Breathing Route Research Articles

Diaphragmatic activity during REM sleep in the adult cat.

Diaphragmatic electromyograms from five adult cats were studied to determine whether diaphragmatic activity, like central respiratory activity, increases in rapid-eye-movement (REM) sleep. Breaths with inspiratory durations between 250 and 2,000 ms were analyzed. 1) There was a greater slope of the moving time average of diaphragmatic activity in REM than in non-REM (NREM) sleep. These greater slopes occurred whether the route of breathing was through the upper airways or through an endotracheal tube and may have resulted from early recruitment of motor units. 2) Mean diaphragmatic activity was also greater, but other variables (peak activity, the area under the curve of diaphragmatic activity, mean intratracheal pressures, inspiratory airflow rates, and tidal volumes) were not greater in REM than in NREM sleep. 3) Diaphragmatic activity was similar in REM sleep and active wakefulness. 4) Across states, slope of the moving time average varied with the duration of inspiration: greater slopes were associated with shorter breaths. These results are consistent with an increase in central respiratory drive in REM sleep that increases the rate of rise of diaphragmatic activity.

Respiratory control during volume-cycled ventilation in normal humans

The purpose of this study was to evaluate the extent of inhibition to respiratory rhythm associated with high volumes of ventilation during volume-cycled mechanical ventilation (neuromechanical inhibition). Two approaches were used. 1) In 18 normal awake subjects, ventilator tidal volume (VT) in the assist/control mode (A/C) was increased in steps from the minimum tolerable level up to 80% of the subject's inspiratory capacity or ventilator's maximum VT. We looked for appearance of intermittent apnea or a reduction in spontaneous rate (f). 2) Another 18 normal awake subjects were placed on controlled mechanical ventilation (CMV). When apnea was established, we abruptly terminated CMV and measured the time before the appearance of the next spontaneous effort. In the assist mode (protocol 1), we did not observe intermittent apnea because VT was increased from [from 944 +/- 198 to 1,867 +/- 277 (SD) ml], and there was only a modest reduction in f (14.1 +/- 3.9 to 12.4 +/- 4.0 breaths/min). End-tidal PCO2 (PETCO2) decreased precipitously as VT was increased. In protocol 2, we did not observe apnea after discontinuation of CMV in any subject. Total breath duration of the first breath after discontinuation did not differ significantly from total breath duration during A/C in the same subjects (4.84 +/- 2.2 vs. 5.2 +/- 2.0 s). This similarly applied regardless of route of breathing (nose vs. mouth) or PETCO2 level at time of discontinuation. We conclude that neuromechanical inhibition is quite weak and provides very little negative feedback that may help control PCO2 in the face of excessive VT and f demands of the subject.

Effect of apparatus on functional residual capacity

As the route of breathing and use of airway apparatus such as mask, mouthpiece and noseclip can alter breathing pattern, this study has used the helium dilution method to estimate the effects of mouthpiece and mask breathing on functional residual capacity (FRC) in the supine position, and the change in FRC that occurs between the sitting and supine positions while breathing by mouthpiece. In 13 normal subjects, breathing by mouthpiece, FRC was smaller, by a median of 1.07 litre (interquartile values 0.73-1.43 litre) in the supine compared with the sitting position (P < 0.01), but residual volume (RV) did not change significantly. FRC measured in the supine position was significantly greater when breathing by mask than by mouthpiece (0.25, 0.04-0.38 litre) and RV was greater by similar amounts (0.20, -0.02 to 0.49 litre). This difference may result from increased inspiratory activity while breathing via the mask.

Effects of breathing route, temperature and volume of inspired gas, and airway anesthesia on the response of respiratory output to varying inspiratory flow.

