Expiratory muscle activity in the awake and sleeping human during lung inflation and hypercapnia.

Expiratory muscle activity in the awake and sleeping human during lung inflation and hypercapnia Y. WAKAI, M. M. WELSH, A. M. LEEVERS, AND J. D. ROAD Departments of Medicine and Radiology, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada WAKAI,~., M.M. WELSH,A.M. LEEVERS,ANDJ. D. ROAD. Expiratory muscle activity in the awake and sleeping human during lung inflation and hypercapnia. J. Appl. Physiol. 72(3): 881-

887, 1992.-Expiratory muscle activity has been shown to occur in awake humans during lung inflation; however, whether this activity is dependent on consciousnessis unclear. Therefore we measuredabdominal muscle electromyograms (intramuscular electrodes) in 13 subjectsstudied in the supine position during wakefulness and non-rapid-eye-movement sleep. Lung inflation was produced by nasal continuous positive airway pressure(CPAP). CPAP at lo-15 cmH,O produced phasic expiratory activity in two subjectsduring wakefulnessbut produced no activity in any subject during sleep. During sleep, CPAP to 15 cmH,O increasedlung volume by 1,260_t 215 (SE) ml, but there wasno changein minute ventilation. The ventilatory threshold at which phasic abdominal muscle activity was first recorded during hypercapnia was 10.3 ,t 1.1 l/min while awake and 13.8 t 1 l/min while asleep(P < 0.05). Higher lung volumes reduced the threshold for abdominal muscle recruitment during hypercapnia. We conclude that lung inflation alone over the range that we studied doesnot alter ventilation or produce recruitment of the abdominal musclesin sleeping humans. The internal oblique and transversus abdominis are activated at a lower ventilatory threshold during hypercapnia, and this activation is influenced by state and lung volume. abdominal muscles;electromyogram; hyperventilation; continuous positive airway pressure

LUNG INFLATION produces a reduction

in resting length of the major inspiratory muscles, a reduction in muscle shortening, and hence a reduction in tidal volume (VT) (19). Increased activation of the inspiratory muscles can prevent the reduction in shortening, or lung volume and resting length may be defended by recruitment of the expiratory muscles. Recruitment of the expiratory muscles during lung inflation can allow passive expansion of the chest wall during the subsequent inspiration, producing an inspiratory assist (20). Although expiratory muscle recruitment in response to lung inflation is strong in quadrupeds (20), the response of the expiratory muscles to lung inflation in humans has been conflicting. Urbscheit et al. (28), Agostoni (2), and Rahn et al. (18) have shown expiratory activity in the abdominal muscles during positive-pressure breathing in humans. However, during sleep abdominal muscle activity was not detected by surface electrodes in response to lung inflation (6). Fine-wire electrodes are a more sensitive means of detecting muscle activity. In addition, recent evidence has

suggested that the deeper layer of abdominal muscles, particularly the transversus abdominis (TA) (9), is recruited preferentially during expiration. Thus surface electrodes that can detect superficial muscle activity may underestimate abdominal muscle recruitment in deeper layers. Because behavioral factors may also play a role in abdominal muscle recruitment in response to this load, we also studied the activity of the individual abdominal expiratory muscles during sleep. Recent evidence shows that the abdominal muscles are recruited at much lower levels of ventilation during hypercapnia (9) than previously thought. However, this ventilatory threshold of expiratory activity may be state dependent. In general, muscle tone decreases when subjects pass from wakefulness to sleep (l4), and the expiratory muscles may be influenced by this effect. Therefore we also compared the level of ventilation at which abdominal muscle activity first occurs between wakefulness and sleep. Lung inflation was produced by continuous positive airway pressure (CPAP) and hypercapnia by CO, rebreathing in 13 naive subjects during both wakefulness and sleep. Abdominal muscle activity was detected in the individual abdominal muscles with fine-wire electrodes. We hypothesized that abdominal muscle expiratory activity if present is state dependent and would decrease during sleep. METHODS

Thirteen healthy humans (7 females and 6 males with normal lung function) ranging in age from 18 to 38 yr were studied. Their anthropometric and pulmonary function data are shown in Table 1. None had experience in respiratory maneuvers, and all were unaware of the scientific purpose of the study. They were in good health at the time of the study and did not have any previous history of sleep disorder or cardiopulmonary or neuromuscular disease. Each subject gave informed consent and was studied during wakefulness and sleep [non-rapid-eye-movement (NREM)] in the supine position. Complete sets of data were obtained from each individual over one continuous session. To measure the raw electromyogram (EMG) of three abdominal muscle layers [external oblique (EO), internal oblique (IO), and TA], we inserted a bipolar fine-wire electrode into each abdominal muscle under ultrasound guidance. The ultrasound probe was placed in the right anterior axillary line at the level of navel, and the three abdominal muscle layers

0161-7567/92 $2.00 Copyright 0 1992 the American Physiological

Society

881

Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (132.174.254.155) on December 14, 2018.

