Effects of lung volume on diaphragm EMG signal strength during voluntary contractions

1998 ◽  
Vol 85 (3) ◽  
pp. 1123-1134 ◽  
Author(s):  
Jennifer Beck ◽  
Christer Sinderby ◽  
Lars Lindström ◽  
Alex Grassino

The use of esophageal recordings of the diaphragm electromyogram (EMG) signal strength to evaluate diaphragm activation during voluntary contractions in humans has recently been criticized because of a possible artifact created by changes in lung volume. Therefore, the first aim of this study was to evaluate whether there is an artifactual influence of lung volume on the strength of the diaphragm EMG during voluntary contractions. The second aim was to measure the required changes in activation for changes in lung volume at a given tension, i.e., the volume-activation relationship of the diaphragm. Healthy subjects ( n = 6) performed contractions of the diaphragm at different transdiaphragmatic pressure (Pdi) targets (range 20–160 cmH2O) while maintaining chest wall configuration constant at different lung volumes. The diaphragm EMG was recorded with a multiple-array esophageal electrode, with control of signal contamination and electrode positioning. The effects of lung volume on the EMG were studied by comparing the crural diaphragm EMG root mean square (RMS), an index of crural diaphragm activation, with an index of global diaphragm activation obtained by normalizing Pdi to the maximum Pdi at the given muscle length (Pdi/P[Formula: see text]) at the different lung volumes. We observed a direct relationship between RMS and Pdi/P[Formula: see text]independent of diaphragm length. The volume-activation relationship of the diaphragm was equally affected by changes in lung volume as the volume-Pdi relationship (60% change from functional residual capacity to total lung capacity). We conclude that the RMS of the diaphragm EMG is not artifactually influenced by lung volume and can be used as a reliable index of diaphragm activation. The volume-activation relationship can be used to infer changes in the length-tension relationship of the diaphragm at submaximal activation/contraction levels.

2001 ◽  
Vol 90 (4) ◽  
pp. 1441-1446 ◽  
Author(s):  
Mario Filippelli ◽  
Riccardo Pellegrino ◽  
Iacopo Iandelli ◽  
Gianni Misuri ◽  
Joseph R. Rodarte ◽  
...  

Lung and chest wall mechanics were studied during fits of laughter in 11 normal subjects. Laughing was naturally induced by showing clips of the funniest scenes from a movie by Roberto Benigni. Chest wall volume was measured by using a three-dimensional optoelectronic plethysmography and was partitioned into upper thorax, lower thorax, and abdominal compartments. Esophageal (Pes) and gastric (Pga) pressures were measured in seven subjects. All fits of laughter were characterized by a sudden occurrence of repetitive expiratory efforts at an average frequency of 4.6 ± 1.1 Hz, which led to a final drop in functional residual capacity (FRC) by 1.55 ± 0.40 liter ( P < 0.001). All compartments similarly contributed to the decrease of lung volumes. The average duration of the fits of laughter was 3.7 ± 2.2 s. Most of the events were associated with sudden increase in Pes well beyond the critical pressure necessary to generate maximum expiratory flow at a given lung volume. Pga increased more than Pes at the end of the expiratory efforts by an average of 27 ± 7 cmH2O. Transdiaphragmatic pressure (Pdi) at FRC and at 10% and 20% control forced vital capacity below FRC was significantly higher than Pdi at the same absolute lung volumes during a relaxed maneuver at rest ( P < 0.001). We conclude that fits of laughter consistently lead to sudden and substantial decrease in lung volume in all respiratory compartments and remarkable dynamic compression of the airways. Further mechanical stress would have applied to all the organs located in the thoracic cavity if the diaphragm had not actively prevented part of the increase in abdominal pressure from being transmitted to the chest wall cavity.


