Inspiratory Muscle Activity Research Articles

Respiratory parameters during professional flute playing

We studied three professional flautists while playing to determine: (1) what respiratory muscles and percent vital capacity (%VC) were used; (2) how mouth pressure (Pm), embouchure resistance (Rem), embouchure aperture (Aem), flow (V̇) and velocity (Vel) affect sound loudness (I) and frequency (F). We measured Pm, esophageal, gastric, transdiaphragmatic, transpulmonary (P l) pressures, diaphragmatic EMG, sound and chest wall displacements directly. Lung volume (V l) was estimated from P l during playing and the static deflation P l–V l curve measured separately; V̇ from ΔV l/Δt; Rem from Pm/(ΔV l/Δt). Staccati and sustained notes at different F and I were performed. I increased mainly with V̇ and F with Vel. V̇ and Vel are independently controlled by Pm and Aem. The variation of mean Pm was small (6–11 cm H 2O) and large for VC (72–83%) suggesting braking inspiratory muscle activity while playing. However, rib cage (RC) and abdominal (Ab) motion were different for each subject. One displaced Ab>RC at high V l and RC>Ab at low V l, another the opposite pattern; the third was in between. We conclude that while different flautists use different strategies to control Pm, the results are similar. Independent control of V and Vel by Pm and Aem allow flautists to control I and F regardless of how Pm is generated.

Chest wall hyperinflation during acute bronchoconstriction in asthma.

The mechanics of the chest wall was studied in seven asthmatic patients before and during histamine-induced bronchoconstriction (B). The volume of the chest wall (VCW) was calculated by three-dimensional tracking of 89 chest wall markers. Pleural (Ppl) and gastric (Pga) pressures were simultaneously recorded. VCW was modeled as the sum of the volumes of the pulmonary-apposed rib cage (VRC,p), diaphragm-apposed rib cage (VRC,a), and abdomen (VAB). During B, hyperinflation was due to the increase in end-expiratory volume of the rib cage (0.63 +/- 0.09 L, p < 0.01), whereas change in VAB was inconsistent (0.09 +/- 0.07 L, NS) because of phasic recruitment of abdominal muscles during expiration. Changes in end-expiratory VRC,p and VRC,a were along the rib cage relaxation configuration, indicating that both compartments shared proportionally the hyperinflation. VRC,p-Ppl plot during B was displaced leftward of the relaxation curve, suggesting persistent activity of rib cage inspiratory muscles throughout expiration. Changes in end-expiratory VCW during B did not relate to changes in FEV(1) or time and volume components of the breathing cycle. We concluded that during B in asthmatic patients: (1) rib cage accounts largely for the volume of hyperinflation, whereas abdominal muscle recruitment during expiration limits the increase in VAB; (2) hyperinflation is influenced by sustained postinspiratory activity of the inspiratory muscles; (3) this pattern of respiratory muscle recruitment seems to minimize volume distortion of the rib cage at end-expiration and to preserve diaphragm length despite hyperinflation.

Lung mechanics and end-expiratory lung volume during hypoxia in rats

We investigated whether an hypoxia-induced increase in airway resistance mediated by vagal efferents participates in the increase in end-expiratory lung volume (EELV) observed in hypoxia. We also assessed the contribution of the end-expiratory activity of the diaphragm (DE) to this phenomenon. Therefore, we measured EELV, total lung resistance (RL), dynamic lung compliance (Cdyn), DE, and minute ventilation (VE) in anesthetized rats during normoxia and hypoxia (10% O(2)) before (control) and after administration of atropine or saline. In the control group, hypoxia increased EELV, Cdyn, DE, and VE but slightly decreased RL. These changes were unaffected by saline or atropine, except that, in the atropine-treated rats, hypoxia did not change RL. These results suggest that 1) the increase in EELV observed in hypoxia cannot result from an increase in airway resistance; 2) the increased and persistent activity of inspiratory muscles during expiration is the most likely cause of the increase in EELV during hypoxia; and 3) the decrease in RL induced by hypoxia could result from the increase in lung volume including EELV.

