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Journal articles on the topic 'Diaphragm electromyogram'
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Supinski, G. S., A. F. DiMarco, F. Hussein, and M. D. Altose. "Alterations in respiratory muscle activation in the ischemic fatigued canine diaphragm." Journal of Applied Physiology 67, no. 2 (August 1, 1989): 720–29. http://dx.doi.org/10.1152/jappl.1989.67.2.720.
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The purpose of the present study was to examine the respiratory motor response to diaphragm fatigue. Studies were performed using in situ diaphragm muscle strips dissected from the left costal diaphragm in anesthetized dogs. The left inferior phrenic artery was isolated, and diaphragmatic strip fatigue was elicited by occluding this vessel. Strip tension, strip electromyographic activity, parasternal electromyographic activity, and the electromyogram of the right hemidiaphragm were recorded during spontaneous breathing efforts before, during, and after periods of phrenic arterial occlusion. In separate trials, we examined the neuromuscular responses to phrenic arterial occlusion at arterial PCO2 (PaCO2) of 40, 55, and 75 Torr. No fatigue and no alteration in electromyographic activities were observed in trials at PaCO2 of 40 Torr. During trials at PaCO2 of 55 and 75 Torr, however, diaphragm tension fell, the peak height of the diaphragm strip electromyogram decreased, and the peak heights of the parasternal and right hemidiaphragm electromyograms increased. Relief of phrenic arterial occlusion resulted in a return of strip tension and all electromyograms toward base-line values. In additional experiments, the left phrenic nerve was sectioned in the chest after producing fatigue. Phrenic section was followed by an increase in the peak height of the left phrenic neurogram (recorded above the site of section). This latter finding suggests that diaphragm strip motor drive may be reflexly inhibited during the development of fatigue by neural traffic carried along phrenic afferents.
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Kimata, H., A. Morita, S. Furuhata, H. Itakura, K. Ikenobu, and Y. Kimura. "Assessment of laughter by diaphragm electromyogram." European Journal of Clinical Investigation 39, no. 1 (January 2009): 78–79. http://dx.doi.org/10.1111/j.1365-2362.2008.02037.x.
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Luo, Y. M., L. C. Johnson, M. I. Polkey, M. L. Harris, R. A. Lyall, M. Green, and J. Moxham. "Diaphragm electromyogram measured with unilateral magnetic stimulation." European Respiratory Journal 13, no. 2 (February 1, 1999): 385–90. http://dx.doi.org/10.1183/09031936.99.13238599.
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Sinderby, C., S. Friberg, N. Comtois, and A. Grassino. "Chest wall muscle cross talk in canine costal diaphragm electromyogram." Journal of Applied Physiology 81, no. 5 (November 1, 1996): 2312–27. http://dx.doi.org/10.1152/jappl.1996.81.5.2312.
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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 influence of cross talk from the abdominal and intercostal muscles on the canine diaphragm electromyogram (EMG). The diaphragm EMG was recorded with bipolar surface electrodes placed on the costal portion of the diaphragm (abdominal side), aligned in the fiber direction, and positioned in a region with a relatively low density of motor end plates. The results indicated that cross talk may occur in the diaphragm EMG, especially during conditions of loaded breathing and light general anesthesia. The cross-talk signals showed characteristics that were entirely different from the diaphragm EMG. Although the diaphragm EMG was typical for signals recorded with electrodes aligned in the fiber direction, the cross-talk signals were characteristic of those obtained with electrode pairs not aligned in the direction of the muscle fibers. Alterations in electrode positioning, interelectrode distance, and/or electrode surface area cannot guarantee the elimination of cross-talk signals, whereas spinal anesthesia at a high thoracic level will paralyze the sources of the cross talk and hence eliminate the cross-talk signals. By taking advantage of the differences in EMG signal characteristics for the diaphragm EMG and cross-talk signals, an index that has the capability to detect cross talk was developed.
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Eikermann, Matthias, Philipp Fassbender, Atul Malhotra, Masaya Takahashi, Shigeto Kubo, Amy S. Jordan, Shiva Gautam, David P. White, and Nancy L. Chamberlin. "Unwarranted Administration of Acetylcholinesterase Inhibitors Can Impair Genioglossus and Diaphragm Muscle Function." Anesthesiology 107, no. 4 (October 1, 2007): 621–29. http://dx.doi.org/10.1097/01.anes.0000281928.88997.95.
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Background It is standard practice to administer a cholinesterase inhibitor (e.g., neostigmine) at the end of a surgical case to reverse suspected effects of neuromuscular blocking agents regardless of whether such residual effects are present. The authors hypothesized that cholinesterase inhibition when given the in absence of neuromuscular blockade (NB) would decrease upper airway dilatory muscle activity and consequently upper airway volume. Methods The authors measured genioglossus and diaphragm electromyograms during spontaneous ventilation in anesthetized, tracheostomized rats before and after administration of neostigmine (0.03, 0.06, or 0.12 mg/kg), after recovery of the train-of-four ratio (quadriceps femoris muscle) to unity after NB (n = 18). For comparison, the authors made the same measurements in rats that had no previous NB (n = 27). In intact anesthetized rats, the authors measured upper airway volume and end-expiratory lung volume by magnetic resonance imaging before and after 0.12 mg/kg neostigmine (n = 9). Results Neostigmine treatment in rats that had fully recovered from NB based on the train-of-four ratio caused dose-dependent decreases in genioglossus electromyogram (to 70.3 +/- 7.6, 49.2 +/- 3.2, and 39.7 +/- 2.3% of control, respectively), decreases in diaphragm electromyogram (to 103.1 +/- 6.5, 83.1 +/- 4.7, and 68.7 +/- 7.3% of control), and decreases in minute ventilation to a nadir value of 79.6 +/- 6% of preneostigmine baseline. Genioglossus electromyogram effects were the same when neostigmine was given with no previous NB. Neostigmine caused a decrease in upper airway volume to 83 +/- 3% of control, whereas end-expiratory lung volume remained constant. Conclusions The cholinesterase inhibitor neostigmine markedly impairs upper airway dilator volume, genioglossus muscle function, diaphragmatic function, and breathing when given after recovery from vecuronium-induced neuromuscular block.