882

ABDOMINAL

1. Anthropometric data of subjects

and pulmonary function

TABLE

Am

MUSCLE

ACTIVATION

Subj

Sex

Yr

Height, cm

Weight, kg

FE& liters

A B

F F F F F F F M M M M M M

37 35 31 29 27 25 24 38 29 27 26 24 18

165 158 165 157 166 162 168 180 180 180 175 172 185

62 53 61 61 54 61 63 80 75 74 68 65 90

3.6

4.1

2.9 3.9 2.5 3.3 3.4 3.4 5.0 4.0 4.5 4.6 5.1

3.3 4.4 3.9 3.9 4.0 5.0 5.6 4.9 5.3 5.2 6.3

c

D E F G H I J K L M FE&,

forced

expiratory

volume

in 1 s; FVC,

forced

vital

9

FVC, liters

capacity.

were visualized easily. The EMG electrode consisted of a pair of Teflon-coated wires (0.254 mm diam; Cooner Wire, CA). These bipolar fine-wire electrodes were first described by Basmajian and Stecko (5) and have been used in the study of skeletal muscles during exercise. The electrodes keep a constant position in the muscle because of small hooks on their tips and cause almost no discomfort after insertion. These wires were held in a 21-gauge needle. The needle was inserted through the skin, and its passage was monitored by the ultrasound probe. The needle was advanced in small steps until the tip was visualized in the desired muscle layer. Although the needle tip can be visualized by ultrasound, the wire electrode cannot. Therefore, to maintain electrode position within a particular muscle, we inserted the electrodes as parallel to the muscle layer as possible, so that once in the muscle belly the electrode could be advanced further by -1 cm. We put a mark on the wire at its exit through the skin, and this mark was measured before and after the session. This length changed in one subject, and the data from this subject were discarded. Subjects then performed several voluntary maneuvers, such as head lift, belly-in isovolume maneuver, cough, and slow expiration to residual volume. These maneuvers were repeated at the end of the experiment. Results that were not reproducible were discarded. The three EMG signals were processed with the use of an amplifier (Grass model P511) and were filtered below 30 Hz and above 3 kHz. A direct current-coupled respiratory inductive plethysmograph (RIP; Respitrace, Ambulatory Monitoring, NY) was used to measure breathing pattern and change in functional residual capacity (FRC). The rib-cage band was placed just under the axilla, and the abdominal band was placed above the iliac crest and below the 10th rib to avoid the rib cage. The RIP was calibrated by the leastsquares method. The sum signal was calibrated by spirobag (800 ml), and the volume signal was obtained from a pneumotachograph (Fleish no. 2). RIP values were within 10% of pneumotachograph volume. In 11 of the 13 subjects, the calibration procedure was repeated at the end of the experiment and was still found to be within 10%. Lung volume was increased by nasal CPAP (CPAP

DURING

HYPERINFLATION

model 7001, Healthdyne, GA) by the use of a tight-fitting nasal mask. Airway pressure was recorded from a port in the mask and was measured by differential pressure transducer (model MP45, Validyne Engineering, CA). The pressure was varied by a remote control system from outside the room. Nasal CPAP was applied over the range of 5-20 cmH,O in 5-cmH,O increments. Breathing was allowed to stabilize for 5 min at each CPAP level before measurements were made. Sleep was monitored with standard silver cup electrodes recording electroencephalographic and electrooculographic signals. Sleep stage was determined with the use of standard criteria. All parameters were recorded on a multichannel pen recorder (Grass, model 7S1230). Ventilatory threshold for abdominal expiratory activity during wakefulness. To explore the effect of hyperinfla-

