Contractile properties of the human diaphragm during chronic hyperinflation

BACKGROUND. In patients with chronic obstructive pulmonary disease (COPD) and hyperinflation of the lungs, dysfunction of the diaphragm may contribute to respiratory decompensation. We evaluated the contractile function of the diaphragm in well-nourished patients with stable COPD, using supramaximal, bilateral phrenic-nerve stimulation, which provides information about the strength and inspiratory action of the diaphragm. METHODS. In eight patients with COPD and five control subjects of similar age, the transdiaphragmatic pressure generated by the twitch response to phrenic-nerve stimulation was recorded at various base-line lung volumes, from functional residual capacity to total lung capacity, and during relaxation and graded voluntary efforts at functional residual capacity (twitch occlusion). RESULTS. At functional residual capacity, the twitch transdiaphragmatic pressure ranged from 10.9 to 26.6 cm of water (1.07 to 2.60 kPa) in the patients and from 19.8 to 37.1 cm of water (1.94 to 3.64 kPa) in the controls, indicating considerable overlap between the two groups. The ratio of esophageal pressure to twitch transdiaphragmatic pressure, an index of the inspiratory action of the diaphragm, was -0.50 +/- 0.05 in the patients, as compared with -0.43 +/- 0.02 in the controls (indicating more efficient inspiratory action in the patients than in the controls). At comparable volumes, the twitch transdiaphragmatic pressure and esophageal-to-transdiaphragmatic pressure ratio were higher in the patients than in normal subjects, indicating that the strength and inspiratory action of the diaphragm in the patients were actually better than in the controls. Twitch occlusion (a measure of the maximal activation of the diaphragm) indicated near-maximal activation in the patients with COPD, and the maximal transdiaphragmatic pressure was 106.9 +/- 13.8 cm of water (10.48 +/- 1.35 kPa). CONCLUSIONS. The functioning of the diaphragms of the patients with stable COPD is as good as in normal subjects at the same lung volume. Compensatory phenomena appear to counterbalance the deleterious effects of hyperinflation on the contractility and inspiratory action of the diaphragm in patients with COPD. Our findings cast doubt on the existence of chronic fatigue of the diaphragm in such patients and therefore on the need for therapeutic interventions aimed at improving diaphragm function.     

Contribution of the diaphragm and the other inspiratory muscles to different levels of tidal volume and static inspiratory effort in the rabbit

1. The contribution of the diaphragm and that of the other inspiratory muscles at different levels of tidal volume and during static inspiratory efforts of various strength has been studied in supine rabbits by blocking phrenic conduction with an electrotonic current. The rabbits were lightly anaesthetized with urethane and pentobarbitone.2. The volume displaced by the extradiaphragmatic muscles (V(tEDM)) in vagotomized rabbits increases linearly with the tidal volume (V(t)), according to the function V(tEDM) = - 3.27 + 0.32 V(t). The relative contribution of extradiaphragmatic muscles (V(tEDM)/V(t) x 100) for resting ventilation is 12% and becomes ca. 25% for the maximum V(t) value attained during re-breathing.3. When the vagi are left intact, the V(tEDM) is always higher because of the compensatory hyperactivity of the extradiaphragmatic muscles due to Hering-Breuer reflexes during the phrenic block.4. The pressure exerted by the extradiaphragmatic muscles, during inspiratory efforts with closed airways, increases linearly with the strength of the effort, without any difference between intact and vagotomized rabbits. The relationship between the pressure exerted by the extradiaphragmatic muscles (P(EDM)) and the pressure exerted by all the inspiratory muscles (P) is expressed by the function P(EDM) = - 3.29 + 0.38P.5. These results indicate that the diaphragm is the main inspiratory muscle at all levels of inspiratory activity.     