1991 ◽  
Vol 70 (1) ◽  
pp. 70-76 ◽  
Author(s):  
D. E. Mayock ◽  
T. A. Standaert ◽  
T. D. Murphy ◽  
D. E. Woodrum

Inspiratory resistive loaded (IRL) breathing results in hypoventilation and diaphragmatic fatigue in the piglet. We studied the effects of 6 h of IRL on ten 1-mo-old piglets. The load was adjusted to increase spontaneously generated transdiaphragmatic pressure five to six times baseline. Six 1-mo-old piglets acted as controls and were identically instrumented but were not subjected to IRL. Measurements of ventilation, blood gases and pH, diaphragmatic electromyogram, force-frequency curve, blood flow, and end-expiratory lung volume were obtained hourly. Diaphragmatic muscle samples were obtained after 6 h for determination of ATP, phosphocreatine, lactate, and glycogen levels. No changes occurred in the control animals. IRL resulted in a significant decrease in ventilation, an increase in diaphragmatic EMG, onset of abdominal expiratory muscle activity, and a fall in end-expiratory lung volume by 1 h. The force-frequency curve adjusted for lung volume change fell by 20% at all frequencies of stimulation at 1 h and by 40% at 6 h. Blood flow to the costal and crural diaphragm increased by 51 and 141%, respectively. No differences were noted in ATP, phosphocreatine, lactate, or glycogen between control and IRL animals. It is concluded that submaximal spontaneous contractions of the piglet diaphragm over a 6-h period cause a substantial decrease in its maximal force-generating capacity that is not related to substrate depletion.


1978 ◽  
Vol 44 (6) ◽  
pp. 829-839 ◽  
Author(s):  
A. Grassino ◽  
M. D. Goldman ◽  
J. Mead ◽  
T. A. Sears

We related diaphragm electromyographic activity (Edi) to transdiaphragmatic pressure (Pdi) in man during graded inspiratory efforts. Estimates of rib cage and abdominal volume displacements were based on their anteroposterior (AP) diameter changes. The diaphragm was assumed to contract isometrically when subjects performed inspiratory efforts against a closed airway at specified abdominothoracic configurations, increasing Edi and Pdi while holding lung volume and rib case and abdominal AP diameters constant. The relationship between Pdi and Edi depends primarily on abdominothoracic configuration rather than lung volume. For equal increments in lung volume, the Pdi developed at constant Edi is four to eight times more sensitive to changes in abdominal than in rib cage AP diameter. We demonstrate an isofunctional state of the diaphragm at different lung volumes, when increases in lung volume and rib cage AP diameter are compensated for by slight decreases in abdominal AP diameter, resulting in a constant relationship between Edi and Pdi. We conclude that diaphragm shortening is reflected more directly in abdominal displacement than in lung volume change.


1986 ◽  
Vol 60 (1) ◽  
pp. 225-231 ◽  
Author(s):  
A. Oliven ◽  
G. S. Supinski ◽  
S. G. Kelsen

Costal strips of diaphragmatic muscle obtained from animals with elastase-induced emphysema generate maximum tension at significantly shorter muscle fiber lengths than muscle strips from control animals. The present study examined the consequences of alterations in the length-tension relationship assessed in vitro on the pressure generated by the diaphragm in vivo. Transdiaphragmatic pressure (Pdi) and functional residual capacity (FRC) were measured in 22 emphysematous and 22 control hamsters 4–5 mo after intratracheal injection of pancreatic elastase or saline, respectively. In 12 emphysematous and 12 control hamsters Pdi was also measured during spontaneous contractions against an occluded airway. To allow greater control over muscle excitation, Pdi was measured during bilateral tetanic (50 Hz) electrical stimulation of the phrenic nerves in 10 emphysematous and 10 control hamsters. Mean FRC in the emphysematous hamsters was 183% of the value in control hamsters (P less than 0.01). During spontaneous inspiratory efforts against a closed airway the highest Pdi generated at FRC tended to be greater in control than emphysematous hamsters. When control hamsters were inflated to a lung volume approximating the FRC of emphysematous animals, however, peak Pdi was significantly greater in emphysematous animals (70 +/- 6 and 41 +/- 8 cmH2O; P less than 0.05). With electrophrenic stimulation, the Pdi-lung volume curve was shifted toward higher lung volumes in emphysematous hamsters. Pdi at all absolute lung volumes at and above the FRC of emphysematous hamsters was significantly greater in emphysematous compared with control animals. Moreover, Pdi continued to be generated by emphysematous hamsters at levels of lung volume where Pdi of control subjects was zero.(ABSTRACT TRUNCATED AT 250 WORDS)


1984 ◽  
Vol 56 (5) ◽  
pp. 1294-1301 ◽  
Author(s):  
A. R. Hill ◽  
D. L. Kaiser ◽  
D. F. Rochester