tion on ventilation and abdominal muscle EMG, we applied CPAP in a random order. To determine the effect of hypercapnia on abdominal muscle recruitment, we determined the level of ventilation [threshold minute ventilation (VE)] where phasic expiratory abdominal muscle activity was first detected. To compare the ventilatory threshold of abdominal muscle activity during wakefulness and sleep, we produced hypercapnia through the CPAP device (at CPAP 5 cmH,O). In this instance, hypercapnic gas (5O%CO,-50%0,) was bled into the tube proximal to the nasal mask. End-tidal CO, was monitored at the nostrils by nasal prongs, and CO, flow rate was controlled to achieve an end-tidal CO, of 7-9%. Ventilator-y threshold for abdominal expiratory muscle activity during sleep. Sleep measurements were similar to

measurements during wakefulness with some alterations. The subjects went to sleep with nasal CPAP at 5 cmH,O. Once a deep level of sleep was obtained (NREM sleep stages 3 or 4), CPAP was applied over the range of 5-20 cmH,O as in the wakefulness protocol. Hypercapnic stimulation of breathing was produced by a protocol similar to the third phase of the wakefulness protocol. The subject breathed spontaneously through the nasal CPAP mask (5 cmH,O). A hypercapnic gas mixture (50%C02-50%0,) was introduced through a side port in the tubing of the CPAP system. The 5O%CO,5O%O, gas mixture was used to keep flow rates to a minimum so as not to waken the subjects. The subjects’ posture was monitored by a video camera, and measurements were made only with the subject in the supine position. End-tidal CO, was gradually increased from 7 to 9% by increasing the flow of CO,. The threshold VE where phasic expiratory abdominal muscle activity was first detected was identified. Then, in addition to hypercapnic breathing at 5 cmH,O CPAP, the protocol was repeated at 10 cmH,O CPAP. Statistics. The data are summarized as means t SE. To determine whether ventilatory parameters (VE, VT, FRC change, mean inspiratory flow) differed among the CPAP levels, we analyzed the data by a Friedman twoway analysis of variance. To determine whether the threshold TE of abdominal muscle activity during sleep increased compared with that of wakefulness and whether the threshold VE of abdominal muscle activity with CPAP at 10 cmH,O + CO, decreased compared with that with CPAP at 5 cmH,O + CO,, we used a one-tailed


ABDOMINAL

MUSCLE

ACTIVATION

W a

Z 20

a

0

CPAP

( cm

H20

)

FIG. 1. Increase in lung volume [functional residual capacity (FRC)] with CPAP during wakefulness and sleep. Values are means _t SE for supine humans.

paired t test. We considered P < 0.05.

differences

significant

at

RESULTS

Ventilatory changes with CPAP. Although all subjects tolerated CPAP at 20 cmH,O while awake, during sleep two subjects had arousals at CPAP 15 cmH,O and eight subjects had arousals at CPAP 20 cmH,O. Lung volume measured by RIP increased with each level of CPAP (Fig. 1). During wakefulness the increase in end-expiratory 600

1

i> 200 1

+ w

0

I 5

I 10

I 15

( cmHn0)

1

T

U a

w2

wakefulness sleep

l> I 20

883

HYPERINFLATION

lung volume (EELV) from CPAP at 5-20 cmH,O was 1,172 t 224 (SE) ml, which equaled 35% of inspiratory capacity. During sleep the increase in lung volume from CPAP at 5-20 cmH,O was 1,260 t 250 (SE) ml, which equaled 36% of inspiratory capacity. Nasal CPAP did not alter VT (Fig. 2) or VE (Fig. 2) during wakefulness or sleep. VT and VE were maintained at various levels of CPAP ranging from 5 to 20 cmH,O during both wakefulness and sleep. The VE during sleep was less than during wakefulness (Fig. 2). The mean decrease in VE from wakefulness to sleep at each level of CPAP was 29.7% (6.02 vs. 4.23 llmin). Activation of abdominal expiratory activity. Hyperinflation produced by nasal CPAP did not produce recruitment of any one of the abdominal muscles during sleep, and only 2 of 13 subjects recruited one abdominal muscle during wakefulness (Table 2). In one of these individuals, three muscles were active through expiration and in the other, only the TA was active. This second individual did not defend FRC (FRC increased 880 ml at a CPAP of 20 cmH,O). Two of 11 subjects who did not activate abdominal muscles defended their FRC (FRC increase was 130 and 150 ml, respectively). These subjects may have recruited their rib cage expiratory muscles: internal intercostal and/or transversus thoracis. When ventilation was stimulated by CO,, abdominal phasic EMG activity was detected both during wakefulness and sleep, and the IO and TA muscles were activated at a lower ventilatory threshold than the EO (Table 2). In Fig. 3, the effect of lung inflation on the ventilatory threshold for abdominal muscle activity during hypercapnia is shown. The minute ventilation at which phasic expiratory abdominal muscle activity was first detected was significantly less at a CPAP of 10 cmH,O than at a CPAP of 5 cmH,O during CO,-stimulated breathing (10.5 t 0.7 vs. 13.5 $- 1.0 l/min; P < 0.05, paired t test) (Fig. 3). Therefore, hyperinflation decreased the ventila-