Respiratory muscle performance with stretch-shortening cycle manoeuvres: maximal inspiratory pressure-flow curves

AIM: To test the hypothesis that the maximal inspiratory muscle (IM) performance, as assessed by the maximal IM pressure-flow relationship, is enhanced with the stretch-shortening cycle (SSC). METHODS: Maximal inspiratory flow-pressure curves were measured in 12 healthy volunteers (35 +/- 6 years) during maximal single efforts through a range of graded resistors (4-, 6-, and 8-mm diameter orifices), against an occluded airway, and with a minimal load (wide-open resistor). Maximal inspiratory efforts were initiated at a volume near residual lung volume (RV). The subjects exhaled to RV using slow (S) or fast (F) manoeuvres. With the S manoeuvre, they exhaled slowly to RV and held the breath at RV for about 4 s prior to maximal inspiration. With the F manoeuvre, they exhaled rapidly to RV and immediately inhaled maximally without a post-expiratory hold; a strategy designed to enhance inspiratory pressure via the SSC. RESULTS: The maximal inspiratory pressure-flow relationship was linear with the S and F manoeuvres (r2 = 0.88 for S and r2 = 0.88 for F manoeuvre, P < 0.0005 in all subjects). With the F manoeuvre, the pressure-flow relationship shifted to the right in a parallel fashion and the calculated maximal power increased by approximately 10% (P < 0.05) over that calculated with the S manoeuvre. CONCLUSION: The maximal inspiratory pressure-flow capacity can be enhanced with SSC manoeuvres in a manner analogous to increases in the force-velocity relationship with SSC reported for skeletal muscles.     

Respiratory muscle performance with stretch‐shortening cycle manoeuvres: maximal inspiratory pressure–flow curves

Aim: To test the hypothesis that the maximal inspiratory muscle (IM) performance, as assessed by the maximal IM pressure–flow relationship, is enhanced with the stretch‐shortening cycle (SSC). Methods: Maximal inspiratory flow–pressure curves were measured in 12 healthy volunteers (35 ± 6 years) during maximal single efforts through a range of graded resistors (4‐, 6‐, and 8‐mm diameter orifices), against an occluded airway, and with a minimal load (wide‐open resistor). Maximal inspiratory efforts were initiated at a volume near residual lung volume (RV). The subjects exhaled to RV using slow (S) or fast (F) manoeuvres. With the S manoeuvre, they exhaled slowly to RV and held the breath at RV for about 4 s prior to maximal inspiration. With the F manoeuvre, they exhaled rapidly to RV and immediately inhaled maximally without a post‐expiratory hold; a strategy designed to enhance inspiratory pressure via the SSC. Results: The maximal inspiratory pressure–flow relationship was linear with the S and F manoeuvres (r² = 0.88 for S and r² = 0.88 for F manoeuvre, P < 0.0005 in all subjects). With the F manoeuvre, the pressure–flow relationship shifted to the right in a parallel fashion and the calculated maximal power increased by approximately 10% (P < 0.05) over that calculated with the S manoeuvre. Conclusion: The maximal inspiratory pressure–flow capacity can be enhanced with SSC manoeuvres in a manner analogous to increases in the force–velocity relationship with SSC reported for skeletal muscles.     

Effect of carbon dioxide on diaphragmatic function in human beings

We studied the effects of acute changes in the partial pressure of arterial carbon dioxide on diaphragmatic contractility and performance in four normal men. To study contractility we measured the ability of the diaphragm to generate pressure at a given level of excitation by determining the relation between the electrical activity of the diaphragm and transdiaphragmatic pressure during a voluntary quasi-isometric inspiratory effort carried out at different levels of end-tidal carbon dioxide. Our results show that contractility was reduced with hypercapnia (when end-tidal carbon dioxide was 7.5 per cent or higher), although hypocapnia (end-tidal carbon dioxide, 3 per cent) had no effect on diaphragmatic contractility. We also studied the development of diaphragmatic fatigue before and during carbon dioxide breathing. Subjects were studied at the same diaphragmatic tension-time index, a value analogous to the more familiar myocardial tension-time index, while the same inspiratory flow was maintained. Electromyographic signs of fatigue appeared at a lower tension-time index during hypercapnia than during normocapnia, indicating that endurance is diminished during hypercapnia. These findings show that acute respiratory acidosis equivalent to an arterial carbon dioxide tension of about 54 mm Hg decreases the contractility and endurance time of the diaphragm in human beings.     