Pontine carbachol elicits multiple rapid eye movementsleep-like neural events in urethane-anaesthetized rats

Microinjection of a cholinergic agonist, carbachol, into the pontine reticular formation of chronically instrumented intact or acutely decerebrate rats and cats has been used extensively to study rapid eye movement sleep mechanisms. In this study, we sought to develop a reduced carbachol model of rapid eye movement sleep-like neural events exhibiting multiple physiological markers of this state, and allowing for the use of invasive electrophysiological techniques. Accordingly, we investigated whether pontine carbachol could produce rapid eye movement sleep-like motor atonia and electrocortical changes in urethane-anaesthetized rats. We recorded cortical and hippocampal electroencephalograms and genioglossus and inspiratory intercostal muscle activities in 13 urethane-anaesthetized, spontaneously breathing, tracheotomized and vagotomized rats. In steady-state periods with high-voltage/low-frequency electroencephalogram activity, carbachol microinjections (15–40 nl, 10 mM) were placed in the medial pontine reticular formation. In 12 rats, carbachol elicited episodes of stereotyped hypotonia of genioglossus but not intercostal muscle activity, typical of rapid eye movement sleep, with a latency and duration of 2.2±0.3 min (mean±S.E.M.) and 11.0±2.9 min, respectively. In four of these rats, also similar to rapid eye movement sleep, the major suppression of genioglossus activity (−74±9%) was accompanied by electroencephalogram desynchronization, appearance of hippocampal theta rhythm, and a respiratory rate increase (+14±3%). In the remaining eight rats, the stereotyped suppression of genioglossus activity (−48±3%) occurred without electroencephalogram desynchronization and hippocampal theta, and was accompanied by a respiratory rate decrease (−6±2%); a pattern of response typical of decerebrate animals. Within a rat, similar patterns of response to repeated carbachol injections at the same anatomical site were obtained. Pontine atropine prevented responses to subsequent carbachol injections. Thus, in urethane-anaesthetized rats, pontine carbachol consistently produced a differential suppression of pharyngeal versus respiratory pump muscle activity, and in a subset of animals, this was also accompanied by cortical and hippocampal electrographic changes typical of rapid eye movement sleep. This shows that complex and stereotyped neuronal events underlying both ascending and descending signs of rapid eye movement sleep can be pharmacologically activated under general anaesthesia. Such a reduced preparation may be useful for studies into the central neuronal mechanisms underlying generation of rapid eye movement sleep; particularly for studies requiring techniques that are difficult to implement in intact, naturally sleeping animals. The acceleration of the respiratory rate observed only when carbachol induced electroencephalogram desynchronization suggests that neural events associated with electrocortical changes contribute to the respiratory rate increases observed in natural rapid eye movement sleep.

Effects of different expiratory maneuvers on inspiratory muscle force output.

We assessed the effects of two different expiratory maneuvers (fast [F] or slow [S]) on the ability of normal subjects (n = 12, age 35 +/- 6 yr) to generate maximal inspiratory pressures and maximal inspiratory flows near residual volume (RV). With the F maneuver, the subject exhaled rapidly to RV and immediately performed a maximal inspiratory effort, whereas with the S maneuver the subject exhaled slowly to RV, paused for 4 to 6 s at RV, and then inspired forcefully. Maximal static inspiratory pressure against an occluded airway (PImax), and maximal dynamic inspiratory pressure (PIdyn) and maximal inspiratory flow (V Imax) with no added resistance, as well as the electromyographic activity of the parasternal muscles, were measured during each maneuver. Both maneuvers were initiated from TLC and were performed randomly. In comparison with the S maneuver, the F maneuver yielded values of higher (mean +/- SE) PImax (148 +/- 5 cm H2O versus 135 +/- 7 cm H2O, p < 0.05), PIdyn (33 +/- 2 cm H2O versus 28 +/- 2 cm H2O, p < 0.05), and V Imax (12.3 +/- 0.4 L/s versus 11.4 +/- 0.6 L/s, p < 0.05). In addition, the rate of rise of PImax, the rate of rise of PIdyn, and the integrated peak electromyographic activity of the parasternal muscles were significantly greater with the F than with the S maneuver, suggesting greater inspiratory muscle (IM) activation. The enhanced IM activation may be related to a specific inspiratory-expiratory muscle interaction similar to the agonist-antagonist interactions described for a pair of skeletal muscles.

Determinants of rib motion in flail chest.