-

E

0

DURING

0:

1 0

I 5

T

wakefulness sleep I 10

I 15

1

20

( cm H20 )

FIG. 2. There was no change in tidal volume (VT) or minute ventilation (frE) with continuous positive airway pressure (CPAP). Values are means t SE; n = 13 during wakefulness; n = 13 during sleep at CPAP 5 and 10 cmH,O; n = 8 and n = 5 at CPAP 15 and 20 cmH,O.


884 TABLE

ABDOMINAL

MUSCLE

ACTIVATION

DURING

HYPERINFLATION

2. Abdominal muscle recruitment during CPAP Wakefulness

CPAP CPAP + CO2

Sleep

EO

IO

TA

EO

IO

TA

l/l3 (13.0) 5/13 (15.3 + 3.6)

l/13 (10.9) 7713 (13.3 + 2.6)

Z/13 (11.1) 9113 (12.6 + 1.5)

o/13

O/l3

o/13

(20.0

3/13 + 2.3)

(15.8

4/13 + 1.9)

(13.0

6113 + 1.1)

Values are no. of subjects who recruited individual abdominal muscles. Values in parentheses indicate mean minute ventilation (l/min t 0.1 SE) where individual abdominal muscle activation was first recorded. CPAP did not produce recruitment of abdominal muscles during sleep, and only 2 of 13 subjects recruited abdominal muscles during wakefulness. IO and TA were activated more frequently than EO during hypercapnia. CPAP, continuous positive airway pressure; EO, external oblique; IO, internal oblique; TA, transversus abdominis.

10 W l

1

CPAP

>

I

5

+ co2

CPAP

10

+ co2

3. Threshold where abdominal muscle recruitment was first recorded during sleep. VE is threshold at which abdominal muscle activity was first detected during CPAP 5 and 1.0 cmH,O plus CO, (0, means t SE) for 5 supine humans. Threshold VE decreased at CPAP 10 cmH,O compared with CPAP 5 cmH20, *P < 0.05. FIG.

tory threshold for abdominal muscle activity during sleep. We also compared abdominal muscle activity during wakefulness and sleep. The ventilatory threshold for abdominal muscle activity was higher during sleep than during wakefulness (10.3 t 1.1 vs. 13.8 t 1 l/min; P < 0.05, paired t test) (Fig. 4). Both thresholds were determined while the subjects were on nasal CPAP at 5 cmH,O. DISCUSSION

Abdominal muscle recruitment and breathing during elevated EELV. Three mechanisms may maintain venti-

lation during hyperinflation: increased inspiratory drive, changes in respiratory timing, and/or expiratory muscle activity. We found that ventilation was maintained during hyperinflation; however, hyperinflation did not produce abdominal muscle activity during NREM sleep. This result is consistent with the report of Begel et al. (6), who reported no abdominal muscle activity using surface electrodes. In this study, wire electrodes inserted into each abdominal muscle layer were used and no EMG activity was detected. Therefore, we conclude that the abdominal muscles are not recruited during hyperinflation

Wakefulness

Sleep

4. Threshold for abdominal muscle recruitment decreased during sleep. VE is threshold at which abdominal muscle activity was first detected with CPAP 5 cmH,O and hypercapnia (0, means & SE) for 8 supine humans. *Significant difference (P < 0.05) between mean VE during sleep and wakefulness. FIG.