The determinants of the response of the respiratory output to inspiratory flow rates (VI) were examined in awake normal subjects. Subjects were connected to a volume-cycle ventilator in the assist/control mode, and VI was increased in steps from 30 to 90 L/min and then back to 30 L/min. VI pattern was square, and all breaths were subject-triggered. In six subjects the effects of breathing route (nasal or mouth) and temperature and volume of inspired gas (Protocol A) and in 8 subjects the effects of airway anesthesia (upper and lower airways; Protocol B) on the response of respiratory output to varying VI were studied. In Protocol B, in order to calculate muscle pressure during inspiration (Pmus), respiratory system mechanics were measured using the interrupter method at end-inspiration. Independent of conditions studied, breathing frequency increased significantly and end-tidal concentration of CO2 decreased as VI increased. The response was graded and reversible and not affected by breathing route, temperature and volume of inspired gas, and airway anesthesia. With and without airway anesthesia (Protocol B), neural inspiratory and expiratory time and neural duty cycle, estimated from Pmus waveform, decreased significantly as VI increased. At all conditions studied, the rate of change in airway pressure prior to triggering the ventilator tended to increase as VI increased. The changes in timing and drive were nearly complete within the first two breaths after transition, with no evidence of adaptation during a given VI period. We conclude that VI exerts an excitatory effect on respiratory output which is independent of breathing route, temperature and volume of inspirate, and airway anesthesia. The response most likely is neural in origin, mediated through receptors not accessible to anesthesia, such as those located in the chest wall or below the airway mucosa.

Breathing route and ventilatory responses to inspiratory resistive loading in humans.

In response to ventilatory loading, a number of compensatory mechanisms can serve to maintain ventilation at or near control levels. To test the hypothesis that respiratory compensation for inspiratory flow-resistive load during nasal breathing may be different from that during oral breathing, we investigated the ventilatory responses to four different magnitudes of inspiratory flow-resistive loads ("control," "light," "moderate," and "severe" loads: 3.5, 15.0, 51.8, 83.3 cm H2O/L/s at a flow rate of 30 L/min, respectively) during nasal breathing and during oral breathing in 11 conscious subjects. With the control, light, and moderate loads, there were no significant differences in tidal volume (VT), respiratory frequency (f), minute ventilation (VI), and end-tidal (partial) carbon dioxide pressure (PETCO2) between nasal and oral breathing. With the severe load, however, VI and f were significantly lower and PETCO2 was significantly higher during nasal breathing than during oral breathing. Occlusion pressure (P0.1) progressively increased during both nasal and oral breathing with increasing magnitudes of loading. However, the value of P0.1 during oral breathing at the severe loading was significantly higher than that during nasal breathing. Our results indicate that ventilatory compensation for the inspiratory flow-resistive load is better during oral breathing than during nasal breathing.

Effect of posture and breathing route on genioglossal electromyogram activity in normal subjects and in patients with the sleep apnea/hypopnea syndrome.

Patients with the sleep apnea/hypopnea syndrome (SAHS) often have more apneas supine that sitting. We have shown radiologically that although the retropalatal airway narrows on lying down, the retroglossal airway widens. We have thus investigated the effect of posture on genioglossal EMG activity in 10 normal subjects and 10 patients with SAHS (58 +/- 29 SD apneas + hypopneas/h) using peroral intramuscular EMG electrodes. Data were analyzed by three-way analysis of variance, with diagnosis, posture, and route as factors. Peak inspiratory and tonic expiratory genioglossal EMG were both than sitting, with no significant difference between normal subjects and SAHS higher (p < 0.001) supine patients, although there was a trend (p < 0.09) toward the supine posture having a greater effect on peak inspiratory EMG in the SAHS patients. There was no significant effect of breathing route on either peak inspiratory (p > 0.9) or tonic expiratory (p > 0.8) genioglossal EMG, but there were significant differences between the groups (p < 0.01), the SAHS patients having higher and the normal subjects lower EMG tone with nasal in comparison with oral breathing on both inspiration and expiration. This study therefore shows that both body posture and breathing route are important determinants of genioglossal EMG tone.

EFFECTS OF SEDATION PRODUCED BY THIOPENTONE ON RESPONSES TO NASAL OCCLUSION IN FEMALE ADULTS

To test the hypothesis that full wakefulness is an important factor in the control of the route of breathing in adult humans, we have studied the responses to nasal occlusion before and during sedation with thiopentone in 14 female subjects. A tightly fitting partitioned face mask separated the nasal and oral breathing routes. Nasal and oral breathing were identified from changes in carbon dioxide concentration and airway pressure in the different compartments of the face mask. Arterial oxygen saturation (SpO2) was monitored simultaneously. Eleven of 14 subjects breathed only through the nose (nasal breathers) both before and during sedation. In these subjects, the time required to initiate oral breathing in response to nasal occlusion during sedation was significantly longer than that before sedation (mean 37.7 (SD 15.5) s vs 3.2 (1.3) s (P < 0.01)). Also, there was a significant difference (P < 0.01) in the smallest values of SpO2 attained during nasal occlusion before (98.0 (0.8)%) and after (89.3 (4.3)%) sedation. In adult humans the ability to maintain adequate ventilation by switching from the nasal to the oral route in response to nasal occlusion is greatly impaired during sedation, probably because of the impairment of conscious influence on the control of the palatal muscles.