We have previously developed a canine model of isolated flail chest to assess the effects of this condition on the mechanics of breathing, and these studies have led to the conclusion that the respiratory displacement of the fractured ribs is primarily determined by the fall in pleural pressure (Delta Ppl) and the action of the parasternal intercostal muscles. The present studies were designed to test the validity of this conclusion. A flail was induced in six supine anesthetized animals by fracturing both dorsally and ventrally the second to fifth ribs on the right side of the chest, after which the phrenic nerve roots were bilaterally sectioned in the neck. Sectioning the phrenic nerves caused a 34% decrease in Delta Ppl, associated with a 39% increase in parasternal intercostal inspiratory EMG activity (p < 0.05), and resulted in a marked reduction in the inspiratory inward displacement of the ribs. In three animals, the inward rib displacement was even reversed into a small outward displacement. When the airway was then occluded at end-expiration to increase Delta Ppl during the subsequent inspiration, all animals again showed a clear-cut inward rib displacement. These observations therefore confirm that in dogs with flail chest, the inspiratory displacement of the fractured ribs is set by the balance between the force related to pleural pressure and that generated by the parasternal intercostals. These observations also point to the critical importance of the pattern of inspiratory muscle activation in determining the magnitude of rib cage paradox in such patients.

Differences in spontaneous breathing pattern and mechanics in patients with severe COPD recovering from acute exacerbation.

The aims of this study were to assess spontaneous breathing patterns in patients with chronic obstructive pulmonary disease (COPD) recovering from acute exacerbation and to assess the relationship between different breathing patterns and clinical and functional parameters of respiratory impairment. Thirty-four COPD patients underwent assessment of lung function tests, arterial blood gases, haemodynamics, breathing pattern (respiratory frequency (fR), tidal volume (VT), inspiratory and expiratory time (tI and tE), duty cycle (tI/ttot), VT/tI) and mechanics (oesophageal pressure (Poes), work of breathing (WOB), pressure-time product and index, and dynamic intrinsic positive end-expiratory pressure (PEEPi,dyn)). According to the presence (group 1) or absence (group 2) of Poes swings during the expiratory phase (premature inspiration), 20 (59%) patients were included in group 1 and 14 (41%) in group 2. Premature inspirations were observed 4.5+/-6.4 times x min(-1) (range 1-31), i.e. 20+/-21% (3.7-100%) of total fR calculated from VT tracings. In group 1 the coefficient of variation in VT, tE, tI/ttot, PEEPi,dyn, Poes and WOB of the eight consecutive breaths immediately preceding the premature inspiration was greater than that of eight consecutive breaths in group 2. There were no significant differences in the assessed parameters between the two groups in the overall population, whereas patients with chronic hypoxaemia in group 1 showed a more severe impairment in clinical conditions, mechanics and lung function than hypoxaemic patients in group 2. In spontaneously breathing patients with chronic obstructive pulmonary disease recovering from an acute exacerbation, detectable activity of inspiratory muscles during expiration was found in more than half of the cases. This phenomenon was not associated with any significant differences in anthropometric, demographic, physiological or clinical characteristics.

Time to peak tidal expiratory flow and the neuromuscular control of expiration.

The ratio of the time needed to reach peak tidal expiratory flow (tPTEF) and the duration of expiration (tE) is used to detect airflow obstruction in young children. tPTEF is decreased in patients with asthma, but knowledge about the physiological determinants of this parameter is scarce. This study examined the relationship between tPTEF and postinspiratory activities of inspiratory muscles and evaluated the effects of changing sensory information from the lung. Airflow patterns and electromyographic (EMG) activity of inspiratory muscles were recorded in seven spontaneously breathing, anaesthetized cats. The trachea was cannulated and, as a result, the larynx and upper airways were bypassed. Changes in postinspiratory muscle activity were induced by changing afferent sensory nerve information (by cooling the vagus nerves, by administration of histamine and by additional application of continuous positive airway pressure (CPAP)). Durations of postinspiratory activities of the diaphragm and intercostal muscles (characterized by their time constants tau diaphr and tau interc) correlated strongly with tPTEF (r=0.85 and 0.77, respectively). Tau diaphr, tau interc and tPTEF were significantly increased during cooling of the vagus nerves (4-8 degrees C) compared with values at 22 and 37 degrees C (p<0.05). Conversely, administration of histamine and CPAP caused significant decreases in tau diaphr, tau interc and tPTEF, which were absent during cooling of the vagus nerves. In conclusion, the time needed to reach peak tidal expiratory flow is highly influenced by the activities of inspiratory muscles during the early phase of expiration which, in turn, depend on the activities of vagal receptors in the lung.