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Sinderby, C., L. Lindstrom, and A. E. Grassino. "Automatic assessment of electromyogram quality." Journal of Applied Physiology 79, no. 5 (November 1, 1995): 1803–15. http://dx.doi.org/10.1152/jappl.1995.79.5.1803.
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Power spectrum analysis of the diaphragm electromyogram (EMGdi) is time consuming, and no criteria have been developed to objectively quantify contamination of the signal. The present work describes a set of computer algorithms that automatically select EMGdi free of the electrocardiogram and numerically quantify the common artifacts that affect the EMGdi. The algorithms were tested 1) on human EMGdi (n = 5) obtained with esophageal electrodes positioned at the level of the gastroesophageal junction, 2) on EMGdi obtained in mongrel dogs (n = 5) with intramuscular electrodes in the costal diaphragm, and 3) on computer-simulated power spectra. For authentic and simulated power spectra, indexes were obtained by the algorithms and were able to quantify signal disturbances induced by noise, electrode motion, esophageal peristalsis (in humans), and non-QRS complex-related electrocardiogram activity. With the index inclusion thresholds set to levels that allowed for a high signal acceptance rate with relatively small artifact-induced fluctuations (10–15%) of the EMGdi center frequency, the computer algorithms were found to be as reliable as or more reliable than other methods, including careful visual selection of the time domain signals by experienced analysts. In conclusion, the frequency domain application of computer algorithms offers a reliable and reproducible means to objectively quantify the sources that contaminate the interference pattern EMG.
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Beck, J., C. Sinderby, J. Weinberg, and A. Grassino. "Effects of muscle-to-electrode distance on the human diaphragm electromyogram." Journal of Applied Physiology 79, no. 3 (September 1, 1995): 975–85. http://dx.doi.org/10.1152/jappl.1995.79.3.975.
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It has been suggested that esophageal recordings of the diaphragm electromyogram (EMGdi) are influenced by changes in chest wall configuration. Whether the changes are of physiological or artifactual origin is unclear. For example, the distance between the esophageal electrode and the diaphragm is likely to alter with chest wall configuration and may lead to misinterpretations of EMGdi. The aims of this study were 1) to evaluate and quantify the effect of the muscle-to-electrode (ME) distance filter on EMGdi, as obtained with a multiple-array esophageal electrode, 2) to take advantage of the ME distance filter to locate the position of the diaphragm with respect to the electrode, and 3) to evaluate the influence of lung volume and chest wall configuration on EMGdi center frequency (CF) while controlling for the ME distance filter and signal quality. Five subjects performed six static contractions of the diaphragm at each of seven chest wall configurations, as evaluated by the method of K. Konno and J. Mead (J. Appl. Physiol. 22: 407–422, 1967). EMGdi was measured with seven pairs of electrodes mounted on an esophageal catheter. The pair of electrodes whose EMGdi power spectra were the least filtered by the ME distance was assumed to be closest to the diaphragm. The results of the study indicated that 1) EMGdi power spectra were strongly affected by the distance between the diaphragm and the electrodes. CF decreased by approximately 1 Hz/mm displacement away from the electrode pair closest to the diaphragm; and 2) no systematic relationship was found between changes in chest wall configuration and CF, when CF was measured from the electrode pair closest to the diaphragm. We conclude that the EMGdi CF can be reliably measured with a multiple-array esophageal electrode that covers the span of diaphragmatic excursion and by selecting the pair of electrodes that is the closest to the diaphragm.
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LaFramboise, W. A., and D. E. Woodrum. "Elevated diaphragm electromyogram during neonatal hypoxic ventilatory depression." Journal of Applied Physiology 59, no. 4 (October 1, 1985): 1040–45. http://dx.doi.org/10.1152/jappl.1985.59.4.1040.
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Diaphragmatic electromyogram (EMG) was obtained in eight 48-h-old unanesthetized monkeys while breathing air and then either of two different hypoxic gas mixtures (12 or 8% O2 in N2) for 5 min. Minute ventilation (VI) rose significantly above control levels by 1 min of hypoxemia while animals were breathing either of the hypoxic gas mixtures as tidal volume (VT) and slope and rate moving average EMG increased. The relative gains in VI were associated with comparable increases in diaphragmatic neural activity per minute (EMG/min = peak EMG X frequency) during this early phase of hypoxemia. VI subsequently fell to control levels (inspired O2 fraction = 12%, arterial PO2 = 23 +/- 3 Torr) or significantly below (inspired O2 fraction = 8%, arterial PO2 = 18 +/- 0.4 Torr) by 5 min of hypoxemia, secondary to changes in VT. Despite the decline in VI, slope and rate moving average EMG, and EMG/min remained statistically above control values by 5 min of hypoxemia, although there was a trend for EMG/min to decrease slightly from the 1-min peak response. These findings demonstrate that hypoxic-induced depression of neural input to the diaphragm is not independently responsible for the biphasic nature of the newborn ventilatory response, although it cannot be ruled out as a contributor. The fall in inspiratory volumes despite constant elevated EMG activity suggests the presence of a change in respiratory mechanics and/or an impairment in diaphragmatic contractile function without offsetting neural compensatory activity.
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Burns, David P., Sarah E. Drummond, Dearbhla Bolger, Amélie Coiscaud, Kevin H. Murphy, Deirdre Edge, and Ken D. O’Halloran. "N-acetylcysteine Decreases Fibrosis and Increases Force-Generating Capacity of mdx Diaphragm." Antioxidants 8, no. 12 (November 24, 2019): 581. http://dx.doi.org/10.3390/antiox8120581.