Comparison of Snoring Measured at Home and During Polysomnographic Studies

Snoring characteristics depend on several factors (sleep position, sleep architecture, breathing route) that can be influenced by changes in sleep habits and by the presence of the different probes and electrodes during polysomnographic studies. Our objective in this study was to compare the characteristics of snoring in the home environment with those of the sleep laboratory where most conventional studies are carried out. Fourteen nonapneic snorers were subjected to three night recording sessions within a two-week period, two at home and one in the sleep laboratory. To eliminate any sleep interference by the apparatus, breathing sounds were recorded with two microphones symmetrically placed on either side of the bed, the signal being preamplified and stored on a VHS hi-fi video recorder. The recorded signal was analyzed by using a spectrum analyzer (real time analyzer) and an equalizer to correct for acoustic resonances of the bedrooms. A snoring event was defined as a breathing sound with a sound pressure level (SPL) greater than 60 dB SPL. The snoring index (number/sleep hour) and the sound intensity of each event were automatically determined. The total sleep time (TST) was similar for the two home recordings (6.8 +/- 0.2 and 7.0 +/- 0.2 h, respectively, mean +/- SEM), but it was significantly shorter during the hospital study (6.0 +/- 0.3 h). The snoring indices obtained at home were 141.4 +/- 33.3 and 144.1 +/- 41.2/h and not statistically different from those obtained during the hospital recording (209.1 +/- 41.5/h). The percentage of TST spent above 60 dB SPL was significantly greater during the polysomnographic study (4.3 +/- 1.2 percent) than during the home recordings (2.5 +/- 0.7 and 2.9 +/- 1.0 percent, respectively). We conclude that the severity of snoring may be overestimated during polysomnographic recordings.

Effect of route of breathing on the ventilatory and arousal responses to hypercapnia in awake and sleeping dogs.

1. The influence of the upper airway on the ventilatory and arousal responses to hypercapnia in wakefulness and sleep was investigated using a chronic animal model. 2. Experiments were performed in five unrestrained dogs trained to sleep naturally in the laboratory. The animal rebreathed through a chronic tracheostoma (thus excluding the upper airway from the breathing circuit), or through the snout (intact upper airway). Resistance to breathing and volume of dead space during quiet tracheal breathing were matched to those in quiet nasal breathing during wakefulness and sleep. CO2 rebreathing tests were performed during wakefulness, rapid eye movement (REM) and non-REM (NREM) sleep, during nasal and tracheal breathing. 3. The ventilatory response to hypercapnia was significantly lower in nasal breathing compared with tracheal breathing, in all behavioural states. This was due to a smaller tidal volume and lower breathing frequency. 4. The ventilatory response to CO2 was lowest during REM sleep, irrespective of route used for breathing. 5. Alveolar partial pressure of CO2 (PA,CO2) level at arousal was identical in NREM nasal and tracheal rebreathing tests. Differences in PA,CO2 levels at arousal between NREM and REM sleep were not significant in nasal tests and only marginally different during tracheal breathing. 6. We conclude that nasal breathing influences the hypercapnic ventilatory response in wakefulness and sleep, and that the presence of CO2 in the upper airway does not affect arousal in NREM and REM sleep.

Fast-Computed Tomographic Evaluation of the Effect of Route of Breathing on Upper Airway Size and Function in Normal Men

