Reproducibility and responsiveness of a noninvasive EMG technique of the respiratory muscles in COPD patients and in healthy subjects.

In the present study, we assessed the reproducibility and responsiveness of transcutaneous electromyography (EMG) of the respiratory muscles in patients with chronic obstructive pulmonary disease (COPD) and healthy subjects during breathing against an inspiratory load. In seven healthy subjects and seven COPD patients, EMG signals of the frontal and dorsal diaphragm, intercostal muscles, abdominal muscles, and scalene muscles were derived on 2 different days, both during breathing at rest and during breathing through an inspiratory threshold device of 7, 14, and 21 cm H2O. For analysis, we used the logarithm of the ratio of the inspiratory activity during the subsequent loads and the activity at baseline [log EMG activity ratio (EMGAR)]. Reproducibility of the EMG was assessed by comparing the log EMGAR values measured at test days 1 and 2 in both groups. Responsiveness (sensitivity to change) of the EMG was assessed by comparing the log EMGAR values of the COPD patients to those of the healthy subjects at each load. During days 1 and 2, log EMGAR values of the diaphragm and the intercostal muscles correlated significantly. For the scalene muscles, significant correlations were found for the COPD patients. Although inspiratory muscle activity increased significantly during the subsequent loads in all participants, the COPD patients displayed a significantly greater increase in intercostal and left scalene muscle activity compared with the healthy subjects. In conclusion, the present study showed that the EMG technique is a reproducible and sensitive technique to assess breathing patterns in COPD patients and healthy subjects.     

Activation of the parasternal intercostals during breathing efforts in human subjects

We have tested the possibility that the electromyographic (EMG) activity present in the parasternal intercostal muscles during quiet inspiration was reflexive, rather than agonistic, in nature. Using concentric needle electrodes we measured parasternal EMG activity in four normal subjects during various inspiratory maneuvers. We found that 1) phasic inspiratory activity was invariably present in the parasternal intercostals during quiet breathing, 2) the parasternal EMG activity was generally increased during attempts to perform the tidal breathing maneuver with the diaphragm alone, 3) parasternal EMG activity was markedly decreased or suppressed in the presence of rib cage distortion during diaphragmatic isovolume maneuvers, and 4) that EMG activity could not be voluntarily suppressed during breathing unless the inspired volume was trivial. We conclude that the parasternal EMG activity detected during quiet inspiration in the normal subjects depends on a central involuntary mechanism and is not related to activation of intercostal mechanoreceptors.     

Differential activation among five human inspiratory motoneuron pools during tidal breathing.

Neural drive to inspiratory pump muscles is increased under many pathological conditions. This study determined for the first time how neural drive is distributed to five different human inspiratory pump muscles during tidal breathing. The discharge of single motor units (n = 280) from five healthy subjects in the diaphragm, scalene, second parasternal intercostal, third dorsal external intercostal, and fifth dorsal external intercostal was recorded with needle electrodes. All units increased their discharge during inspiration, but 41 (15%) discharged tonically throughout expiration. Motor unit populations from each muscle differed in the timing of their activation and in the discharge rates of their motor units. Relative to the onset of inspiratory flow, the earliest recruited muscles were the diaphragm and third dorsal external intercostal (mean onset for the population after 26 and 29% of inspiratory time). The fifth dorsal external intercostal muscle was recruited later (43% of inspiratory time; P < 0.05). Compared with the other inspiratory muscles, units in the diaphragm and third dorsal external intercostal had the highest onset (7.7 and 7.1 Hz, respectively) and peak firing frequencies (12.6 and 11.9 Hz, respectively; both P < 0.05). There was a unimodal distribution of recruitment times of motor units in all muscles. Neural drive to human inspiratory pump muscles differs in timing, strength, and distribution, presumably to achieve efficient ventilation.     

Effects of diaphragmatic ischemia on the inspiratory motor drive.