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Respiratory muscle weakness occurs due to dystrophin deficiency in Duchenne muscular dystrophy (DMD). The mdx mouse model of DMD shows evidence of impaired respiratory muscle performance with attendant inflammation and oxidative stress. We examined the effects of N-acetylcysteine (NAC) supplementation on respiratory system performance in mdx mice. Eight-week-old male wild type (n = 10) and mdx (n = 20) mice were studied; a subset of mdx (n = 10) received 1% NAC in the drinking water for 14 days. We assessed breathing, diaphragm, and external intercostal electromyogram (EMG) activities and inspiratory pressure during ventilatory and non-ventilatory behaviours. Diaphragm muscle structure and function, cytokine concentrations, glutathione status, and mRNA expression were determined. Diaphragm force-generating capacity was impaired in mdx compared with wild type. Diaphragm muscle remodelling was observed in mdx, characterized by increased muscle fibrosis, immune cell infiltration, and central myonucleation. NAC supplementation rescued mdx diaphragm function. Collagen content and immune cell infiltration were decreased in mdx + NAC compared with mdx diaphragms. The cytokines IL-1β, IL-6 and KC/GRO were increased in mdx plasma and diaphragm compared with wild type; NAC decreased systemic IL-1β and KC/GRO concentrations in mdx mice. We reveal that NAC treatment improved mdx diaphragm force-generating capacity associated with beneficial anti-inflammatory and anti-fibrotic effects. These data support the potential use of NAC as an adjunctive therapy in human dystrophinopathies.
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Goldman, Ernesto, Christer Sinderby, Lars Lindstrom, and Alex Grassino. "Influence of Atracurium on the Diaphragm Mean Action Potential Conduction Velocity in Canines." Anesthesiology 90, no. 3 (March 1, 1999): 855–62. http://dx.doi.org/10.1097/00000542-199903000-00029.
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Background It has been shown that progressive neuromuscular blockade (NMB) affects the electromyogram power spectrum and compound muscle action potential duration in skeletal muscle. These measures are linked to the mean muscle action potential conduction velocity (APCV), but no studies have confirmed a relation between the mean APCV and NMB. The aim of this study was to determine whether diaphragm mean APCV is affected by NMB. Methods The effects of NMB on diaphragm mean APCV were evaluated in five mongrel dogs. Progressive NMB was induced by slow intravenous infusion of atracurium. During spontaneous breathing, the diaphragm mean APCV was determined by electromyogram signals, in the time and frequency domains. The magnitude of NMB was quantified by the amplitude of the compound muscle action potential and by changes in muscle shortening during supramaximal stimulation of the phrenic nerve. Results Progressive NMB was associated with a decrease in diaphragm mean APCV. At approximately 70% reduction in the compound muscle action potential amplitude, diaphragm mean APCV had decreased more than 20%. Recovery after NMB was characterized by a restoration of the mean APCV to control values. Conclusion This study shows that progressive NMB paralyzes motor units within the diaphragm in an orderly manner, and the blockade first affects muscle fibers with high APCV before it affects fibers with lower APCV.
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Sinderby, Christer, Jennifer Beck, Jadranka Spahija, Jan Weinberg, and Alex Grassino. "Voluntary activation of the human diaphragm in health and disease." Journal of Applied Physiology 85, no. 6 (December 1, 1998): 2146–58. http://dx.doi.org/10.1152/jappl.1998.85.6.2146.
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Intersubject comparison of the crural diaphragm electromyogram, as measured by an esophageal electrode, requires a reliable means for normalizing the signal. The present study set out 1) to evaluate which voluntary respiratory maneuvers provide high and reproducible diaphragm electromyogram root-mean-square (RMS) values and 2) to determine the relative diaphragm activation and mechanical and ventilatory outputs during breathing at rest in healthy subjects ( n = 5), in patients with severe chronic obstructive pulmonary disease (COPD, n = 5), and in restrictive patients with prior polio infection (PPI, n = 6). In all groups, mean voluntary maximal RMS values were higher during inspiration to total lung capacity than during sniff inhalation through the nose ( P = 0.035, ANOVA). The RMS (percentage of voluntary maximal RMS) during quiet breathing was 8% in healthy subjects, 43% in COPD patients, and 45% in PPI patients. Despite the large difference in relative RMS ( P = 0.012), there were no differences in mean transdiaphragmatic pressure ( P= 0.977) and tidal volumes ( P = 0.426). We conclude that voluntary maximal RMS is reliably obtained during an inspiration to total lung capacity but a sniff inhalation could be a useful complementary maneuver. Severe COPD and PPI patients breathing at rest are characterized by increased diaphragm activation with no change in diaphragm pressure generation.
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van Lunteren, E., M. A. Haxhiu, E. C. Deal, J. S. Arnold, and N. S. Cherniack. "Respiratory changes in thoracic muscle length during bronchoconstriction." Journal of Applied Physiology 63, no. 1 (July 1, 1987): 221–28. http://dx.doi.org/10.1152/jappl.1987.63.1.221.
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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.
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Bockelmann, Niclas, Jan Graßhoff, Lasse Hansen, Giacomo Bellani, Mattias P. Heinrich, and Philipp Rostalski. "Deep Learning for Prediction of Diaphragm Activity from the Surface Electromyogram." Current Directions in Biomedical Engineering 5, no. 1 (September 1, 2019): 17–20. http://dx.doi.org/10.1515/cdbme-2019-0005.
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AbstractThe electrical activity of the diaphragm (EAdi) is a novel monitoring parameter for patients under assisted ventilation and is used for assessing the patient’s neural respiratory drive. It is recorded by an array of electrodes placed inside the esophagus at the level of the diaphragm. A noninvasive alternative is the measurement of the electromyogram by means of skin surface electrodes (sEMG). The respiratory sEMG signal, however, is subject to electrocardiographic interference and crosstalk from other muscles and may also pick up a different part of the muscular activity. In this work, we propose to use a deep neural network to predict the electrical activity of the diaphragm as measured by a nasogastric catheter from sEMG measurements. We use a ResNet based architecture and train the network to directly regress the EAdi as a supervised learning task - we further investigate a heatmap based regression approach. The proposed methods are evaluated on a clinical dataset consisting of 77 recordings from mechanically ventilated patients. For the direct regression task, the network’s predictions reach a Pearson correlation coefficient (PCC) of 0.818 with EAdi on the hold-out set. The heatmap regression increases the PCC to 0.830 while at the same time achieving a lower mean absolute error, indicating a superior performance. From our results we conclude that sEMG measurements may be used to predict the internal activity of the diaphragm as measured invasively using a nasogastric catheter.