Nasal obstruction is associated with increased sleep disordered breathing (SDB), even in normal subjects. This increase in SDB may result from narrowing of the orohypopharyngeal (OHP) or retroglossal segment of the upper airway (UA) due to retropositioning of the jaw and tongue base as the mouth is opened and route of breathing changed from nasal to oral. It is postulated that significant narrowing of the OHP occurs with oral breathing even in the awake state. To ascertain the effect of route of breathing on the UA, fast-CT was used to study the UA response to the route of breathing in 30 normal, awake men, with each subject breathing via the nasal and oral routes under the following conditions: end-inspiration during tidal breathing (VTei) and functional residual capacity (FRC). In the velopharyngeal (VP) or retropalatal segment of the UA, minimum (Amin) and mean (Amean) cross-sectional areas (CSA) decreased 49 +/- 11 percent and 16 +/- 6 percent, respectively, with oral compared with nasal breathing at FRC. In the OHP, Amin at FRC increased by 26 +/- 15 percent with oral compared with nasal breathing with no significant change in Amean. Similar changes in CSA of both the VP and OHP were observed at VTei. Genioglossal electromyographic (EMGgg) activity increased from 12 +/- 1 microV breathing nasally to 27 +/- 4 microV breathing orally at FRC. Although the CSA of the VP segment decreased with conversion from nasal to oral breathing, Amin of the OHP segment was unexpectedly observed to increase with oral breathing. The doubling of EMGgg activity with oral breathing suggests that active contraction of the genioglossus may function to increase the patency of the OHP segment during oral breathing in supine, awake, normal subjects.

Effects of topical nasal anaesthesia on shift of breathing route in adults

The position of the soft palate is known to determine the breathing route, but the physiological mechanisms that bring about a shift from nasal to oral breathing are unclear. To test the hypothesis that activation of receptors in the nasal passage may be involved in reflex initiation of oral breathing after nasal obstruction, we investigated respiratory responses to nasal occlusion before and after topical lignocaine anaesthesia of the nasal passages. Eleven volunteers were fitted with custom-made partitioned face masks, which separated nasal and oral passages. Air flow through each passage was detected by changes in airway pressure and carbon dioxide concentration. Nine subjects were habitual nasal breathers both before and after topical anaesthesia with 4% lignocaine. Among these subjects, the time to initiate oral breathing in response to nasal occlusion was significantly shorter before anaesthesia than afterwards (mean 4.4 [SD 2.5] vs 10.8 [7.4] s, p less than 0.01). Similarly, the time to resume nasal breathing after release of nasal occlusion was significantly shorter before topical anaesthesia than afterwards (6.9 [4.9] vs 12.1 [7.8] s, p less than 0.01). Topical anaesthesia did not affect respiration rate, end-tidal carbon dioxide concentration, or arterial oxygen saturation. These findings suggest that in human beings sensory information from receptors in the nasal passage has an important role in controlling the shift of breathing route.

Influence of nasal airflow temperature and pressure on alae nasi electrical activity

The influence of nasal airflow, temperature, and pressure on upper airway muscle electromyogram (EMG) was studied during steady-state exercise in five normal subjects. Alae nasi (AN) and genioglossus EMG activity was recorded together with nasal and oral airflows and pressures measured simultaneously by use of a partitioned face mask. At constant ventilations between 30 and 50 l/min, peak inspiratory AN activity during nasal breathing (7.2 +/- 1.4 arbitrary units) was greater than that during oral breathing (1.0 +/- 0.3 arbitrary units; P less than 0.005). In addition, the onset of AN EMG activity preceded inspiratory flow by 0.38 +/- 0.03 s during nasal breathing but by only 0.17 +/- 0.04 s during oral breathing (P less than 0.04). When the subject changed from nasal to oral breathing, both these differences were apparent on the first breath. However, peak AN activity during nasal breathing was uninfluenced by inspiration of hot saturated air (greater than 40 degrees C), by external inspiratory nasal resistance, or by changes in the expiratory route. The genioglossus activity did not differ between nasal and oral breathing (n = 2). Our findings do not support reflex control of AN activity sensitive to nasal flow, temperature, or surface pressure. We propose a centrally controlled feedforward modulation of phasic inspiratory AN activity linked with the tonic drive to the muscles determining upper airway breathing route.

Relationship between alae nasi activation and breathing route during exercise in humans

We studied the relationship between alae nasi muscle (AN) activation and breathing route in normal subjects during exercise. Nasal and oral airflow were measured simultaneously using a partitioned face mask and were recorded with the AN electromyogram. Subjects breathed via 1) the nose and mouth (NM) 2) the nose only (N), or 3) the mouth only (M). As ventilation (VE) rose progressively, the peak phasic inspiratory AN activity (IAAN) increased for all breathing routes. IAAN during N [11.8 +/- 2.0 arbitrary units (AU)] was greater than during NM (3.3 +/- 1.3 AU) and M (2.4 +/- 1.0 AU; P less than 0.01) measured at the highest common VE (over a 10-l/min range). At the highest 20% of IAAN recorded during NM, the total VE during N (24 +/- 5 l/min). However, for the same IAAN, nasal VE during NM (27 +/- 3 l/min) was similar to that during N. Thus, as ventilation increases during exercise, AN activity and nasal ventilation are tightly correlated, independently of flow through the mouth. This suggests either reflex modulation of AN activity by nasal flow or coordination of AN activation with the flow-partitioning mechanism of the upper airway.

