulness and sleep.
Respir. Physiol.
93:
57-70,
1993[Medline].
19.
Rist, K. E.,
J. A. Daubenspeck,
and
J. F. McGovern.
Effects of non-REM sleep upon respiratory drive and the respiratory pump in humans.
Respir. Physiol.
63:
241-256,
1986[Medline].
20.
Rodenstein, D. O.,
and
D. C. Stanescu.
The soft palate and breathing.
Am. Rev. Respir. Dis.
134:
311-325,
1986[Medline].
21.
Simon, P. M.,
J. A. Dempsey,
D. M. Landry,
and
J. B. Skatrud.
Effect of sleep on respiratory muscle activity during mechanical ventilation.
Am. Rev. Respir. Dis.
147:
32-37,
1993[Medline].
22.
Tabachnik, E.,
N. L. Muller,
A. C. Bryan,
and
H. Levison.
Changes in ventilation and chest wall mechanics during sleep in normal adolescents.
J. Appl. Physiol.
51:
557-564,
1981
23.
Tangel, D. J.,
W. S. Mezzanotte,
and
D. P. White.
Influence of sleep on tensor palatini EMG and upper airway resistance in normal men.
J. Appl. Physiol.
70:
2574-2581,
1991
24.
Tangel, D. J.,
W. S. Mezzanotte,
and
D. P. White.
The influence of sleep on the activity of tonic vs. inspiratory phasic muscles in normal men.
J. Appl. Physiol.
73:
1058-1068,
1992
25.
Trinder, J.,
F. Whitworth,
A. Kay,
and
P. Wilkin.
Respiratory instability during sleep onset.
J. Appl. Physiol.
73:
2462-2469,
1992
26.
Wheatley, J. R.,
W. S. Mezzanotte,
D. J. Tangel,
and
D. P. White.
Influence of sleep on genioglossus muscle activation by negative pressure in normal men.
Am. Rev. Respir. Dis.
148:
597-605,
1993[Medline].
27.
Wheatley, J. R.,
D. J. Tangel,
W. S. Mezzanotte,
and
D. P. White.
Influence of sleep on response to negative airway pressure of tensor palatini muscle and retropalatal airway.
J. Appl. Physiol.
75:
2117-2124,
1993
28.
White, D. P.
Occlusion pressure and ventilation during sleep in normal humans.
J. Appl. Physiol.
61:
1279-1287,
1986
29.
White, D. P.
Pathophysiology of obstructive sleep apnoea.
Thorax
50:
797-804,
1995[Medline].
30.
Wiegand, L.,
C. W. Zwillich,
and
D. P. White.
Collapsibility of the human airway during normal sleep.
J. Appl. Physiol.
66:
1800-1808,
1989
This article has been cited by other articles:
|
|
 |
|
  D. J. Eckert and A. Malhotra Pathophysiology of Adult Obstructive Sleep Apnea Proceedings of the ATS, February 15, 2008; 5(2): 144 - 153. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. F. Bailey, K. W. Fridel, and A. D. Rice Sleep/Wake Firing Patterns of Human Genioglossus Motor Units J Neurophysiol, December 1, 2007; 98(6): 3284 - 3291. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-L. Lo, A. S Jordan, A. Malhotra, A. Wellman, R. A Heinzer, M. Eikermann, K. Schory, L. Dover, and D. P White Influence of wakefulness on pharyngeal airway muscle activity Thorax, September 1, 2007; 62(9): 799 - 805. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Pierce, D. White, A. Malhotra, J. K. Edwards, D. Kleverlaan, L. Palmer, and J. Trinder Upper airway collapsibility, dilator muscle activation and resistance in sleep apnoea Eur. Respir. J., August 1, 2007; 30(2): 345 - 353. [Abstract] [Full Text] [PDF]
|
|
|
|