To assess the effects of lung volume and chest wall configuration on electromechanical coupling of the abdominal muscles, we examined the relationship between abdominal muscle pressure ( Pmus ) and electrical activity ( EMGab ) in eight normal subjects during expiratory efforts at lung volumes ranging from functional residual capacity (FRC) to FRC + 2.0 liters. At and above FRC, increases of lung volume did not significantly alter either the Pmus - EMGab relationship or abdominal surface linear dimensions, although expiratory efforts displaced the abdomen inward from its relaxed position. We attribute the constancy of delta Pmus /delta EMG above FRC to the negligible effects of increasing lung volume on abdominal configuration and muscle length. Expiratory efforts performed at lung volumes below FRC resulted in a wider range of abdominal indrawing . Under these conditions the EMGab required to augment Pmus by 30–40 cmH2O increased as the abdomen was displaced inward. This decrease of delta Pmus /delta EMGab appears to reflect muscle shortening, flattening of the abdominal wall, and possibly deformation of the rib cage.


2006 ◽  
Vol 101 (3) ◽  
pp. 794-798 ◽  
Author(s):  
Aladin M. Boriek ◽  
Ben Black ◽  
Rolf Hubmayr ◽  
Theodore A. Wilson

Transdiaphragmatic pressure is a result of both tension in the muscles of the diaphragm and curvature of the muscles. As lung volume increases, the pressure-generating capability of the diaphragm decreases. Whether decrease in curvature contributes to the loss in transdiaphragmatic pressure and, if so, under what conditions it contributes are unknown. Here we report data on muscle length and curvature in the supine dog. Radiopaque markers were attached along muscle bundles in the midcostal region of the diaphragm in six beagle dogs of ∼8 kg, and marker locations were obtained from biplanar images at functional residual capacity (FRC), during spontaneous inspiratory efforts against a closed airway at lung volumes from FRC to total lung capacity, and during bilateral maximal phrenic nerve stimulation at the same lung volumes. Muscle length and curvature were obtained from these data. During spontaneous inspiratory efforts, muscle shortened by 15–40% of length at FRC, but curvature remained unchanged. During phrenic nerve stimulation, muscle shortened by 30 to nearly 50%, and, for shortening exceeding 52%, curvature appeared to decrease sharply. We conclude that diaphragm curvature is nearly constant during spontaneous breathing maneuvers in normal animals. However, we speculate that it is possible, if lung compliance were increased and the chest wall and the diameter of the diaphragm ring of insertion were enlarged, as in the case of chronic obstructive pulmonary disease, that decrease in diaphragm curvature could contribute to loss of diaphragm function.


1979 ◽  
Vol 46 (6) ◽  
pp. 1071-1075 ◽  
Author(s):  
N. A. Saunders ◽  
S. M. Kreitzer ◽  
R. H. Ingram

Patterns of rib cage (RC) deformation were studied in six normal subjects during moderate static inspiratory efforts such that esophageal pressure (Pes) as an index of transthoracic pressure fell to between -30 and -60 cmH2O during each maneuver. At lung volumes below 50% inspiratory capacity (IC), static inspiratory efforts deformed RC to a more elliptical shape; RC lateral diameter became smaller and RC lateral diameter became larger. However, at high lung volumes (greater than 50% IC) the opposite change in RC dimensions occurred despite similar changes in Pes, i.e., the RC became more circular. These differences in RC deformation did not appear to be a possive consequence of increased lung volume because the RC could be voluntarily deformed to a more circular shape at low lung volume when a) subjects performed static inspiratory efforts mainly with their intercostal and accessory muscles rather than their diaphragm as judged by a smaller change in transdiaphragmatic pressure for the same Pes; or b) subjects statically contracted their diaphragm with it held in a relatively flattened configuration as assessed by a large abdominal AP dimension. We suggest that deformation of the RC during static inspiratory efforts is not as predictable as has previously been suggested but depends on the pattern of contraction and configuration of the respiratory muscles.