Abdominal muscle activity in conscious dogs: effect of sleep and route of breathing

Abdominal muscle activity (EMG abd) was studied in 4 adult dogs during wakefulness and sleep. The dogs were previously prepared with a permanent side-hole tracheal stoma, and were trained to sleep with a tightly-fitting snout mask, hermetically sealed in place. They breathed either through a cuffed endotracheal tube inserted distally into the tracheal stoma (tracheal) the upper airway, with the tracheal stoma plugged (nasal). Sleep state was determined by behavioural, electroencephalographic and electromyographic criteria. EMG abd activity was measured using fine bipolar needles inserted into the abdominal muscle layers. Expiratory EMG abd augmented progressively from sleep onset to SWS regardless of route of breathing, and without major changes in the animal's ventilation. Maximal EMG abd occurred in SWS during nasal breathing; EMG abd increased from a mean of 16.6 ± 0.3 mV awake, to 23.8 ± 0.3 mV in SWS, representing an overall increase of 55.0 ± 7.5% from the awake level. EMG abd increased similarly during tracheal breathing, with an overall increase of 62.0 ± 15.4% in SWS. We conclude that the consistent augmentation of expiratory EMG abd activity in sleep indicates that expiration in the dog is an active process, which is enhanced during nasal breathing and NREM sleep.

Breathing route influences upper airway muscle activity in awake normal adults.

Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21-38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.

Effect of the larynx on ventilation and respiratory pattern in anesthetized rabbits.

The effects of the larynx on ventilation and pattern of breathing have been investigated in anesthetized, spontaneously breathing rabbits. Breathing was either via a tracheostomy or via a supralaryngeal tube in control condition, after laryngeal denervation and after subsequent bilateral midcervical vagotomy. Laryngeal resistance was measured in all experimental conditions when breathing was through the larynx. In control conditions the presence of the larynx in the breathing circuit, as compared to breathing through the tracheostomy, slightly but significantly lowered inspiratory and expiratory airflows, tidal volume, and minute ventilation and increased tracheal pressure. Inspiratory and expiratory durations were not significantly changed. Expiratory laryngeal resistance was higher than inspiratory. Laryngeal deafferentation did not significantly modify values of the respiratory variables. Subsequent motor denervation of the larynx enhanced the decrease in ventilatory parameters due to adding the larynx to the circuit and lengthened the respiratory cycle. Inspiratory laryngeal resistance increased sevenfold and expiratory resistance threefold. Subsequent midcervical vagotomy induced a further increase in inspiratory and expiratory durations and augmented tidal volume independent of the route of breathing, and also reduced laryngeal resistance previously increased by motor denervation. These results reveal the ventilatory effects of the larynx and show the importance of its patency in the pattern of breathing.

Effect of maturation on oral breathing in sleeping premature infants

To evaluate the influence of postnatal maturation on oral breathing, we measured nasal and oral ventilation during sleep and the ventilatory response to nasal occlusion in 11 preterm infants. Studies were repeated at 31-32, 33-34, and 35-36 weeks postconceptional age. Premature infants had rare episodes of spontaneous oronasal breathing during sleep. The frequency of oral breathing in response to nasal occlusion increased with advancing postconceptional age, from 8% +/- 8% at 31-32 weeks to 26% +/- 18% at 33-34 weeks and 28% +/- 33% at 35-36 weeks. Oral breathing in preterm infants, unlike that in term infants, was characterized by intermittent airway obstruction leading to a significant decrease in respiratory rate, tidal volume, minute ventilation, and tcpo2 (P less than 0.005). When inspiratory (Rl) and expiratory (RE) resistances during nasal and oral breathing were compared, Rl increased from 41 +/- 30 to 234 +/- 228 (P less than 0.004) and RE from 62 +/- 16 to 145 +/- 43 cm H2O X L-1 X sec (P less than 0.004). The ability of preterm infants to use the oral route of breathing thus increases with advancing postnatal maturation, but its effectiveness may remain limited by high oral airway resistance.

Breathing route during sleep.