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Brice, A. G., H. V. Forster, L. G. Pan, T. F. Lowry, and C. L. Murphy. "Respiratory muscle electromyogram responses to acute hypoxia in awake ponies." Journal of Applied Physiology 68, no. 3 (March 1, 1990): 1024–32. http://dx.doi.org/10.1152/jappl.1990.68.3.1024.
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We determined the effect of acute hypoxia on the ventilatory (VE) and electromyogram (EMG) responses of inspiratory (diaphragm) and expiratory (transversus abdominis) muscles in awake spontaneously breathing ponies. Eleven carotid body-intact (CBI) and six chronic carotid body-denervated (CBD) ponies were studied during normoxia (fractional inspired O2 concn [FIO2] = 0.21) and two levels of hypoxia (FIO2 approximately 0.15 and 0.12; 6-10 min/period). Four CBI and five CBD ponies were also hilar nerve (pulmonary vagal) denervated. Mean VE responses to hypoxia were greater in CBI ponies (delta arterial PCO2 = -4 and -7 Torr in CBI during hypoxic periods; -1 and -2 Torr in CBD). Hypoxia increased the rate of rise and mean activity of integrated diaphragm EMG in CBI (P less than 0.05) and CBD (P greater than 0.05) ponies relative to normoxia. Duration of diaphragm activity was reduced in CBI (P less than 0.05) but unchanged in CBD ponies. During hypoxia in both groups of ponies, total and mean activities per breath of transversus abdominis were reduced (P less than 0.05) without a decrease in rate of rise in activity. Time to peak and total duration of transversus abdominis activity were markedly reduced by hypoxia in CBI and CBD ponies (P less than 0.05). Hilar nerve denervation did not alter the EMG responses to hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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Beck, J., C. Sinderby, L. Lindstrom, and A. Grassino. "Influence of bipolar esophageal electrode positioning on measurements of human crural diaphragm electromyogram." Journal of Applied Physiology 81, no. 3 (September 1, 1996): 1434–49. http://dx.doi.org/10.1152/jappl.1996.81.3.1434.
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We aimed to describe how the human diaphragm electromyogram (EMGdi) is filtered at different positions within the esophageal hiatus, i.e., in the close proximity of the diaphragm, when obtained with an array of bipolar electrode pairs mounted on an esophageal catheter. We defined the electrically active crural diaphragm musculature that covers the esophagus as the electrically active region of the diaphragm (EARdi) and its center as the EARdi center. EMGdi signals were obtained via a multiple-array esophageal catheter consisting of seven sequential electrode pairs with three different electrode configurations. Subjects (n = 5) performed voluntary contractions of the diaphragm at functional residual capacity. Visual inspection of the signals revealed reversal of signal polarity on either side of the EARdi center. Extreme correlation values (r values close to -1 at 0-ms time offset) were observed for the correlation of signals on either side of the EARdi center. The root mean square (RMS) was reduced at the EARdi center; moving peripherally from the EARdi center (caudally and cephalad), the RMS increased to a peak (range of 2.1-4.1 dB for the different electrode configurations) and then decreased for the most peripheral electrode pairs. From a position where the RMS values peaked, center frequency values increased at the EARdi center (range of 26-29 Hz for the different electrode configurations). Computer simulation yielded similar data to the experimental results. We conclude that electrode positioning within the EARdi severely influences center frequency and RMS values and that the center of the EARdi can be identified via cross-correlation analysis.
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Luo, Y. M., M. I. Polkey, L. C. Johnson, R. A. Lyall, M. L. Harris, M. Green, and J. Moxham. "Diaphragm EMG measured by cervical magnetic and electrical phrenic nerve stimulation." Journal of Applied Physiology 85, no. 6 (December 1, 1998): 2089–99. http://dx.doi.org/10.1152/jappl.1998.85.6.2089.
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The purpose of the study was to compare electrical stimulation (ES) and cervical magnetic stimulation (CMS) of the phrenic nerves for the measurement of the diaphragm compound muscle action potential (CMAP) and phrenic nerve conduction time. A specially designed esophageal catheter with three pairs of electrodes was used, with control of electrode positioning in 10 normal subjects. Pair A and pair B were close to the diaphragm ( pair A lower than pair B); pair C was positioned 10 cm above the diaphragm to detect the electromyogram from extradiaphragmatic muscles. Electromyograms were also recorded from upper and lower chest wall surface electrodes. The shape of the CMAP measured with CMS (CMS-CMAP) usually differed from that of the CMAP measured with ES (ES-CMAP). Moreover, the latency of the CMS-CMAP from pair B (5.3 ± 0.4 ms) was significantly shorter than that from pair A (7.1 ± 0.7 ms). The amplitude of the CMS-CMAP (1.00 ± 0.15 mV) was much higher than that of ES-CMAP (0.26 ± 0.15 mV) when recorded from pair C. Good-quality CMS-CMAPs could be recorded in some subjects from an electrode positioned very low in the esophagus. The differences between ES-CMAP and CMS-CMAP recorded either from esophageal or chest wall electrodes make CMS unreliable for the measurement of phrenic nerve conduction time.
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Beck, Jennifer, Christer Sinderby, Lars Lindström, and Alex Grassino. "Crural diaphragm activation during dynamic contractions at various inspiratory flow rates." Journal of Applied Physiology 85, no. 2 (August 1, 1998): 451–58. http://dx.doi.org/10.1152/jappl.1998.85.2.451.
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The purpose of this study was to evaluate the influence of velocity of shortening on the relationship between diaphragm activation and pressure generation in humans. This was achieved by relating the root mean square (RMS) of the diaphragm electromyogram to the transdiaphragmatic pressure (Pdi) generated during dynamic contractions at different inspiratory flow rates. Five healthy subjects inspired from functional residual capacity to total lung capacity at different flow rates while reproducing identical Pdi and chest wall configuration profiles. To change the inspiratory flow rate, subjects performed the inspirations while breathing across two different inspiratory resistances (10 and 100 cmH2O ⋅ l−1 ⋅ s), at mouth pressure targets of −10, −20, −40, and −60 cmH2O. The diaphragm electromyogram was recorded and analyzed with control of signal contamination and electrode positioning. RMS values obtained for inspirations with identical Pdi and chest wall configuration profiles were compared at the same percentage of inspiratory duration. At inspiratory flows ranging between 0.1 and 1.4 l/s, there was no difference in the RMS for the inspirations from functional residual capacity to total lung capacity when Pdi and chest wall configuration profiles were reproduced ( n = 4). At higher inspiratory flow rates, subjects were not able to reproduce their chest wall displacements and adopted different recruitment patterns. In conclusion, there was no evidence for increased demand of diaphragm activation when healthy subjects breathe with similar chest wall configuration and Pdi profiles, at increasing flow rates up to 1.4 l/s.