The expiratory flow pattern and the neuromuscular control of breathing in cats.

During spontaneous breathing inspiratory muscle activity does not stop immediately at the start of expiration, but decays at a rate which can be influenced importantly by pulmonary receptors. 1 When the contribution of this decaying activity to the expiratory flow pattern is suppressed by a short end-inspiratory occlusion, the time constant of the respiratory system (τRS = RRS/ERS) can be estimated from the expiratory flow pattern using equation 1 and P(t) = 0.4 KeywordsContinuous Positive Airway PressurePeak Expiratory FlowNeuromuscular ControlDecay ActivityResidual Standard DeviationThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Respiratory activity of the rat posterior cricoarytenoid muscle.

An anatomic and electrophysiological study of the rat posterior cricoarytenoid (PCA) muscle is described. The intramuscular nerve distribution of the PCA branch of the recurrent laryngeal nerve was demonstrated by a modified Sihler's stain. The nerve to the PCA was found to terminate in superior and inferior branches with a distribution that appeared to be confined to the PCA muscle. Electromyography (EMG) recordings of PCA muscle activity in anesthetized rats were obtained under stereotaxic control together with measurement of phrenic nerve discharge. A total of 151 recordings were made in 7 PCA muscles from 4 rats. Phasic inspiratory activity with a waveform similar to that of phrenic nerve discharge was found in 134 recordings, while a biphasic pattern with both inspiratory and post-inspiratory peaks was recorded from random sites within the PCA muscle on 17 occasions. The PCA EMG activity commenced 24.6 +/- 2.2 milliseconds (p < .0001) before phrenic nerve discharge. The results are in accord with findings of earlier studies that show that PCA muscle activity commences prior to inspiratory airflow and diaphragmatic muscle activity. The data suggest that PCA and diaphragm motoneurons share common or similar medullary pre-motoneurons. The earlier onset of PCA muscle activity may indicate a role for medullary pre-inspiratory neurons in initiating PCA activity.

Effects of uni- and bilateral phrenicotomy on active and passive respiratory mechanics in rats

Eighteen spontaneously breathing anesthetized rats were selected to belong to three groups: control (C), unilateral (U), and bilateral phrenicotomy (B). Eight days after surgery, the passive and active mechanical properties of the respiratory system, the shape of the occlusion pressure wave, the decay of inspiratory muscle activity during expiration and control of breathing were analysed. Passive and active elastances increased significantly from C to U and from U to B. Passive and active time constants decreased either in uni- or bilateral phrenicotomies. Passive and active resistances remained unaltered. The intensity of respiratory drive increased from C to U and B. In conclusion, uni- and bilateral phrenicotomies increase the elastic load of the respiratory system, because of both its passive and active components, which raised the respiratory neuromuscular drive of the remaining muscles. Consequently, minute ventilation remained unchanged. The higher frequency was allowed for, by a shorter time constant of the respiratory system and by a faster decay of post-inspiratory muscle activity.

Physiological effects and optimisation of nasal assist-control ventilation for patients with chronic obstructive pulmonary disease in respiratory failure.

BACKGROUND: A study was undertaken to investigate the effects of non-invasive assist-control ventilation (ACV) by nasal mask on respiratory physiological parameters and comfort in acute on chronic respiratory failure (ACRF)....

Respiratory mechanics in patients with tense cirrhotic ascites.