To assess the effect of diaphragmatic ischemia on the inspiratory motor drive, we studied the in situ isolated and innervated left diaphragm in anesthetized, vagotomized, and mechanically ventilated dogs. The arterial and venous vessels of the left diaphragm were catheterized and isolated from the systemic circulation. Inspiratory muscle activation was assessed by recording the integrated electromyographic (EMG) activity of the left and right costal diaphragms and parasternal intercostal and alae nasi muscles. Tension generated by the left diaphragm during spontaneous breathing attempts was also measured. In eight animals, left diaphragmatic ischemia was induced by occluding the phrenic artery for 20 min, followed by 10 min of reperfusion. This elicited a progressive increase in EMG activity of the left and right diaphragms and parasternal and alae nasi muscles to 170, 157, 152, and 128% of baseline values, respectively, an increase in the frequency of breathing efforts, and no change in left diaphragmatic spontaneous tension. Thus the ratio of left diaphragmatic EMG to tension rose progressively during ischemia. During reperfusion, only the frequency of breathing efforts and alae nasi EMG recovered completely. In four additional animals, left diaphragmatic ischemia was induced after the left phrenic nerve was sectioned. Neither EMG activity of inspiratory muscles nor respiratory timing changed significantly during ischemia. In conclusion, diaphragmatic ischemia increases inspiratory motor drive through activation of phrenic afferents. The changes in alae nasi activity and respiratory timing indicate that this influence is achieved through supraspinal pathways.     

Regional intercostal activity during coughing and vomiting in decerebrate cats.

Regional variations in the discharge patterns of the internal and external intercostal muscles of the middle and caudad thorax were studied in decerebrate, spontaneously breathing cats during coughing and vomiting. Coughing, induced by electrical stimulation of the superior laryngeal nerves, consisted of increased and prolonged diaphragmatic activity followed by a burst of abdominal activity. Mid-thoracic external and internal intercostal muscles discharged synchronously with the diaphragm and abdominal muscles, respectively. Caudal external and internal intercostal muscles, however, discharged synchronously with the abdominal muscles. Vomiting, induced by stimulation of the lower thoracic vagi, consisted of a series of synchronous bursts of diaphragmatic and abdominal activity (retching) followed by a prolonged abdominal discharge after the cessation of diaphragmatic activity (expulsion). Caudal external and internal intercostals discharged in phase with diaphragmatic and abdominal activity but both mid-thoracic intercostal muscles discharged out of phase with these muscles. These results indicate major differences in the control and functional roles of intercostal muscles at different thoracic levels during these behaviours.     

Respiratory muscle activity in the assessment of bronchial responsiveness in asthmatic children

We investigatedwhether an increase in transcutaneous electromyographic (EMG) activityof the diaphragm and intercostal muscles corresponds with theconcentration of histamine that induces a 20% fall in the forcedexpiratory volume in one second(FEV₁; PC₂₀). Eleven asthmatic children(mean age 11.9 yr) were studied after they were given histaminechallenge. EMG activity atPC₂₀ or at the highest histamineconcentration was compared with activity at baseline by calculating theratio of the mean peak-to-peak excursion at the highest histamine doseto that at baseline [EMG activity ratio (EMGAR)]. In allchildren reaching PC₂₀, anincrease in diaphragmatic and intercostal EMGAR was observed. Noincrease was found at the dose step beforePC₂₀ was reached. In sixchallenges, no fall in FEV₁ wasinduced, and no increase in EMGAR was seen. In two challenges, no fallin FEV₁ was induced, but increasein diaphragmatic or intercostal EMGAR was observed. Increase in the electrical activity of the diaphragm and intercostal muscles in asthmatic children corresponds closely to a 20% fall inFEV₁ induced by histaminechallenge.

     

Respiratory responses in reversible diaphragm paralysis

The effects of diaphragm paralysis on respiratory activity were assessed in 13 anesthetized, spontaneously breathing dogs studied in the supine position. Transient diaphragmatic paralysis was induced by bilateral phrenic nerve cooling. Respiratory activity was assessed from measurements of ventilation and from the moving time averages of electrical activity recorded from the intercostal muscles and the central end of the fifth cervical root of the phrenic nerve. The degree of diaphragm paralysis was evaluated from changes in transdiaphragmatic pressure and reflected in rib cage and abdominal displacements. Animals were studied both before and after vagotomy breathing O2, 3.5% CO2 in O2, or 7% CO2 in O2. In dogs with intact vagi, both peak and rate of rise of phrenic and inspiratory intercostal electrical activity increased progressively as transdiaphragmatic pressure fell. Tidal volume decreased and breathing frequency increased as a result of a shortening in expiratory time. Inspiratory time and ventilation were unchanged by diaphragm paralysis. These findings were the same whether O2 or CO2 in O2 was breathed. After vagotomy, no significant change in phrenic or inspiratory intercostal activity occurred with diaphragm paralysis in spite of increased arterial CO2 partial pressure. Ventilation and tidal volume decreased significantly, and respiratory timing was unchanged. These results suggest that mechanisms mediated by the vagus nerves account for the compensatory increase in respiratory electrical activity during transient diaphragm paralysis. That inspiratory time is unchanged by diaphragm paralysis whereas the rate or rise of phrenic nerve activity increases suggest that reflexes other than the Hering-Breuer reflex contribute to the increased respiratory response.     