in the supine sleeping human. We did not attempt to detect phasic expiratory activity in the rib cage expiratory muscles. However, when CPAP increased from 5 to 20 cmH,O during sleep, lung volume increased by 1,260 t 215 ml [27 t 8.6% of vital capacity (VC)] or 84 ml/ cmH,O airway pressure (1.85% VC/cmH,O). This value is close to the passive compliance of the respiratory system reported for humans of 2% VC/cmH,O (13). Therefore we conclude that the rib cage expiratory muscles did not have an important effect on lung volume because the increase in lung volume produced by CPAP was close to that predicted by the passive characteristics of the respiratory system. If the expiratory muscles were not recruited, then how were VT and VE defended? Begel et al. (6) found that inspiratory duration shortened, expiratory duration lengthened, and breathing frequency fell during hyperinflation. We found no significant change in respiratory timing or mean inspiratory flow (Fig. 5). Another potential mechanism that defends VT and ventilation during CPAP is a reduction in upper airway resistance. The cross-sectional area of the upper airway increases with nasal CPAP in obstructive sleep apnea patients (1). Na-


ABDOMINAL

0

5

CPAP

MUSCLE

ACTIVATION

--e-

wakefulness

-

sleep

10

15

20

( cm H20 )

FIG. 5. There was no change in mean inspiratory flow (VTJTI) with CPAP. Values are means _t SE for 13 supine humans.

sal CPAP appears to have a specific effect on reducing upper airway resistance in addition to the reduction in resistance produced by the increase in lung volume (23). However, Henke et al. (11) recorded total pulmonary resistance in sleeping snorers and found that only small increases in CPAP of 2.5-5 cmH,O were enough to reduce pulmonary resistance to wakefulness levels. The degree to which further reductions in pulmonary resistance could unload the inspiratory muscles at higher levels of CPAP may determine the increase in inspiratory muscle activation needed to defend VT. We used the RIP (calibrated by least-squares method) to measure FRC change and VT. According to the recent study of Werchowski et al. (29), in normal subjects over a large number of determinations, RIP values for FRC change and VT at elevated EELV correlate with pneumotachographic measurements. Therefore our measurements as a group were thought to be accurate. The increase in EELV during wakefulness was similar to the increase in EELV during sleep (Fig. 2). In contrast to these human experiments, many experiments in animals have shown that the abdominal muscles are recruited during positive pressure breathing (7) and that EELV is kept constant (20). This defense of EELV is abolished by vagotomy (19). Our data suggest that there is a weak or no effect of the vagus nerve in this aspect of the control of breathing in humans. However, the threshold for abdominal muscle recruitment during hypercapnit breathing occurred at lower levels of ventilation when lung volume was increased during sleep (13.5 t 1.0 I/min, CPAP at 5 cmH,O vs. 10.5 t 0.7 l/min, CPAP at 10 cmH,O). Several mechanisms may be postulated to explain this difference. The abdominal muscles can be lengthened considerably at high lung volumes as shown by a study in dogs (16). Indeed, the IO and TA muscles of the deep internal layer of the abdominal wall are lengthened much more than the EO and rectus abdominis dur-