Inspiratory muscle adaptations following pressure or flow training in humans

Skeletal muscle adapts differently to training with high forces or with high velocities. The effects of these disparate training protocols on the inspiratory muscles were investigated in ten healthy volunteers. Five subjects trained using high force (pressure) loads (pressure trainers) and five trained using high velocity (flow) loads (flow trainers). Pressure training entailed performing 30 maximal static inspiratory efforts against a closed airway. Flow training entailed performing 30 sets of three maximal dynamic inspiratory efforts against a minimal resistance. Training was supervised and carried out 5 days a week for 6 weeks. Inspiratory flow rates and oesophageal pressure-time curves were measured before and after training. Peak inspiratory pressures during maximal static and dynamic efforts and peak flows during the maximal dynamic efforts were calculated. The time-to-peak pressure and rate of rise in peak pressure during maximal static and dynamic manoeuvres were also calculated before and following training. Maximal static pressure increased in the pressure training group and maximal dynamic pressure increased in the flow training group. Both groups increased the rate of pressure production (dP/dt) during their respective maximal efforts. The post-training decrease in time-to-peak pressure was proportionately greater in the flow trainers than in the pressure trainers. The differences in time-to-peak pressure between the two groups were consistent with the different effects of force and velocity training on the time-to-peak tension of skeletal muscle.     

Effects of theophylline on diaphragmatic strength and fatigue in patients with chronic obstructive pulmonary disease

We studied the effects of theophylline on diaphragmatic strength and fatigue in 15 patients with severe chronic obstructive pulmonary disease. Diaphragmatic strength was assessed by measurement of the transdiaphragmatic pressure generated at functional residual capacity during a maximal inspiratory effort against closed airways. Diaphragmatic fatigue was induced by resistive loaded breathing. The electrical activity of the diaphragm was recorded with an esophageal electrode during the fatigue runs, and the high-low ratio of the electrical signal was analyzed to assess diaphragmatic fatigue. Studies were performed before and after 7 and 30 days of theophylline administration (mean plasma level, 13 +/- 2 mg per liter). A control group received a placebo instead of theophylline. Theophylline increased maximal transdiaphragmatic pressure by 16 per cent after 7 days of administration (P less than 0.01), and this increase persisted after 30 days. No significant change in maximal transdiaphragmatic pressure was observed in the group given the placebo. Theophylline also suppressed diaphragmatic fatigue in all patients who received it. We conclude that theophylline has a potent and long-lasting effect on diaphragmatic strength and fatigue in patients with fixed airway obstruction.     

Diaphragm and intercostal surface EMG and muscle performance after acute inspiratory muscle loading

We examined the effect of an acute bout of submaximal non-fatiguing inspiratory loading (IL) on maximal inspiratory pressure (MIP), and on the activation of the diaphragm (DI) and intercostals (IC) using surface electromyography (sEMG). After baseline measurements, 12 healthy subjects performed two sets of 30 inspiratory efforts at a load equivalent to 40% of their initial MIP. MIP and maximal DI and IC sEMG activity were recorded after the first and second set of IL, and 15 min after task cessation. After IL, MIP reached (+/-S.E.M.) 111+/-4% (P=0.032) of baseline values, and during MIP, DI and IC root mean square (RMS) sEMG amplitude increased significantly above baseline (143+/-21%, P=0.039 and 137+/-33%, P=0.016, respectively). The significant increase in MIP and RMS amplitude after IL suggests that MIP efforts were initially submaximal, and that prior loading enabled full activation. The changes in DI and IC RMS amplitude may also reflect an improvement in the synergy between them during these maximal efforts.     

Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure

We studied the effects of hypophosphatemia on diaphragmatic function in eight patients with acute respiratory failure who were artificially ventilated. Their mean serum phosphorus level was 0.55 +/- 0.18 mmol per liter (normal value, 1.20 +/- 0.10). The contractile properties of the diaphragm were assessed by measuring the transdiaphragmatic pressure generated at functional residual capacity during bilateral supramaximal electrical stimulation of the phrenic nerves. Diaphragmatic function was evaluated in each patient before and after correction of hypophosphatemia, which was achieved by administration of 10 mmol of phosphorus (as KH2PO4) as a continuous infusion for four hours. After phosphate infusion, the mean serum phosphorus level increased significantly (1.33 +/- 0.21 mmol per liter, P less than 0.0001). The increase in serum phosphorus was accompanied by a marked increase in the transdiaphragmatic pressure after phrenic stimulation (17.25 +/- 6.5 cm H2O as compared with 9.75 +/- 3.8 before phosphate infusion, P less than 0.001). Changes in the serum phosphorus level and transdiaphragmatic pressure were well correlated (r = 0.73). These results strongly suggest that hypophosphatemia impairs the contractile properties of the diaphragm during acute respiratory failure, and they emphasize the importance of maintaining normal serum inorganic phosphate levels in such patients.     

Trend of maximal inspiratory pressure in mechanically ventilated patients: predictors

INTRODUCTION: It is known that mechanical ventilation and many of its features may affect the evolution of inspiratory muscle strength during ventilation. However, this evolution has not been described, nor have its predictors been studied. In addition, a probable parallel between inspiratory and limb muscle strength evolution has not been investigated. OBJECTIVE: To describe the variation over time of maximal inspiratory pressure during mechanical ventilation and its predictors. We also studied the possible relationship between the evolution of maximal inspiratory pressure and limb muscle strength. METHODS: A prospective observational study was performed in consecutive patients submitted to mechanical ventilation for > 72 hours. The maximal inspiratory pressure trend was evaluated by the linear regression of the daily maximal inspiratory pressure and a logistic regression analysis was used to look for independent maximal inspiratory pressure trend predictors. Limb muscle strength was evaluated using the Medical Research Council score. RESULTS: One hundred and sixteen patients were studied, forty-four of whom (37.9%) presented a decrease in maximal inspiratory pressure over time. The members of the group in which maximal inspiratory pressure decreased underwent deeper sedation, spent less time in pressure support ventilation and were extubated less frequently. The only independent predictor of the maximal inspiratory pressure trend was the level of sedation (OR=1.55, 95% CI 1.003 - 2.408; p = 0.049). There was no relationship between the maximal inspiratory pressure trend and limb muscle strength. CONCLUSIONS: Around forty percent of the mechanically ventilated patients had a decreased maximal inspiratory pressure during mechanical ventilation, which was independently associated with deeper levels of sedation. There was no relationship between the evolution of maximal inspiratory pressure and the muscular strength of the limb.     

Diaphragmatic effects of selective resection of the upper phrenic nerve root in dogs

The aim of this study was to evaluate the effects on the diaphragm of upper phrenic nerve root resections in dogs. During laryngeal reinnervation, selective resections of the upper phrenic nerve root (C5) were performed unilaterally (right side, n=7; Group A) and bilaterally (n=6; Group B) and compared to non denervated animals (n=5). After 8 months, a diaphragmatic evaluation was performed: X-ray, EMG, transdiaphragmatic pressure (Pdi) after ipsi- and bilateral tetanic stimulation of the phrenic nerves and a bilateral histological study of five hemidiaphragmatic regions. EMG alterations were significantly more severe in Group B than in Group A, for the left (p<0.05) and right hemidiaphragms (p<0.01). No differences in the X-rays were noted between the three groups. The Pdi of the three groups after occlusion and phrenic nerve stimulations (unilateral and bilateral) were not statistically different. Histological data demonstrated that there were no differences in fibre irregularity, predominant fibre type or fibrosis between the three groups. Macroscopic and microscopic atrophy, which was mainly present on the anterior regions of the hemidiaphragms, was significantly higher in Group B than in Group A and undenervated dogs (p<0.05). In conclusion, resection of the upper phrenic nerve root of one phrenic nerve (right side) have limited effect on the diaphragm in dogs. However, resection of the upper phrenic nerve root on both sides resulted in a significant effect on the EMGs and histology of the entire diaphragm without any significant consequences on transdiaphragmatic pressure.     