Lung volumes are decreased by tense ascites and increase after large volume paracentesis (LVP). The overall effect of ascites and LVP on the respiratory function is poorly understood. We studied eight cirrhotic patients with tense ascites before and after LVP. Inspiratory muscle force (maximal transdiaphragmatic pressure (Pdi,max), and the lowest pleural pressure (Pp1,min)) was assessed while the patients were seated. Rib cage and abdominal volume displacements, as well as pleural and gastric pressures were measured during quiet breathing while the patients were supine. Pdi,max and Ppl,min were normal and did not change after LVP (from 84.2+/-19.7 to 85.2+/-17.0 cmH2O and from 68.3+/-19.7 to 74+/-15.9 cmH2O, respectively). The abdominal contribution to the generation of tidal volume was greater than that of the rib cage (79 vs 21%), a pattern which did not change after LVP (73 and 27%). Before LVP, tidal swings both of pleural pressure (Ppl,sw) and transdiaphragmatic pressure (Pdi,sw) were large (15.3+/-4.3 and 18.5+/-3.9 cmH2O, respectively) and the load on inspiratory muscles was increased as a consequence of elevated dynamic elastance of the lung (El,dyn) (11.4+/-2.6 cmH2O x L(-1)) and ("intrinsic") positive end-expiratory pressure (PEEPi) (4.3+/-3.5 cmH2O). LVP reduced the load on the inspiratory muscles, as shown by the significant decrease in Ppl,sw (10.6+/-2.0 cmH2O), Pdi,sw (12.8+/-3.0 cmH2O), El,dyn (10.0+/-2.0 cmH2O x L(-1)) and PEEPi (1.1+/-1.3 cmH2O). The amount of fluid removed was closely related to changes in Ppl,sw and PEEPi. We conclude that the strength of the inspiratory muscles is normal or reduced in seated cirrhotic patients. In the supine position, tense ascites results in an increase in lung elastic load and development of positive end-expiratory pressure, with a consequent overload and increased activation of inspiratory muscles. Large volume paracentesis decreases overloading and activation, but does not change the strength of the inspiratory muscles.

Nasal mask pressure waveform and inspiratory muscle rest during nasal assisted ventilation.

In mechanically ventilated patients, pressure and flow tracings can be used to assess respiratory pump muscle activity or rest. When the ventilation is delivered through an endotracheal tube, the respiratory system can be considered a one-compartment model, and activation of the respiratory muscles results in deformations and variability of the pressure tracings. This is also true when mechanical ventilation is delivered nasally. With intermittent positive-pressure ventilation delivered through a nasal mask (nIPPV), we have recently shown that the glottis can interfere with ventilation even in the absence of diaphragmatic surface electromyographic (EMG) activity. On the basis of our observations, we suggested that when mechanical ventilation is delivered through a nasal means of access, the respiratory system cannot be considered a one-compartment model. To confirm this hypothesis, we submitted one healthy subject to nIPPV while his glottis was continuously monitored through a fiberoptic bronchoscope and his diaphragmatic activity was monitored with a bipolar esophageal electrode. During wakefulness or sleep, we observed irregularities in the nasal mask pressure waveform, in nasal mask peak pressure, and in actual VT despite the absence of respiratory pump muscle activity. These irregularities were related to significant variations in the glottic width, rather than to the reappearance of transient phasic inspiratory muscle activity. We conclude that during nIPPV, deformations in the mask pressure waveform can be induced by variations in the glottic aperture without activation of the diaphragm. Thus, when mechanical ventilation does not bypass the glottis, the respiratory system does not behave like a one-compartment model, and EMG remains the only reliable technique for assessing diaphragmatic muscle activity.

Respiratory muscle coordination in acute spinal dogs

Our objectives were (1) to test whether respiratory muscles of spinal dogs can generate the alternating pattern of activation seen in intact animals and (2) to characterize the responsiveness of spinal rhythms to mechanical ventilation. We recorded the electromyographic activities of inspiratory muscles (diaphragm and parasternal intercostals) and expiratory muscles (triangularis sterni and transversus abdominis) in ten anesthetized dogs before and after transection of the cervical cord at levels C1–C2 ( n = 2), C2–C3 ( n = 6), and C8 ( n = 2). In 9 10 dogs, we observed short lasting (3–4 min) rhythmic ventilatory muscle activity for up to 3 h after transection. Inspiratory and expiratory muscles contracted simultaneously, suggesting an absence of mechanism(s) responsible for reciprocal muscle activation on a spinal level. Five of ten dogs showed tonic rib cage activity during apnea that was phasically modulated during mechanical ventilation. From the absence of alternating inspiratory and expiratory muscle activity in acute spinalized dogs, we conclude that dogs do not have a spinal pattern generator for respiration.

Histamine-induced end-tidal inspiratory activity and lung receptors in cats.