DURING

HYPERINFLATION

885

ing lung inflation (16). Russel et al. (22) have shown abdominal y-motoneuron control in cats. Therefore feedback control by muscle spindles activated by lengthening of the abdominal muscles may have augmented muscle recruitment. Alternatively, vagal afferents stimulated by the increase in lung volume may have played a role in these conditions and lowered the ventilatory threshold. Wakefulness itself increases muscle tone and may have augmented expiratory muscle activity in response to hyperinflation (14). However, we detected abdominal muscle activation during wakefulness in only 2 of 13 subjects, and those subjects both hyperventilated. This finding is different from the observations of Urbscheit et al. (28), who found phasic abdominal muscle EMG during CPAP in awake supine subjects. This difference may be explained by the fact that their subjects showed a marked increase in VE during CPAP, and indeed the two subjects who activated their abdominal muscles in our study also hyperventilated. Abdominal muscle activation is known to occur in hyperpnea due to voluntary hyperventilation (lo), hypercapnic breathing (27), and exercise (17). Therefore we assume that their observed abdominal muscle recruitment was associated with the hyperpnea. Several factors may cause these different ventilatory responses, for example, the methods of applying positive pressure, subject posture, or previous experience with positive pressure breathing. Regardless of the mechanism, conscious factors clearly may play a role in modifying ventilatory and abdominal muscle response during CPAP. However, during sleep when these factors are eliminated, there was no change in ventilation and no activation of abdominal muscles.. On average, the decrease in VE during NREM sleep compared with wakefulness is reported to be w 15% (13), whereas we report a 30% decrease. The largest decrease in VE reported was 22% (4.9 vs. 3.8 I/min) by Shore et al. (24). These measurements, however, were all made without the addition of CPAP, and our subjects all went to sleep with CPAP at 5 cmH,O. We believe our volume calibration of RIP was accurate (the difference between RIP volume and pneumotachograph volume was within 10% and remained so on awakening in the 11 of 13 in whom it was measured). Therefore we assume that our subjects had a small augmentation of breathing during wakefulness due to conscious factors, which could account for the greater decrease in ventilation from wakefulness to sleep. Abdominal muscle activity during hypercapnia. We found that the IO and TA muscles are activated at a lower level of ventilation during hypercapnia and that this activation can occur at low levels of ventilation. De Troyer et al. (9) found that the TA was recruited at a VE of 10.6-18.3 l/min during hypercapnic breathing in the sitting position. Although the subjects’ positions were different in the two studies, the threshold level of VE where TA recruitment occurred was similar to the results reported here. Strohl et al. (25) reported abdominal muscle recruitment at a VE of 18-56 l/min in the standing position using surface electrodes. Campbell (8) used needle electrodes and found a ventilation of 40-60 l/min was needed to recruit the abdominal muscles. Probably the inability to obtain signals from the TA or the IO with surface electrodes and not inserting electrodes into the


886

ABDOMINAL

MUSCLE

ACTIVATION

deeper abdominal muscles produced the high ventilatory threshold for abdominal muscle recruitment in these studies. The IO as well as TA were recruited earlier and more frequently than EO in our study. The reason why previous studies using intramuscular recordings have not measured IO activity is unclear. But our recent study in dogs (16) showed that during expiratory threshold loading, active expiratory shortening was evident particularly in the IO. In addition, the IO and TA have been shown to receive significantly greater blood flow than the EO and RA during expiratory loading in anesthetized dogs (21). Goldman et al. (10) reported that the abdominal muscle layers acted together in breathing and had a high threshold of recruitment (88 t 13 l/min) in humans. They used a computerized tomography scan to separate each abdominal layer, but the actual insertion of wire electrodes was based on predetermined expected depth of the muscle without real-time monitoring. We conclude that in humans the internal muscles of the abdominal wall are activated preferentially and that this pattern of activation is similar to that found in dogs (16). Because of their fiber orientation to the abdominal compartment, these muscles appear most effective at abdominal compression (16). We found that the threshold of abdominal muscle recruitment during hypercapnic breathing increased during sleep. Some mechanisms may be considered. Ventilatory response to CO, is well known to be state dependent (decreases in sleep vs. wakefulness). However, we compared the level of ventilation where the abdominal muscles were first recruited. This level, we assume, was at a higher CO, during sleep. By comparing the threshold ventilation at which abdominal muscle recruitment occurred during wakefulness and sleep, we also assume that we are comparing expiratory muscle recruitment at Similar levels Of inspiratory motor neuron Output. VE may underestimate inspiratory motor neuron output in sleep because of an increase in upper airway resistance, but we used CPAP 5 cmH,O during wakefulness and sleep. This level of CPAP should reduce resistance to wakefulness levels (11). The expected decrease in FRC (4,12) that occurs when subjects pass from wakefulness to sleep may have been obviated by nasal CPAP; however, if FRC did decrease, this would result in an increase in ventilation for any given amount of inspiratory motor neuron output, assuming chest wall configuration was unchanged. Given these assumptions, we conclude that sleep may reduce the responsiveness of expiratory motoneurons more than inspiratory motoneurons compared with wakefulness. A reduction in expiratory motoneuron output is in keeping with a general decrease in muscle tone that occurs when passing from wakefulness to sleep (14). The expiratory muscles would appear to be more susceptible to this effect compared with the main inspiratory muscles. We thank Bernice Robillard for valuable assistance in typing the manuscript and Geoffrey Edge11 for technical help with the polysomnography. This study was supported by the British Columbia Health Care Research Foundation. J. D. Road was a scholar of the British Columbia Health Care Research Foundation. Address for reprint requests: J. D. Road, Dept. of Medicine, Univer-