Peak-potentialities of inspiratory musculature as disclosed by tracheal occlusion

Interest was focussed on maximal inspiratory efforts which anesthetized rabbits are able to display when acutely made dyspnoic by prolonged tracheal occlusion. Such efforts were characterized by the mean intrapleural pressure decrease per breath and by the maximum of intrapleural pressure decrease reached during inspiration. These efforts could not be intensified by additional biochemical and/or biophysical means such as hypercapnia, hypoxia, artificial pneumothorax, thoracic compression, etc. They were most pronounced around the 25th second after onset of tracheal occlusion.They could, however, be altered pharmacodynamically. Methylphenidate was found to be of particular interest. It enhanced the mean intrapleural pressure decrease per breath and intensified the maximum of inspiratory effort while, at the same time, leaving respiratory frequency nearly unaltered.The possible medicinal usefulness of the approach pursued is briefly discussed.     

Characteristics of inspiratory inhibition by occlusion of both external carotid and basilar arteries in cats.

Effects of the occlusion of both the external carotid and basilar arteries on the inspiratory activity were studied in anesthetized, vagotomized, paralyzed, and artificially ventilated cats. Integrated phrenic nerve activity was used as an index of the inspiratory activity. Blood pressure in the lingual artery, located downstream from the occluded external carotid arteries, was measured as the arterial pressure of the upper brain stem during occlusion. The basilar artery was occluded at the boundary between the medulla and pons. Occlusions of the external carotid arteries and basilar artery suppressed the phrenic nerve activity to finally disappear within 1 min (phrenic nerve apnea, 45 out of 50 occlusions in 6 cats). The blood pressure in the upper brain stem was 16.6 +/- 5.7 mmHg (mean +/- S.D.) during occlusions. These effects of occlusion on the phrenic nerve activity were also observed during hypercapnia and hypoxia, although they were not so remarkable as those during normocapnia and normoxia. The results indicate that the upper part of the brain stem operates a profound facilitatory mechanism on the medullary inspiratory activity.     

Differential effects of low-intensity motor cortical stimulation on the inspiratory activity in scalene muscles during voluntary and involuntary breathing

To assess the cortical contribution to breathing, low-intensity transcranial magnetic stimulation (TMS) was delivered over the motor cortex in 10 subjects during: (i) voluntary static inspiratory efforts, (ii) hypocapnic voluntary ventilation (end-tidal CO(2), 2.7±0.4% mean±SD), and (iii) hypercapnic involuntary ventilation (end-tidal CO(2), 6.0±0.7%). Electromyographic activity (EMG) was recorded from the scalene muscles (obligatory inspiratory muscles) and was significantly suppressed by TMS at short latency (17.2±1.7ms). The scalene EMG was reduced to 76±8% and 76±7% in voluntary breathing and the static inspiratory effort, respectively, but only to 91±10% during the involuntary ventilation, significantly less than during the two voluntary tasks (p<0.005). Thus, with differences in chemical drive to breathe, TMS shows differences in the cortical contribution to inspiratory activity in scalene muscles. Voluntary breathing showed larger suppression than involuntary breathing, when the suppression was marginal. The results strongly suggest that drive from fast-conducting corticospinal neurones contributes to inspiratory activity in scalenes during voluntary breathing but is not required during involuntary breathing.     