Respiratory changes in thoracic muscle length during bronchoconstriction

The purpose of the present study was to assess the effects of bronchoconstriction on respiratory changes in length of the costal diaphragm and the parasternal intercostal muscles. Ten dogs were anesthetized with pentobarbital sodium and tracheostomized. Respiratory changes in muscle length were measured using sonomicrometry, and electromyograms were recorded with bipolar fine-wire electrodes. Administration of histamine aerosols increased pulmonary resistance from 6.4 to 14.5 cmH2O X l-1 X s, caused reductions in inspiratory and expiratory times, and decreased tidal volume. The peak and rate of rise of respiratory muscle electromyogram (EMG) activity increased significantly after histamine administration. Despite these increases, bronchoconstriction reduced diaphragm inspiratory shortening in 9 of 10 dogs and reduced intercostal muscle inspiratory shortening in 7 of 10 animals. The decreases in respiratory muscle tidal shortening were less than the reductions in tidal volume. The mean velocity of diaphragm and intercostal muscle inspiratory shortening increased after histamine administration but to a smaller extent than the rate of rise of EMG activity. This resulted in significant reductions in the ratio of respiratory muscle velocity of shortening to the rate of rise of EMG activity after bronchoconstriction for both the costal diaphragm and the parasternal intercostal muscles. Bronchoconstriction changed muscle end-expiratory length in most animals, but for the group of animals this was statistically significant only for the diaphragm. These results suggest that impairments of diaphragm and parasternal intercostal inspiratory shortening occur after bronchoconstriction; the mechanisms involved include an increased load, a shortening of inspiratory time, and for the diaphragm possibly a reduction in resting length.     

Chest wall muscle cross talk in canine costal diaphragm electromyogram

Sinderby, C., S. Friberg, N. Comtois, and A. Grassino.Chest wall muscle cross talk in the canine costal diaphragm electromyogram. J. Appl. Physiol.81(5): 2312-2327, 1996.The present paper describes the influenceof cross talk from the abdominal and intercostal muscles on the caninediaphragm electromyogram (EMG). The diaphragm EMG was recorded withbipolar surface electrodes placed on the costal portion of thediaphragm (abdominal side), aligned in the fiber direction, andpositioned in a region with a relatively low density of motor endplates. The results indicated that cross talk may occur in thediaphragm EMG, especially during conditions of loaded breathing andlight general anesthesia. The cross-talk signals showed characteristicsthat were entirely different from the diaphragm EMG. Although thediaphragm EMG was typical for signals recorded with electrodes alignedin the fiber direction, the cross-talk signals were characteristic ofthose obtained with electrode pairs not aligned in the direction of themuscle fibers. Alterations in electrode positioning, interelectrodedistance, and/or electrode surface area cannot guarantee theelimination of cross-talk signals, whereas spinal anesthesia at a highthoracic level will paralyze the sources of the cross talk and henceeliminate the cross-talk signals. By taking advantage of thedifferences in EMG signal characteristics for the diaphragm EMG andcross-talk signals, an index that has the capability to detect crosstalk was developed.