DURING

HYPERINFLATION

sity Hospital (UBC), 2211 Westbrook Mall, Vancouver, British Columbia V6T 2B5, Canada. Received 26 December 1990; accepted in final form 30 September 1991. REFERENCES 1, ABBEY, N. C., A. J. BLOCK, D. GREEN, A. MANCUSO, AND D. W. HELLARD. Measurement of pharyngeal volume by digitized magnetic resonance imaging. Am. Rev. Respir. Dis. 140: 717-723,1989. 2. AGOSTONI, E. Diaphragm activity and thoracoabdominal mechanics during positive pressure breathing. J. Appl. Physiol. 17: 215220,1962. 3. ALEX, C. G., R. M. ARONSON, E. ONAL, AND M. LOPATA. Effects of continuous positive airway pressure on upper airway and respiratory muscle activity. J. Appl. Physiol. 62: 2026-2030, 1987. 4. BALLARD, R. D., C. G. IRVIN, R. J. MARTIN, J. PAK, R. PANDEY, AND D. P. WHITE. Influence of sleep on lung volume in asthmatic patients and normal subjects. J. Appl. Physiol. 68: 2034-2041,199O. 5. BASMAJIAN, J. V., AND G. STECKO. A new bipolar electrode for electromyography. J. Appl. Physiol. 17: 849, 1962. 6. BEGEL, R. L., J. B. SKATRUD, AND J. A. DEMPSEY. Ventilatory compensation for changes in functional residual capacity during sleep. J. Appl. Physiol. 62: 1299-1306, 1987. 7. BISHOP, B. Abdominal muscle and diaphragm activities and cavity pressures in pressure breathing. J. Appl. Physiol. 18: 37-42, 1963. 8. CAMPBELL, E. J. M. An electromyographic study of the role of the abdominal muscles in breathing. J. Physiol. Lond. 117: 222-233, . 1952. 9. DE TROYER, A., M. ESTENNE, V. NINANE, D. V. GANSBEKE, AND M. GORINI. Transversus abdominis muscle function in humans. J. Appl. Physiol. 68: 1010-1016, 1990. 10. GOLDMAN, J. M., R. P. LEHN, A. B. MILLAR, AND J. R. SILVER. An electromyographic study of the abdominal muscles during postural and respiratory manoeuvers. J. Neurol. Neurosurg. Psychiatry 50: 866-869,1987. 11. HENKE, K. G., J. A. DEMPSEY, M. S. BADR, J. M. KOWITZ, AND J. B. SKATRUD. Effect of sleep-induced increases in upper airway resistance on respiratory muscle activity. J. Appl. Physiol. 70: 158168,1991. 12. HUDGEL, D. W., AND P. DEVADATTA. Decrease in functional residual capacity during sleep in normal humans. J. Appl. Physiol. 57: 1319-1322,1984. 13. JOHNSON, L. F., JR., AND J. MEAD. Volume-pressure relationships during pressure breathing and voluntary relaxation. J. Appl. Physiol. 18: 505-508, 1963. 14 KLEITMAN, N. Sleep and Wakefulness. Chicago, IL: Univ. of Chicago Press, 1963, p. 552. 15. KRIEGER, J. Breathing during sleep in normal subjects. In: Principles and Practice of Sleep Medicine, edited by M. H. Kryger, T. Roth, and W. C. Dement. Philadelphia, PA: Saunders, 1989, p. 257-268. 16. LEEVERS, A. M., AND J. D. ROAD. Mechanical response to hyperinflation of the two abdominal muscle layers. J. Appl. Physiol. 66: 2189-2195,1989. 17. LORING, S. H., AND J. MEAD. Abdominal muscle use during quiet breathing and hyperpnea in uninformed subjects. J. Appl. Physiol. 52:700-704,1982. 18. RAHN, H., A. B. OTIS, L. E. CHAPWICK AND W. 0. FENN. The pressure-volume diagram of the thorax and lung. Am. J. Physiol. 146: 161-178,1946. 19. ROAD, J. D., AND A. M. LEEVERS. Effect of lung inflation on diaphragmatic shortening. J. Appl. Physiol. 65: 2383-2389, 1988. 20. ROAD, J. D., AND A. M. LEEVERS. Inspiratory and expiratory muscle function during continuous positive airway pressure in dogs. J. AppZ. Physiol. 68: 1092-1100, 1990. 21. ROBERTSON, C. H., JR., W. L. ESCHENBACHER, AND R. L. JOHNSON, JR. Respiratory muscle blood flow distribution during expiratory resistance. J. Clin. Invest. 60: 473-480, 1977. 22. RUSSEL, J. A., B. P. BISHOP, AND R. E. HYATT. Discharge of abdominal a! and y motoneurons during expiratory loading in cats. Exp. Neurol. 97: 179-192,1987. 23. SI%RII%, F., Y. CORMIER, J. COUTURE, AND M. DESMEULES. Changes in upper airway resistance with lung inflation and positive airway pressure. J. Appl. Physiol. 68: 1075-1079, 1990. 24. SHORE, E. T., R. P. MILLMAN, D. A. SILAGE, D. C. MUNG, AND A. L. PACK. Ventilatory and arousal patterns during sleep in nor-