Nasal obstruction has been associated with apneic episodes during sleep. However, the normal distribution of nasal and oral air flow while asleep has not been investigated. To determine the normal route of ventilation during sleep, we studied 7 healthy men and 7 healthy women using a sealed face mask that mechanically separated nasal and oral air flow. Standard sleep staging techniques were employed. The subjects slept 297 +/- 29 (SEM) min, with a mean of 197 +/- 15 min of ventilation recorded. Ventilation was decreased during sleep as has been previously demonstrated. However, during sleep, we found that men breathed a greater percentage of total ventilation through the mouth (29.0 +/- 8.2%) than did women (5.0 +/- 1.0%, p less than 0.02). The same trend applied during wakefulness but did not reach significance (p = 0.06). Although none was symptomatic, 4 subjects, all men, had more than 3 apneas per hour. These 4 men had a greater percentage of mouth ventilation (37.3 +/- 19.0%) than did the other 10 subjects with few or no apneas (8.1 +/- 2.7%, p less than 0.02). It was also noted that increasing age in men was associated with an increasing percentage of mouth ventilation (r = 0.83 p less than 0.03) but this relationship was not observed in women. We conclude that mouth breathing may be associated with apneas during sleep and that breathing through the mouth occurs commonly in men, particularly in those who are older. This suggests that nasal breathing may be important in the maintenance of ventilatory rhythmicity during sleep.

Pattern of inhalation of tobacco smoke in pipe, cigarette, and never smokers.

There is controversy on whether both primary and secondary pipe smokers do inhale tobacco smoke. We studied inhalation of tobacco smoke in 6 primary and 6 secondary pipe smokers and compared it with that in 20 cigarette smokers and 11 never smokers. Respiratory movements were assessed with inductive plethysmography, nasal flow through measurements of nasal pressure, oral flow with an oral thermistor, puffing through pressure measurements in the cigarette holder or the pipe, and upper airways by fluoroscopy. In all pipe smokers except 1, breathing and smoking appeared as independent activities. The former was exclusively nasal, whereas the latter was exclusively oral. Smoke was sucked and puffed by a to-and-fro movement of the tongue sliding along the soft palate. The oropharyngeal isthmus was closed (or only intermittently opened) by the apposition of the soft palate and the tongue, thus preventing overt inhalation of smoke. In most cigarette smokers, smoking interfered with the breathing route. Once smoke was sucked into the mouth, the oropharyngeal isthmus opened and inspiration proceeded through both mouth (with inhalation of smoke) and nose. Cigarette smoking interfered also with the evenness of ventilation. Never smokers avoided inhalation by oropharyngeal closure followed by oral expiration. We conclude that the oropharyngeal isthmus is the essential gate controlling smoke inhalation. Most secondary pipe smokers are able to change their smoking pattern and avoid overt inhalation when switching from cigarette to pipe smoking. The inhalation pattern appears to be acquired in the course of the smoking history.

Influence of the respiratory route on the resting breathing pattern in humans.

It has been shown that the pattern of breathing is modified when breathing through a mouthpiece (MP) with a noseclip (NC), although the reasons for this are not clear. We studied 14 healthy naïve subjects during unrestrained breathing, while connected to a spirometer without NC, and while connected to a spirometer with NC. Breathing pattern, studied with an inductive plethysmograph (Respitrace), was recorded during 4 min in each case, once a steady state was attained. During unrestrained breathing, all subjects breathed exclusively through the nose. During spirometric testing without NC, 9 of 14 subjects still breathed through the nose only (since the oropharynx is closed by the soft palate and the tongue, and flow proceeds through the nose). Tidal volume (VT), frequency (f), minute ventilation (VE), inspiratory time, mean inspiratory flow, and duty cycle (Tl/Ttot) were not different during the first 2 procedures (p greater than 0.1 by analysis of variance). By contrast, during spirometric testing with NC, mean VT increased from 530 (during unrestrained breathing) to 700 ml (p less than 0.02), whereas f decreased from 14.9 to 13.6 breaths X min-1 (p greater than 0.05), VE did not change, and Tl/Tot increased from 37 to 41% (p less than 0.05). These data suggest that the change in the pattern of breathing depends on the breathing route. To further confirm this, we asked 8 separate subjects to simply breathe through either the nose or the mouth (half of them starting with mouth breathing, half with nose breathing) while respiration was monitored with the Respitrace without any connection to the airways.(ABSTRACT TRUNCATED AT 250 WORDS)