     

Diaphragm length adjustments with body position changes in the awake dog

Sonomicrometry was used to measure end-expiratory length and tidal shortening of the costal and crural diaphragm in awake chronically instrumented dogs in the right lateral decubitus, standing, and sitting postures. End-expiratory length did not change significantly in standing but fell by 11.5% for the costal and by 14.4% for the crural segment in sitting, when compared with decubitus position. Tidal shortening of both segments did not change significantly in the three postures. From decubitus to sitting, diaphragmatic electromyogram (EMG) activity increased only in some dogs, not significantly for the group. The inspiratory swing of abdominal pressure was always positive in decubitus and negative in standing and sitting. In the latter two postures, abdominal pressure increased gradually during expiration and fell in inspiration, suggesting a phasic expiratory contraction of abdominal muscles. We conclude that diaphragmatic tidal shortening is maintained in the different postures assumed by the awake dog during resting breathing. It seems that the main compensatory mechanism for changes in diaphragmatic operational length is a phasic expiratory contraction of the abdominal muscles rather than an increase in diaphragmatic EMG activity.     

Patterns of intercostal muscle activity in humans

Coordination of activity of inspiratory intercostal muscles in conscious human subjects was studied by means of an array of electromyograph (EMG) electrodes. Bipolar fine wire electrodes were placed in the second and fourth parasternal intercostal muscles and in two or three external intercostal muscles in the midaxillary line from the fourth to eighth intercostal spaces. Subjects breathed quietly or rebreathed from a bag containing 8% CO2 in O2 in both supine and upright postures. Respiration was monitored by means of flow, volume, and separate rib cage and abdominal volumes. Onset of EMG activity in each breath was found near the beginning of inspiration in the uppermost intercostal spaces but progressively later in inspiration in lower spaces, indicating that activity spreads downward across the rib cage through inspiration. At higher ventilation stimulated by CO2, activity spread further and faster downward. In voluntary deep breathing, external intercostal muscles tended to be recruited earlier in inspiration than in CO2-stimulated breathing. The change from supine to sitting resulted in small and inconsistent changes. There was no lung volume or rib cage volume threshold for appearance of EMG activity in any of the spaces.     

Electrical and mechanical activity of respiratory muscles during hypercapnia

In nine anesthetized supine spontaneously breathing dogs, we compared moving average electromyograms (EMGs) of the costal diaphragm and the third parasternal intercostal muscles with their respective respiratory changes in length (measured by sonomicrometry). During resting O2 breathing the pattern of diaphragm and intercostal muscle inspiratory shortening paralleled the gradually incrementing pattern of their moving average EMGs. Progressive hypercapnia caused progressive increases in the amount and velocity of respiratory muscle inspiratory shortening. For both muscles there were linear relationships during the course of CO2 rebreathing between their peak moving average EMGs and total inspiratory shortening and between tidal volume and total inspiratory shortening. During single-breath airway occlusions, the electrical activity of both the diaphragm and intercostal muscles increased, but there were decreases in their tidal shortening. The extent of muscle shortening during occluded breaths was increased by hypercapnia, so that both muscles shortened more during occluded breaths under hypercapnic conditions (PCO2 up to 90 Torr) than during unoccluded breaths under normocapnic conditions. These results suggest that for the costal diaphragm and parasternal intercostal muscles there is a close relationship between their electrical and mechanical behavior during CO2 rebreathing, this relationship is substantially altered by occluding the airway for a single breath, and thoracic respiratory muscles do not contract quasi-isometrically during occluded breaths.     

Differential respiratory muscle recruitment induced by clonidine in awake goats

The purpose of this study was to test thehypothesis that dysrhythmic breathing induced by the₂-agonist clonidine isaccompanied by differential recruitment of respiratory muscles. Inadult goats (n = 14) electromyographic(EMG) measurements were made from inspiratory muscles (diaphragm andparasternal intercostal) and expiratory muscles [triangularissterni (TS) and transversus abdominis (Abd)]. EMG of thethyroarytenoid (TA) muscle was used as an index of upper airway(glottal) patency. Peak EMG activities of all spinal inspiratory andexpiratory muscles were augmented by central and peripheralchemoreceptor stimuli. Phasic TA was apparent in the postinspiratoryphase of the breathing cycle under normoxic conditions. Duringdysrhythmic breathing episodes induced by clonidine, TS and Abdactivities were attenuated or abolished, whereas diaphragm andparasternal intercostal activities were unchanged. There was no tonicactivation of TS or Abd EMG during apneas; however, TA activity becametonic throughout the apnea. We conclude that1) ₂-adrenoceptor stimulationresults in differential recruitment of respiratory muscles duringrespiratory dysrhythmias and 2) apneas are accompanied by active glottic closure in the awake goat.