Hyperinflation in acute asthma has been associated with inspiratory muscle activity, which persist during expiration. The main objective of the present study was to evaluate the role of rapidly adapting receptors (RARs), slowly adapting receptors (SARs) and C-fibre endings in generating end-tidal inspiratory activity (ETIA). ETIA was induced by intravenous administration of histamine and continuous negative airway pressure (CNAP) in anaesthetized, spontaneously breathing cats. To differentiate between reflex activities from the three types of lung receptors, both vagus nerves were cooled to eight different temperatures (Tvg) between 4 and 37 degrees C. It is known that CNAP stimulates RARs and inhibits SARs. Histamine was used to stimulate RARs, and this was combined with continuous positive airway pressure (CPAP) to further stimulate SARs. ETIA was evoked in the diaphragm and in parasternal intercostal muscles by both stimuli (histamine and CNAP) in 8 out of 18 cats. After vagotomy, neither histamine nor CNAP evoked ETIA any more. At Tvg = 37 degrees C, CPAP suppressed histamine-induced ETIA; whereas, this suppression was diminished at Tvg between 14 and 8 degrees C. ETIA sharply declined for Tvg between 8 degrees and 4 degrees C, and at Tvg = 4 degrees C ETIA had virtually disappeared. At Tvg = 37 degrees and 22 degrees C values of ETIA during CNAP were larger than those in response to histamine; whereas, at Tvg = 10 degrees C comparable ETIA values were obtained. It was shown that ETIA is a vagal reflex activity in which C-fibre endings are not involved. Histamine-induced ETIA originates from stimulation of RARs, and is inhibited by stimulation of SARs. Mechanical stimulation of RARs is a forceful stimulus to induce ETIA. This suggests that hyperinflation in acute asthma might be due, at least in part, to ETIA resulting from an imbalance between SAR and RAR activity.

Respiratory response to positive inspiratory pressure in the cat: effects of CO2 and vagal integrity.

Effects of inspiratory pressure support (IPS) on respiration and activity of inspiratory muscles were tested in eight anesthetized cats by recording the diaphragmatic electromyogram (EMGdi) and respiratory variables at four levels of positive inspiratory airway pressure (5, 10, 15, and 20 cmH2O); onset of IPS was triggered by the inspiratory effort of the animal. When IPS was applied with room air (IPSAir) the respiratory frequency (f) was reduced compared with spontaneous breathing and the tidal volume (VT) was significantly increased, which resulted in a fall of arterial PCO2 (PaCO2) at IPS airway pressures (Paw) above 5 cmH2O. Despite this increase in VT, the amplitude of the integrated EMGdi (Adi) was reduced during IPS at all levels of Paw. When arterial hypocapnia is corrected by addition of CO2 to the inspirate, the values of VT at any given Paw were virtually identical with those during IPSAir, but IPS-mediated changes in f and Adi were smaller than those during IPSAir. IPS was also performed after bilateral vagotomy. Vagotomy itself caused VT and Adi to increase, and f to decrease, during spontaneous breathing. In comparison with the corresponding treatment before vagotomy, IPSAir led to a less severe reduction in Adi. As a result, VT was more enhanced and Paco2 was more reduced after vagotomy than before, both during spontaneous breathing and during IPSAir at all levels of Paw. When, however, isocapnia was restored with IPS with CO2 in the vagotomized animal, diaphragmatic activity and f became very similar to their values during spontaneous breathing, whereas VT remained elevated as a result of the high positive airway pressure. Our data suggest that in anesthetized cats IPS leads to a diminution of diaphragm activity and that this reduction can be entirely attributed to 1) the hypocapnia, resulting from increased VT, and 2) the stimulation of pulmonary vagal afferent fibers at positive airway pressure.