The influence of inspiratory muscle work history and specific inspiratory muscle training upon human limb muscle fatigue

The purpose of this study was to assess the influence of the work history of the inspiratory muscles upon the fatigue characteristics of the plantar flexors (PF). We hypothesized that under conditions where the inspiratory muscle metaboreflex has been elicited, PF fatigue would be hastened due to peripheral vasoconstriction. Eight volunteers undertook seven test conditions, two of which followed 4 week of inspiratory muscle training (IMT). The inspiratory metaboreflex was induced by inspiring against a calibrated flow resistor. We measured torque and EMG during isometric PF exercise at 85% of maximal voluntary contraction (MVC) torque. Supramaximal twitches were superimposed upon MVC efforts at 1 min intervals (MVC_TI); twitch interpolation assessed the level of central activation. PF was terminated ( T _lim) when MVC_TI was <50% of baseline MVC. PF T _lim was significantly shorter than control (9.93 ± 1.95 min) in the presence of a leg cuff inflated to 140 mmHg (4.89 ± 1.78 min; P = 0.006), as well as when PF was preceded immediately by fatiguing inspiratory muscle work (6.28 ± 2.24 min; P = 0.009). Resting the inspiratory muscles for 30 min restored the PF T _lim to control. After 4 weeks, IMT, inspiratory muscle work at the same absolute intensity did not influence PF T _lim, but T _lim was significantly shorter at the same relative intensity. The data are the first to provide evidence that the inspiratory muscle metaboreflex accelerates the rate of calf fatigue during PF, and that IMT attenuates this effect.     

Mouth pressure twitches induced by cervical magnetic stimulation to assess inspiratory muscle fatigue

This study aimed at determining whether twitch mouth pressure (TwPmo) induced by cervical magnetic stimulation (CMS) was sensitive to inspiratory muscle fatigue produced by whole body exercise (WBE) in normal subjects. Twenty subjects performed one or two of the following protocols: (i). cycling at 85% V(O(2),max) until exhaustion; (ii). inspiratory resistive load (IRL) breathing at 62% of maximal inspiratory pressure until task failure. In eight subjects, oesophageal (TwPoes), gastric (TwPga) and transdiaphragmatic (TwPdi) pressures were recorded. The TwPmo was significantly reduced (P<0.05) 20 min after both WBE and IRL, from 17.5+/-4.4 to 15.9+/-3.9 cmH(2)O and from 19.4+/-4.9 to 17.7+/-4.5 cmH(2)O, respectively. Subsequently to IRL, the TwPdi decrease was associated with a reduction in TwPoes/TwPga ratio; not after WBE. Independently of the mode of ventilatory loading, inspiratory muscle fatigue was detected. Thus, inspiratory muscle fatigue after WBE can be assessed in normal subjects with a noninvasive technique.     

Diaphragmatic silent period to transcranial magnetic cortical stimulation for assessing cortical motor control of the diaphragm

This study was designed to determine whether a silent period could be elicited in the diaphragm electromyographic (EMG) activity by transcranial magnetic stimulation (TMS) of the motor cortex and, if so, to assess the influence of reflex or voluntary control of breathing on diaphragmatic cortical silent period (cSP). Diaphragmatic EMG activity was recorded in six healthy volunteers after motor cortex TMS triggered by the inspiratory flow peak and applied during forced inspiration (FI), voluntary hyperventilation (vHV) and reflex hyperventilation (rHV) to a CO(2) stimulus. Electrophysiological and respiratory parameters were studied, including diaphragmatic cSP duration and transdiaphragmatic pressure swing (DeltaPdi). A diaphragmatic cSP was found and correlated with DeltaPdi values. DeltaPdi and cSP duration were similar in the vHV and rHV conditions but were significantly increased during FI. This study established for the first time the existence of a diaphragmatic cSP to motor cortex TMS. The diaphragmatic cSP duration depended on the magnitude of the respiratory effort, as assessed by DeltaPdi, but not on the mechanism (volitional or reflex) of diaphragm activation.     