     

Reflex compensation of voluntary inspiration when immersion changes diaphragm length

When immersion alters inspiratory muscle operating lengths, spontaneously breathing humans maintain a constant tidal volume by reflex adjustment of inspiratory muscle activation (Reid et al. J. Appl. Physiol. 58: 1136-1142, 1985). We term this the operational length compensation reflex. The present experiment demonstrates that similar adjustments occur during voluntary respiratory maneuvers. Each of seven naive subjects sat in a tank with water at hip level. We trained them to reproduce an inspired volume (+/- 10%) at constant inspiratory duration. They received verbal feedback during training but not during the experiment. We measured surface electromyograms (EMGs) of diaphragm and intercostal muscles and tidal volume. After the subjects were trained, we made repeated measurements of 10 trained breaths with water at the hip and then again after raising water level to the xiphoid (which decreases lung volume and increases operating length of the diaphragm). In 30 of 42 trials there was a substantial fall in peak diaphragm EMG. In 10 trials this was sufficient to prevent any change in tidal volume. Inspiratory flow was more closely regulated than tidal volume. Subjects were not aware of making adjustments in drive.     

Inhomogeneous response of expiratory muscle activity to cold block of the ventral medullary surface.

We assessed the effects of cooling the ventral medullary surface (VMS) on the activity of chest wall and abdominal expiratory muscles in eight anesthetized artificially ventilated dogs after vagotomy and denervation of the carotid sinus nerves. Electromyograms (EMGs) of the triangularis sterni, internal intercostal, abdominal external oblique, abdominal internal oblique, and transversus abdominis muscles were measured with EMG of the diaphragm as an index of inspiratory activity. Bilateral localized cooling (2 x 2 mm) in the thermosensitive intermediate part of the VMS produced temperature-dependent reduction in the EMG of diaphragm and abdominal muscles. The rib cage expiratory EMGs were little affected at 25 degrees C; their amplitudes decreased at lower VMS temperatures (less than 20 degrees C) but by significantly fewer degrees than the diaphragmatic and abdominal expiratory EMGs at a constant VMS temperature. With moderate to severe cooling (less than 20 degrees C) diaphragmatic EMG disappeared, but rib cage expiratory EMGs became tonic and resumed a phasic pattern shortly before the recovery of diaphragmatic EMG during rewarming of the VMS. These results indicate that the effects of cooling the VMS differ between the activity of rib cage and abdominal expiratory muscles. This variability may be due to inhomogeneous inputs from the VMS to expiratory motoneurons or to a different responsiveness of various expiratory motoneurons to the same input either from the VMS or the inspiratory neurons.     

Dissociation between diaphragmatic and rib cage muscle fatigue

To assess rib cage muscle fatigue and its relationship to diaphragmatic fatigue, we recorded the electromyogram (EMG) of the parasternal intercostals (PS), sternocleidomastoid (SM), and platysma with fine wire electrodes and the EMG of the diaphragm (DI) with an esophageal electrode. Six normal subjects were studied during inspiratory resistive breathing. Two different breathing patterns were imposed: mainly diaphragmatic or mainly rib cage breathing. The development of fatigue was assessed by analysis of the high-to-low (H/L) ratio of the EMG. To determine the appropriate frequency bands for the PS and SM, we established their EMG power spectrum by Fourier analysis. The mean and SD for the centroid frequency was 312 +/- 16 Hz for PS and 244 +/- 48 Hz for SM. When breathing with the diaphragmatic patterns, all subjects showed a fall in H/L of the DI and none had a fall in H/L of the PS or SM. During rib cage emphasis, four out of five subjects showed a fall in H/L of the PS and five out of six showed a fall in H/L of the SM. Four subjects showed no fall in H/L of the DI; the other two subjects were unable to inhibit diaphragm activity to a substantial degree and did show a fall in H/L of the DI. Activity of the platysma was minimal or absent during diaphragmatic emphasis but was usually strong during rib cage breathing. We conclude that fatigue of either the diaphragm or the parasternal and sternocleidomastoid can occur independently according to the recruitment pattern of inspiratory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Integrated approach for in vivo evaluation of respiratory muscles mechanics