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LUO, YUAN M, REBECCA A LYALL, M. LOU HARRIS, GERRARD F RAFFERTY, MICHAEL I POLKEY, and JOHN MOXHAM. "Quantification of the Esophageal Diaphragm Electromyogram with Magnetic Phrenic Nerve Stimulation." American Journal of Respiratory and Critical Care Medicine 160, no. 5 (November 1999): 1629–34. http://dx.doi.org/10.1164/ajrccm.160.5.9809068.
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Road, J. D., A. M. Leevers, E. Goldman, and A. Grassino. "Respiratory muscle coordination and diaphragm length during expiratory threshold loading." Journal of Applied Physiology 70, no. 4 (April 1, 1991): 1554–62. http://dx.doi.org/10.1152/jappl.1991.70.4.1554.
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Active expiration is produced by the abdominal muscles and the rib cage expiratory muscles. We hypothesized that the relative contribution of these two groups to expiration would affect diaphragmatic length and, hence, influence the subsequent inspiration. To address this question we measured the respiratory muscle response to expiratory threshold loading in spontaneously breathing anesthetized dogs. Prevagotomy, the increase in lung volume (functional residual capacity) and decrease in initial resting length of the diaphragm were attenuated by greater than 50% of values predicted by the passive relationships. Diaphragmatic activation (electromyogram) increased and tidal volume (VT) was preserved. Postvagotomy, effective expiratory muscle recruitment was abolished. The triangularis sterni muscle remained active, and the increase in lung volume was attenuated by less than 15% of that predicted by the passive relationship. Diaphragmatic length was shorter than predicted. VT was not restored, even though costal diaphragmatic and parasternal intercostal electromyogram increased. During expiratory threshold loading with abdominal muscles resected and vagus intact, recruitment of the rib cage expiratory muscles produced a reduction in lung volume comparable with prevagotomy; however, diaphragmatic length decreased markedly. Both the rib cage and abdominal expiratory muscles may defend lung volume; however, their combined action is important to restore diaphragmatic initial length and, accordingly, to preserve VT.
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Hsu, Shih-Hui, and Kun-Ze Lee. "Effects of serotonergic agents on respiratory recovery after cervical spinal injury." Journal of Applied Physiology 119, no. 10 (November 15, 2015): 1075–87. http://dx.doi.org/10.1152/japplphysiol.00329.2015.
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Unilateral cervical spinal cord hemisection (i.e., C2Hx) usually interrupts the bulbospinal respiratory pathways and results in respiratory impairment. It has been demonstrated that activation of the serotonin system can promote locomotor recovery after spinal cord injury. The present study was designed to investigate whether serotonergic activation can improve respiratory function during the chronic injury state. Bilateral diaphragm electromyogram and tidal volume were measured in anesthetized and spontaneously breathing adult rats at 8 wk post-C2Hx or C2laminectomy. A bolus intravenous injection of a serotonin precursor [5-hydroxytryptophan (5-HTP), 10 mg/kg], a serotonin reuptake inhibitor (fluoxetine, 10 mg/kg), or a potent agonist for serotonin 2A receptors (TCB-2, 0.05 mg/kg) was used to activate the serotonergic system. Present results demonstrated that 5-HTP and TCB-2, but not fluoxetine, significantly increased the inspiratory activity of the diaphragm electromyogram ipsilateral to the lesion for at least 30 min in C2Hx animals, but not in animals that received sham surgery. However, the tidal volume was not increased after administration of 5-HTP or TCB-2, indicating that the enhancement of ipsilateral diaphragm activity is not associated with improvement of the tidal volume. These results suggest that exogenous activation of the serotonergic system can specifically enhance the ipsilateral diaphragmatic motor outputs, but this approach may not be sufficient to improve respiratory functional recovery following chronic cervical spinal injury.
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Ando, Ryosuke, Toshiyuki Ohya, Kenta Kusanagi, Jun Koizumi, Hayato Ohnuma, Keisho Katayama, and Yasuhiro Suzuki. "Effect of inspiratory resistive training on diaphragm shear modulus and accessory inspiratory muscle activation." Applied Physiology, Nutrition, and Metabolism 45, no. 8 (August 2020): 851–56. http://dx.doi.org/10.1139/apnm-2019-0906.
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This study aimed to elucidate changes in diaphragm and accessory inspiratory muscle (sternocleidomastoid (SCM) muscle and intercostal muscle (IC)) function after a 6-week training program. Nineteen male elite collegiate swimmers were assigned to either a control group (n = 9) or training group (n = 10). The subjects in the training group performed 30 maximum inspirations at a load resistance of 50% of maximum inspiratory mouth pressure (PImax) using an inspiratory muscle training device. These were conducted twice per day and 6 days per week. At baseline and after 6 weeks, PImax, shear modulus of the diaphragm, and electromyograms (EMG) of the SCM and IC during a maximal inspiratory maneuver were evaluated. Relative change in PImax was greater in the training group than in controls. The shear modulus during a PImax maneuver had increased significantly in both groups after 6 weeks. EMG amplitudes of the SCM increased in the training group after 6 weeks, but not in the control group. EMG amplitudes of the IC did not change after 6 weeks in either group. These results suggest that 6-week inspiratory resistive training significantly improves the activation of the SCM, which could be one of the major mechanisms behind increases in inspiratory muscle strength after resistive training. Novelty Six-week inspiratory resistive training increased diaphragm stiffness during maximal inspiration maneuver. Six-week inspiratory resistive training increased electromyogram amplitudes of the sternocleidomastoid during maximal inspiration maneuver.