Mechanisms of genioglossus responses to inspiratory resistive load in rabbits

The purpose of the present study has been to determine whether pharyngeal dilator muscles participate in inspiratory load compensatory responses and if so, to elucidate role of upper airway mechanoreceptors in these responses. The experiments were performed on anaesthetized rabbits. Each animal was tested in three ways by the imposition of inspiratory resistive load: (1) at upper airways via face mask, (2) at the tracheostomic cannula placed below larynx (all upper airway receptors were 'bypassed') and (3) at the mouth after the section of the hypoglossus nerves (motor denervation of genioglossus muscle). The inspiratory load applied to the upper airways evoked significant increases in integrated genioglossus activity (to 129 +/- 14.7% of control) and its inspiratory duration (to 113 +/- 5% of control) already within the first loaded breath (P < 0.05). The increases in the inspiratory activity of musculius genioglossus were relatively greater than the simultaneous increases in the activity of the diaphragm. Motor denervation of the pharynx dilator muscles (including m. genioglossus) increased airway resistance to 184 +/- 19% of control (P < 0.05) and induced obstructive alterations in the breathing pattern during unloaded breathing: decrease in maximal inspiratory flow (-13%) and increase in the level of negative oesophageal pressure (+14%) and the peak diaphragm activity (+6%). After nervi hypoglossus sections additional increases in motor and pressure outputs were required in order to maintain unaltered ventilation at the same degree of loading as before denervation. The results indicate that the pharyngeal dilator muscles have a role in compensation of added inspiratory load. Activation of these muscles facilitate the load compensating function of 'pump' muscles by decreasing airway resistance. Tracheostomy did not reduce the genioglossus response to inspiratory loading, ruling out any role for upper airways receptors in the genioglossus response to inspiratory load compensations.     

Motor control of the costal and crural diaphragm--insights from transcranial magnetic stimulation in man

The costal and crural parts of the diaphragm differ in their embryological development and physiological function. It is not known if this is reflected in differences in their motor cortical representation. We compared the response of the costal and crural diaphragms using varying intensities of transcranial magnetic stimulation of the motor cortex at rest and during submaximal and maximal inspiratory efforts. The costal and crural motor evoked potential recruitment curves during submaximal inspiratory efforts were similar. The response to stimulation before, during and at 10 and 30 min after 44 consecutive maximal inspiratory efforts was also the same. Using paired stimulations to investigate intra-cortical facilitatory and inhibitory circuits we found no difference between the costal and crural response with varying interstimulus intervals, or when conditioning and test stimulus intensity were varied. We conclude that supraspinal control of the costal and crural diaphragm is identical during inspiratory tasks.     

Expiratory activity of the inspiratory muscles during cough.

To investigate the neural mechanism of the expiratory activity of the inspiratory muscles during a cough, EMG of the respiratory muscles were recorded in anesthetized and tracheostomized dogs. A laparoscope was used to minimize injury to the abdominal muscles for implantation of the electrodes into the costal diaphragm. During the expulsive phase of a cough, the diaphragm was active in 7 of 12 dogs and the external intercostal muscle was active in 3 of 6 dogs. During a cough, the expiratory activity of the diaphragm, after the termination of its inspiratory activity, started at 52.9 +/- 24.6 ms, and that of external intercostal muscle started at 51.1 +/- 20.5 ms. The expiratory activity of the internal intercostal muscle and of the transversus abdominis started at 34.3 +/- 13.0 and 27.8 +/- 15.2 ms, respectively. The onset of expiratory activity of the inspiratory muscles is significantly later than that of expiratory muscles. Continuous activity in the expiratory muscles evoked by airway occlusion, i.e., Hering-Breuer reflex, was suppressed during the inspiratory phase of a cough, but not suppressed during the expulsive phase even when the expiratory activity of the diaphragm was observed. We concluded that the expiratory activity of inspiratory muscles is controlled independently of both expiratory activity of the expiratory muscles and inspiratory activity of the inspiratory muscles.