The respiratory muscles constitute the respiratory pump, which determines the efficacy of ventilation. Any functional disorder in their performance may cause insufficient ventilation. This study was designed to quantitatively explore the relative contribution of major groups of respiratory muscles to global lung ventilation throughout a range of maneuvers in healthy subjects. A computerized experimental system was developed for simultaneous noninvasive measurement of inspired/expired airflow, mouth pressure and up to 8 channels of EMG surface signals from major respiratory muscles which are located near the skin (e.g., sternomastoid, external intercostal, rectus abdominis and external oblique) during various respiratory maneuvers. Lung volumes values were calculated by integration of airflow data. Hill's muscle model was utilized to calculate the forces generated by the muscles from the acquired EMG data. Analysis of EMG measurements and respiratory muscles forces revealed the following characteristics: (a) muscle activity increased with increased breathing effort, (b) inspiratory muscles contributed to inspiration even at relatively low flow rates, while expiratory muscles are recruited at higher flow rates, (c) the forces generated by the muscle depended on the muscle properties as well as on their EMG performance and (d) the pattern of the muscle's force curves varied between subjects, but were generally consistent for the same subject regardless of breathing effort.     

Effects of progressive hypoxia on parasternal, costal, and crural diaphragm activation

The distribution of motor drive to the costal and crural diaphragm and parasternal intercostal muscles was evaluated during progressive isocapnic hypoxia in anesthetized dogs. Bipolar stainless steel wire electrodes were placed unilaterally into the costal and crural portions of the diaphragm and into the parasternal intercostal muscle in the second or third intercostal space. Both peak and rate of rise of electromyographic activity of each chest wall muscle increased in curvilinear fashion in response to progressive hypoxia. Both crural and parasternal intercostal responses, however, were greater than those of the costal diaphragm. The onset of crural activation preceded that of the costal portion of the diaphragm and parasternal intercostal muscle activation. Despite differences in the degree of activation among the various chest wall muscles, the rate of increase in activation for any given muscle was linearly related to the rate of increases for the other two. This suggests that respiratory drive during progressive hypoxia increases in fixed proportion to the different chest wall inspiratory muscles. Our findings lend further support to the concept that the costal and crural diaphragm are governed by separate neural control mechanisms and, therefore, may be considered separate muscles.     

Hypoventilation after acute phrenicotomy of the urethane anaesthetized rats.

The aim of this study was to explore the mechanism resulting in hypoventilation in rats with denervated diaphragm. Bilateral cervical phrenicotomy (PX) was performed in 15 male rats anaesthetized with urethane (1.3 g/kg i.p.); other 8 rats were sham operated (SX). Ventilation, PaCO2 and the integrated EMG of the external intercostal muscles (iEMG) were measured before and after the surgery, at regular intervals, up to 4 hours postoperatively. During the 4 hours after PX there was a progressive decrease in minute ventilation and an increase in PaCO2 compared with the control values and with that in the SX rats. The increase in PaCO2 was accompanied by an increase in the peak amplitude of the iEMG to 155 +/- 18% of control values after PX and to 228 +/- 33% 4 hours later. Despite the augmented EMG activity tidal volume gradually decreased. The iEMG of the intercostal muscles, however, did not reach a maximum because the shortlasting stimulation of breathing by acute hypercapnia and hypoxia as the result of added dead space (0.5 ml) increased the iEMG still further. These results indicate that both the central and peripheral mechanisms contribute to hypoventilation in anaesthetized rats with denervated diaphragm.     

The interaction between breathing and swallowing in healthy individuals

In this article, we aimed at investigating the interaction between breathing and swallowing patterns in normal subjects. Ten healthy volunteers were included in the study. Diaphragm EMG activity was recorded by a needle electrode inserted into the 7th or 8th intercostal space. Swallowing was monitored by submental EMG activity, and laryngeal vertical movement was recorded by using a movement sensor. A single voluntary swallow was initiated during either the inspiration or expiration phases of respiration, and changes in EMG activity were evaluated. When a swallow coincided with either inspiration or expiration, the duration of the respiratory phase was prolonged. Normal subjects were able to voluntarily swallow during inspiration. During the inspiration phase with swallowing, diaphragmatic activity did not ceased and during the expiration phase with swallowing, there was a muscle activity in the diaphragm muscle.