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Mittal, R. K., D. F. Rochester, and R. W. McCallum. "Sphincteric action of the diaphragm during a relaxed lower esophageal sphincter in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 1 (January 1, 1989): G139—G144. http://dx.doi.org/10.1152/ajpgi.1989.256.1.g139.
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We studied the effects of involuntary and voluntary contraction of the diaphragm on esophagogastric junction (EGJ) pressure during esophageal distension in healthy human volunteers. The EGJ pressure was monitored using a Dent sleeve device. Along with the pressure we concurrently monitored diaphragm electromyogram (EMG) using intra-esophageal bipolar electrodes that were placed on the nonpressure sensing surface of the sleeve device. Graded esophageal distensions were performed by graded inflations of a 2-cm-diameter balloon that was positioned 7 cm above the EGJ. The graded esophageal distensions caused a graded increase in the amplitude of lower esophageal sphincter (LES) relaxation (end-expiratory EGJ pressure). In a majority of the subjects, esophageal distension had no effect on spontaneous inspiratory EGJ pressure increase and diaphragm EMG. During sustained LES relaxation of greater than 70% induced by sustained esophageal distention, graded voluntary contractions of the diaphragm induced proportional increases in the EGJ pressure and diaphragm EMG. The EGJ pressure and diaphragm EMG were similar during diaphragmatic contraction both before and during esophageal distension. During a maximal and sustained diaphragm contraction, esophageal distension had no effect on the EGJ pressure. We conclude that there are two distinct sphincteric mechanisms at the EGJ, the LES and crural diaphragm, and they respond differently to distension of the distal esophagus.
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Kassim, Z., C. Jolley, J. Moxham, A. Greenough, and G. F. Rafferty. "Diaphragm electromyogram in infants with abdominal wall defects and congenital diaphragmatic hernia." European Respiratory Journal 37, no. 1 (June 1, 2010): 143–49. http://dx.doi.org/10.1183/09031936.00007910.
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Kim, M. J., W. S. Druz, and J. T. Sharp. "Effect of muscle length on electromyogram in a canine diaphragm strip preparation." Journal of Applied Physiology 58, no. 5 (May 1, 1985): 1602–7. http://dx.doi.org/10.1152/jappl.1985.58.5.1602.
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The relationship between diaphragm electromyogram (EMG), isometric force, and length was studied in the canine diaphragm strip with intact blood supply and innervation under three conditions: supramaximal tetanic (100 Hz) phrenic nerve stimulation (STPS; n = 12), supramaximal phrenic stimulation at 25 Hz (n = 15), and submaximal phrenic stimulation at 25 Hz (n = 5). In the same preparation, the EMG-length relationship was also examined with direct muscle stimulation when the neuromuscular junction was blocked. EMG from three different sites and via two types of electrodes (direct or sewn-in and surface) were recorded during isometric contraction at different lengths. Direct EMGs were recorded from two bipolar electrodes sutured into the strip, one near its central end and the other near its costal end. A third EMG electrode configuration summed potentials from the whole strip by recording potentials between central and costal sites. Surface EMGs were recorded by a bipolar spring clip electrode that made contact with upper and lower surfaces of the muscle strip with light pressure. In all conditions of stimulation with different types of electrodes, all EMGs decreased significantly (P less than 0.05) when muscle length was changed from 50 to 120% of resting length (L0). Minimal and maximal force outputs were observed at 50 and 120% of L0, respectively, in all experiments. The results of this study indicated that the muscle length is a significant variable that affects the EMG recording and that the diaphragmatic EMG may not be an accurate reflection of phrenic nerve activity.
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Peri, Elisabetta, Lin Xu, Christian Ciccarelli, Nele L. Vandenbussche, Hongji Xu, Xi Long, Sebastiaan Overeem, Johannes P. van Dijk, and Massimo Mischi. "Singular Value Decomposition for Removal of Cardiac Interference from Trunk Electromyogram." Sensors 21, no. 2 (January 15, 2021): 573. http://dx.doi.org/10.3390/s21020573.
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A new algorithm based on singular value decomposition (SVD) to remove cardiac contamination from trunk electromyography (EMG) is proposed. Its performance is compared to currently available algorithms at different signal-to-noise ratios (SNRs). The algorithm is applied on individual channels. An experimental calibration curve to adjust the number of SVD components to the SNR (0–20 dB) is proposed. A synthetic dataset is generated by the combination of electrocardiography (ECG) and EMG to establish a ground truth reference for validation. The performance is compared with state-of-the-art algorithms: gating, high-pass filtering, template subtraction (TS), and independent component analysis (ICA). Its applicability on real data is investigated in an illustrative diaphragm EMG of a patient with sleep apnea. The SVD-based algorithm outperforms existing methods in reconstructing trunk EMG. It is superior to the others in the time (relative mean squared error < 15%) and frequency (shift in mean frequency < 1 Hz) domains. Its feasibility is proven on diaphragm EMG, which shows a better agreement with the respiratory cycle (correlation coefficient = 0.81, p-value < 0.01) compared with TS and ICA. Its application on real data is promising to non-obtrusively estimate respiratory effort for sleep-related breathing disorders. The algorithm is not limited to the need for additional reference ECG, increasing its applicability in clinical practice.
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Luo, Yuan Ming, John Moxham, and Michael I. Polkey. "Diaphragm electromyography using an oesophageal catheter: current concepts." Clinical Science 115, no. 8 (September 12, 2008): 233–44. http://dx.doi.org/10.1042/cs20070348.
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The usefulness of diaphragm electromyography recorded from an oesophageal electrode depends on a reliable signal which is free of artefact. The diaphragm EMG (electromyogram) recorded from chest wall surface electrodes may be unreliable because of signal contamination from muscle activity other than the diaphragm. Initially, the oesophageal electrode catheter for human studies had only one electrode pair, which could be difficult to position accurately and was influenced by a change in lung volume. Recently, a multipair oesophageal electrode has been developed which allows a high-quality EMG to be recorded. In the present review, the progress of oesophageal electrode design is outlined. The effects of signal contamination, electrode movement and particularly the effect of change in lung volume on the diaphragm EMG are discussed. The diaphragm EMG, recorded from a multipair oesophageal electrode, is useful to assess neural respiratory drive and diaphragm function in different groups of patients with respiratory disease, including patients with neuromuscular disease and sleep-disordered breathing, and those in the intensive care unit. When combined with cervical and cranial magnetic stimulation, an oesophageal electrode can be used to partition the central respiratory response time and phrenic nerve conduction time.