Effect of inspiratory pressure support on the arousal response to CO2 in sleeping dogs

The aim of the present study was to test the hypothesis that afferent mechanoreceptor stimuli from the respiratory muscles contribute to the arousal response to CO2 from both non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. We studied three dogs implanted with electromyographic (EMG) electrodes in the costal diaphragm and transversus abdominis muscles. During sleep, the animals were exposed to supplemental CO2 in O2 to maintain a constant level of end-tidal PCO2 (50 Torr for NREM, 56 Torr for REM) and breathed either spontaneously (SB) or with inspiratory pressure support (IPS). The arousal response was quantified as the time from initiation of CO2 administration to arousal. EMG activity of the costal diaphragm on IPS was decreased to approximately 70% (P < 0.01) of that during SB trials for both NREM and REM, whereas EMG activity of the transversus abdominis muscles did not differ between SB and IPS for either sleep state. The mean time to arousal was increased during NREM from 128.3 +/- 24.7 s (SB) to 216.8 +/- 38.7 s (IPS) (P < 0.025) and was increased during REM from 144.9 +/- 26.1 s (SB) to 219.0 +/- 23.8 s (IPS) (P < 0.001). In summary, in support of our hypothesis, we found that suppression of inspiratory muscle activity, without augmented expiratory muscle activity, delayed the arousal response to hypercapnia during both NREM and REM sleep.

Changes in breathing pattern in the normal horse at rest up to age one year.

Changes in pattern of airflow, sequence of respiratory muscle activation and generated pressures were measured serially in a group of foals during the first year post partum, in order to describe the maturation of the equine breathing pattern. In neonatal foals, inspiration and expiration were both primarily active and airflow pattern was essentially monophasic. By age 1 year, foals displayed essentially the same breathing pattern previously described in adult horses, utilising a combination of active and passive inspiration and expiration to breathe around, rather than from, the relaxation volume of the respiratory system (Vrx). A strong temporal relationship during growth was found between the timing of changes observed in airflow pattern and in the neuromuscular strategy of breathing. The transition to the adult breathing pattern appeared to involve a time delay in activation of both inspiratory and expiratory muscle groups, establishing a passive and active component to both inspiration and expiration. Throughout the study period, concurrent with the increase in delay of abdominal muscle activation, the expiratory flow pattern became progressively more biphasic in appearance. The time of appearance of a consistent biphasic inspiratory flow pattern was considerably later, at approximately age 1 year and coincided with the appearance of a delay in inspiratory muscle activation. From our results, we conclude that the transition from the neonatal to the adult breathing strategy in the horse appears not to be induced by the time course of chest wall stiffening during maturation. While changes in relative body proportions and size of abdominal contents during growth may influence the transition in breathing, our results also indicate that respiratory control mechanisms play an essential role in the expression of the polyphasic breathing pattern.

Neuromechanical regulation of respiratory motor output in ventilator-dependent C1-C3 quadriplegics.

To evaluate the role of phrenic and sternocleidomastoid afferents as alternate sources of inhibitory feedback during mechanical ventilation, we studied five C2-C3 quadriplegics with sensory denervation of the rib cage and diaphragm, six C1-C2 quadriplegics with additional loss of sensory feedback from the neck muscles, and seven normal subjects. We compared the return of inspiratory muscle activity [the recruitment threshold (PCO2RT)] during mechanical ventilation between subject groups after stepwise increases in end-tidal PCO2 (PETCO2) either by increasing the inspired fraction of CO2 (FICO2), decreasing tidal volume (VT; 50 ml/min), or decreasing frequency (f; 1 breath/2 min). Normal subjects were mechanically hyperventilated via a nasal mask until inspiratory activity was undetectable. Efferent input to the sternocleidomastoid was intact at both levels of spinal cord injury, but phasic activity was not evident at the quadriplegics' baseline resting ventilation. The PCO2RT was defined as the level of PETCO2 at which phasic activity of the diaphragm in normal subjects and of the sternocleidomastoid in C1-C2 and C2-C3 quadriplegics recurred. The mean PCO2RT (in response to raising PETCO2 via increased FICO2 while maintaining a high VT and f) was not significantly different (P = 0.6) between normal subjects (43 +/- 3 Torr) and C2-C3 quadriplegics (38 +/- 5 Torr). Both subject groups demonstrated a frequency- and volume-related inhibition, as evidenced by a substantially lower PCO2RT when PETCO2 was raised by reducing either VT or f. In contrast to the C2-C3 quadriplegics, the C1-C2 quadriplegics responded with a similar PCO2RT among the three different mechanical ventilation trials, independent of whether PETCO2 was raised with high VT and f, with reduced VT, or with reduced f. We conclude that feedback from at least some part of the chest wall is required to produce a volume- and frequency-dependent inhibition of inspiratory muscle activity observed during mechanical ventilation.