1992 ◽  
Vol 72 (3) ◽  
pp. 1064-1067 ◽  
Author(s):  
S. Yan ◽  
T. Similowski ◽  
A. P. Gauthier ◽  
P. T. Macklem ◽  
F. Bellemare

The transdiaphragmatic pressure twitches (PdiT) in response to single maximal shocks delivered bilaterally to the phrenic nerves were recorded as a function of lung volume when the diaphragm was fresh and when fatigued. All relationships were linear and negatively sloped (all r greater than 0.85). From these relationships PdiT was found to decrease with fatigue more rapidly and to recover more quickly at high than at low lung volumes. Complete recovery of PdiT at all lung volumes was greater than 1 h. Contraction and relaxation rate constants of PdiT did not change significantly with fatigue. We conclude that fatigue affects diaphragm contractility more at high than at low lung volumes and that changes in diaphragm contractility are best reflected in the measurement of PdiT as a function of lung volume.


2005 ◽  
Vol 288 (4) ◽  
pp. R1021-R1027 ◽  
Author(s):  
Aladin M. Boriek ◽  
Willy Hwang ◽  
Linda Trinh ◽  
Joseph R Rodarte

Both diaphragm shape and tension contribute to transdiaphragmatic pressure, but of the three variables, tension is most difficult to measure. We measured transdiaphragmatic pressure and the global shape of the in vivo canine diaphragm and used principles of mechanics to compute the tension distribution. Our hypotheses were that 1) tension in the active diaphragm is nonuniform with greater tension in the central tendon than in the muscular regions; 2) maximum tension is essentially oriented in the muscle fiber direction, whereas minimum tension is orthogonal to the fiber direction; and 3) during submaximal activation change in the in vivo global shape is small. Metallic markers, each 2 mm in length, were implanted surgically on the peritoneal surface of the diaphragm at 1.5- to 2.0-cm intervals along the muscle bundles at the midline, ventral, middle, and dorsal regions of the left costal diaphragm and along a muscle bundle of the crural diaphragm. Postsurgery, a biplane videofluoroscopic system was used to determine the in vivo three-dimensional coordinates of the markers at end expiration and end inspiration during quiet breathing as well as at end-inspiratory efforts against an occluded airway at lung volumes of functional residual capacity and at one-third maximum inspiratory capacity increments in volume to total lung capacity. A surface was fit to the marker locations using a two-dimensional spline algorithm. Diaphragm surface was modeled as a pressurized membrane, and tension distribution in the active diaphragm was computed using the ANSYS finite element program. We showed that the peak of the diaphragm dome was closer to the ventral surface than to the dorsal surface and that there was a depression or valley in the crural region. In the supine position, during inspiratory efforts, the caudal displacement of the dorsal region of the diaphragm was greater than that of the dome, and the valley along the crural diaphragm was accentuated. In contrast, at lower lung volumes in the prone posture, the caudal displacement of the dome was greater than that of the crural region. At end of inspiration, transdiaphragmatic pressure was ∼6.5 cmH2O, and tensions were nonuniform in the diaphragm. Maximum principal stress σ1 of central tendon was found to be greater than σ1 of the costal region, and that was greater than σ1 of the crural region, with values of 14–34, 14–29, and 4–14 g/cm, respectively. The corresponding data of the minimum principal stress σ2 were 9–18, 3–9, and 0–1.5 g/cm, respectively. Maximum principal tension was approximately parallel to the muscle fibers, whereas minimum tension was essentially orthogonal to the longitudinal direction of the muscle fibers. In the muscular region, σ1 was ∼3-fold σ2, whereas in the central tendon, σ1 was only ∼1.5-fold σ2.


1960 ◽  
Vol 15 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
Emilio Agostoni ◽  
Hermann Rahn

The abdominal (gastric) pressures as well as the intrathoracic pressures were recorded in man during various respiratory maneuvers such as complete relaxation, moderate inspiratory and expiratory efforts, maximal inspiratory and expiratory efforts, and during maximal abdominal pressure efforts. Each maneuver was systematically carried out at various lung volumes. From these measurements it is possible to determine the transdiaphragmatic pressure difference and thus obtain information concerning the activity of the diaphragm during these various maneuvers. During relaxation pressure maneuvers and during moderate expiratory pressure efforts the transdiaphragmatic pressure difference is zero. During maximal inspiratory efforts the pressure is about 100 cm H2O more positive on the abdominal side than on the thoracic side of the diaphragm regardless of the lung volume. A similar difference is found during a maximal abdominal contraction whether during this maneuver the alveolar pressure is zero or whether a high alveolar expiratory pressure is developed. These findings are discussed in terms of reflex contractions of the diaphragm which limit the pressures and volumes that can be obtained in the lung. Submitted on May 2, 1960


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