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Doud, J. R., S. E. Dornseif, and J. M. Walsh. "Comparison of diaphragmatic EMG power spectra: spontaneous contractions vs. evoked compound action potentials." Journal of Applied Physiology 76, no. 4 (April 1, 1994): 1830–35. http://dx.doi.org/10.1152/jappl.1994.76.4.1830.
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The electromyogram (EMG) power spectrum from spontaneous diaphragm contractions has been used to identify the development of fatigue. However, power spectral analysis of the spontaneous diaphragmatic EMG signal is limited and subject to error. In contrast, power spectral analysis of the compound diaphragm action potential (CDAP) may be superior. The aim of the present study was to determine whether the EMG power spectra of evoked CDAPs correlate with those of spontaneous diaphragm contractions. Four anesthetized mechanically ventilated dogs with spontaneous isometric diaphragm contractions were studied using a mechanically isolated in situ diaphragm preparation. CDAPs were elicited via phrenic nerve stimulation, and intramuscular wire electrodes recorded EMG. Diaphragm temperature was changed from 40 to 30 degrees C to elicit changes in the EMG power spectra. The EMG signal from 10 spontaneous contractions and 10 CDAPs were acquired at 1 degrees C intervals. Fast Fourier transform was applied to both spontaneous and CDAP data yielding the power spectra, which were represented by their center frequencies (fc). The CDAP fc correlated well with the EMG fc obtained from spontaneous contractions (r = 0.99). We conclude that evoked CDAPs may provide an accurate alternative to spontaneous contractions for EMG power spectral analysis of the diaphragm.
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Singh, Bhajan, Janine A. Panizza, and Kevin E. Finucane. "Diaphragm electromyogram root mean square response to hypercapnia and its intersubject and day-to-day variation." Journal of Applied Physiology 98, no. 1 (January 2005): 274–81. http://dx.doi.org/10.1152/japplphysiol.01380.2003.
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Diaphragm activation can be quantified by measuring the root mean square of crural EMG (RMSdi) (Beck J, Sinderby C, Lindstrom L, and Grassino A, J Appl Physiol 85: 1123–1134, 1998). To examine intersubject and day-to-day variation in the RMSdi-Pco2 relationship, end-tidal Pco2, minute ventilation (V̇e), respiratory frequency (fB), and RMSdi were measured in seven healthy subjects on two occasions during steady-state ventilation at seven levels of inspired O2 fraction (FiCO2) from 0 to 0.08 in random order. RMSdi was measured with a multielectrode esophageal catheter and controlled for signal contamination and diaphragm position. RMSdi was normalized for values obtained during quiet breathing at functional residual capacity, at FiCO2 of 0.04, and during an inspiratory capacity maneuver (RMSdi%max) as well as ECG R-wave amplitude at functional residual capacity (RMSdi/ECGR), fB, and thickness of the costal diaphragm measured by ultrasound. RMSdi increased linearly with Pco2 (mean r2 = 0.83 ± 0.10); at the highest FiCO2, RMSdi%max was 40.2 ± 11.6%. Relative to the intersubject variation in the V̇e-Pco2 relationship, intersubject variations in the slopes and intercepts of the RMSdi-Pco2 relationships were 1.7 and 1.8 times, respectively, and RMSdi%max-Pco2 relationships 0.9 and 1.3 times, respectively, and were unrelated to fB and diaphragm thickness. Relative to the day-to-day variation in the V̇e-Pco2 relationship, day-to-day variation in the slopes and intercepts of the RMSdi-Pco2 relationships were 2.8 and 4.4 times, respectively, and RMSdi/ECGR-Pco2 relationships 1.3 and 2.2 times, respectively. It was concluded that the RMSdi-Pco2 relationship measures chemosensitivity and is best compared between subjects via RMSdi%max and on separate occasions in the same subject via RMSdi/ECGR.
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Luo, Y. M., N. Hart, N. Mustfa, R. A. Lyall, M. I. Polkey, and J. Moxham. "Effect of diaphragm fatigue on neural respiratory drive." Journal of Applied Physiology 90, no. 5 (May 1, 2001): 1691–99. http://dx.doi.org/10.1152/jappl.2001.90.5.1691.
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To test the hypothesis that diaphragm fatigue leads to an increase in neural respiratory drive, we measured the esophageal diaphragm electromyogram (EMG) during CO2 rebreathing before and after diaphragm fatigue in six normal subjects. The electrode catheter was positioned on the basis of the amplitude and polarity of the diaphragm compound muscle action potential recorded simultaneously from four pairs of electrodes during bilateral anterior magnetic phrenic nerve stimulation (BAMPS) at functional residual capacity. Two minutes of maximum isocapnic voluntary ventilation (MIVV) were performed in six subjects to induce diaphragm fatigue. A maximal voluntary breathing against an inspiratory resistive loading (IRL) was also performed in four subjects. The reduction of transdiaphragmatic pressure elicited by BAMPS was 22% (range 13–27%) after 2 min of MIVV and was similar, 20% (range 13–26%), after IRL. There was a linear relationship between minute ventilation (V˙e) and the root mean square (RMS) of the EMG during CO2 rebreathing before and after fatigue. The mean slope of the linear regression of RMS on V˙e was similar before and after diaphragm fatigue: 2.80 ± 1.31 vs. 3.29 ± 1.40 for MIVV and 1.51 ± 0.31 vs 1.55 ± 0.31 for IRL, respectively. We conclude that the esophageal diaphragm EMG can be used to assess neural drive and that diaphragm fatigue of the intensity observed in this study does not affect respiratory drive.