ABDOMINAL ma1 young and elderly subjects. J. Appl.

MUSCLE Physiol.

ACTIVATION

59: 1607-1615,

1985. 25. STROHL, KOSCH.

K. P., J. MEAN, R. B. BANZETT, S. H. LORING, AND P. C. Regional difference in abdominal muscle activity during various maneuvers in humans. J. Appk Physiol. 51: 1471-1476,

1981. 26. TABACHNIK,

E., N. L. Changes in ventilation normal adolescents. J. 27. TAKASAKI, Y., D. ORR,

A. C. BRYAN, AND H. LEVISON. and chest wall mechanics during sleep in

MULLER, Appl.

Physiol.

J. POPKEN,

51: 557-564,

1981.

A. XIE, AND T. D. BRADLEY.

DURING

HYPERINFLATION

887

Effect of hypercapnia and hypoxia on respiratory muscle activation in humans. J. Appl. Physiol. 67: 1776-1784, 1989. 28. URBSCHEIT, N., B. BISHOP, AND H. BACHOFEN. Immediate effects of continuous positive pressure breathing on abdominal expiratory activity, minute ventilation, and end-tidal PCO~ of conscious man. Phys. Ther. 53: 258-265, 1973. 29. WERCHOWSKI, J. L., M. H. SANDERS, J. SCIURBA, AND R. M. ROGERS. Inductance

surement of CPAP-induced

J. Appl.

Physiol.

P. COSTANTINO, F. C. plethysmograph meachange in end-expiratory lung volume.

68: 1732-1738,

1990.


Activity of abdominal muscle motoneurons during hypercapnia.

Expiratory muscle activity during pulmonary edema in the anesthetized dog.

Vagal afferents essential for abdominal muscle activity during lung inflation in cats.

Abdominal muscle activity during CO2 rebreathing in sleeping neonates.

Vagal afferent control of abdominal expiratory activity in response to hypoxia and hypercapnia in rats.

Temperature effects on the inflation reflex during expiratory time in the cat.

Effect of expiratory resistive loading in expiratory muscle strength training on orbicularis oris muscle activity.

Regional venous outflow, blood volume, and sympathetic nerve activity during hypercapnia and hypoxic hypercapnia.

Expiratory muscle recruitment during inspiratory flow-resistive loading and exercise.

Single-neuron activity and eye movements during human REM sleep and awake vision.

Dynamic lung inflation during high frequency oscillation in neonates.

Lung inflation with hydrogen during the cold ischemia phase decreases lung graft injury in rats.

Respiratory-related activity of cricothyroid muscle in awake normal humans.

The ventilatory response to muscle afferent activation during concurrent hypercapnia in humans: central and peripheral mechanisms.

An automated and reliable method for breath detection during variable mask pressures in awake and sleeping humans.

Responses of pial arterioles after prolonged hypercapnia and hypoxia in the awake rabbit.

A possible role of lung cAMP and cGMP for lung histamine release during chronic hypercapnia.

Relationship of respiratory effort sensation to expiratory muscle fatigue during expiratory threshold loading.

Effect of lung inflation on pulmonary resistance during NREM sleep.

EMG activity of cricothyroid and chin muscles during wakefulness and sleeping in the sleep apnea syndrome.

Lung density changes with growth and inflation.

Respiratory muscle blood flow distribution during expiratory resistance.

Habituation during sleeping and waking.

Ventricular external constraint by the lung and pericardium during positive end-expiratory pressure.