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Eikermann, Matthias, Philipp Fassbender, Sebastian Zaremba, Amy S. Jordan, Carl Rosow, Atul Malhotra, and Nancy L. Chamberlin. "Pentobarbital Dose-dependently Increases Respiratory Genioglossus Muscle Activity while Impairing Diaphragmatic Function in Anesthetized Rats." Anesthesiology 110, no. 6 (June 1, 2009): 1327–34. http://dx.doi.org/10.1097/aln.0b013e3181a16337.
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Background Anesthetics depress both ventilatory and upper airway dilator muscle activity and thus put the upper airway at risk for collapse. However, these effects are agent-dependent and may involve upper airway and diaphragm muscles to varying degrees. The authors assessed the effects of pentobarbital on upper airway dilator and respiratory pump muscle function in rats and compared these results with the effects of normal sleep. Methods Tracheostomized rats were given increasing doses of pentobarbital to produce deep sedation then light and deep anesthesia, and negative pressure airway stimuli were applied (n = 11). To compare the effects of pentobarbital with those of natural sleep, the authors chronically instrumented rats (n = 10) with genioglossus and neck electromyogram and electroencephalogram electrodes and compared genioglossus activity during wakefulness, sleep (rapid eye movement and non-rapid eye movement), and pentobarbital anesthesia. Results Pentobarbital caused a dose-dependent decrease in ventilation and in phasic diaphragmatic electromyogram by 11 +/- 0.1%, but it increased phasic genioglossus electromyogram by 23 +/- 0.2%. Natural non-rapid eye movement sleep and pentobarbital anesthesia (10 mg/kg intraperitoneally) decreased respiratory genioglossus electromyogram by 61 +/- 29% and 45 +/- 35%, respectively, and natural rapid eye movement sleep caused the greatest decrease in phasic genioglossus electromyogram (95 +/- 0.3%). Conclusions Pentobarbital in rats impairs respiratory genioglossus activity compared to the awake state, but the decrease is no greater than seen during natural sleep. During anesthesia, in the absence of pharyngeal airflow, phasic genioglossus activity is increased in a dose-dependent fashion.
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Brichant, J. F., M. Gorini, and A. De Troyer. "Respiratory response to abdominal and rib cage muscle paralysis in dogs." Journal of Applied Physiology 74, no. 5 (May 1, 1993): 2309–17. http://dx.doi.org/10.1152/jappl.1993.74.5.2309.
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To assess the respiratory response to abdominal and rib cage muscle paralysis, we measured tidal volume, esophageal and gastric pressures, arterial blood gases, and the electromyogram (EMG) of the diaphragm during progressive epidural anesthesia (lidocaine 2%) in 35 supine anesthetized dogs. The EMG activity of the diaphragm was measured with fine-wire electrodes; the abdominal cavity was thus left intact. Paralysis of the abdominal muscles alone did not produce any alterations. In contrast, when all rib cage muscles were also paralyzed, there were substantial increases in the peak height and the rate of rise of diaphragmatic EMG activity that were associated with a decrease in tidal volume and an increase in arterial PCO2 (PaCO2); swings in transdiaphragmatic pressure, however, were unchanged. The increased diaphragmatic activation due to rib cage muscle paralysis persisted after bilateral cervical vagotomy and was well explained by the increased PaCO2. These observations indicate that in the dog 1) the rib cage muscles contribute significantly to tidal volume, and their paralysis causes, through the increased hypercapnic drive, a compensatory increase in diaphragmatic activation; and 2) the rib cage inspiratory muscles enhance the diaphragm's ability to generate pressure during breathing.
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Kline, L. R., J. C. Hendricks, R. O. Davies, and A. I. Pack. "Control of activity of the diaphragm in rapid-eye-movement sleep." Journal of Applied Physiology 61, no. 4 (October 1, 1986): 1293–300. http://dx.doi.org/10.1152/jappl.1986.61.4.1293.
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Respiration in rapid-eye-movement sleep (REMS) is known to be highly variable. The purpose of this study was to investigate the source of this variability and to determine which ordering principles remained operative in REM sleep. In unrestrained, naturally sleeping cats we recorded the electroencephalogram, electrooculogram, neck electromyogram, and diaphragmatic electromyogram (EMG) and computed its moving average (MAdi). As a reference, we first examined MAdi during “tonic” REMS, since breathing is fairly regular in this state. “Control” ranges for peak amplitude (PEMG), inspiratory time (TI), duration of postinspiratory inspiratory activity, expiratory time, and the calculated inspiratory slope (PEMG/TI) were determined by overlaying individual breath traces of the time course of MAdi during tonic REMS to form a composite tracing. Next, the time course of the EMG during individual breaths in slow-wave sleep (SWS) and a complete period of consecutive breaths in REMS (both tonic and phasic) were compared with this tonic REMS composite. The number of eye movements per breath was tabulated as an index of phasic activity. The inspiratory slopes during SWS and tonic REMS were similar. However, during phasic REMS, many breaths displayed either increases (excitation) or decreases (inhibition) in slope compared with the “typical” breaths seen in tonic REMS. The occurrence of these altered slopes increased with the frequency of phasic events. TI was inversely related to the slope of the EMG, which tended to minimize changes in PEMG.(ABSTRACT TRUNCATED AT 250 WORDS)
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Reid, W. D., T. Blogg, B. J. Wiggs, P. D. Pare, and R. L. Pardy. "Diaphragmatic plate electrode stimulation of the hamster diaphragm." Journal of Applied Physiology 67, no. 4 (October 1, 1989): 1341–48. http://dx.doi.org/10.1152/jappl.1989.67.4.1341.
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We developed a new technique of diaphragmatic stimulation by apposing plate electrodes directly against the diaphragm (DPS) in adult Golden Syrian hamsters. The electrophysiological and the mechanical responses to DPS were compared with those with phrenic nerve stimulation. In four animals, evaluation of the electromyogram before and after curare demonstrated that plate electrode stimulation occurred via the phrenic nerve filaments. In four animals, similar transdiaphragmatic pressure was produced at maximal current with DPS and phrenic nerve stimulation. Using DPS increasing current beyond a certain level resulted in recruitment of muscles besides the diaphragm. In six animals, an external abdominal pressure of 15 cmH2O produced maximal transdiaphragmatic pressure, suggesting that the diaphragm was contracting near optimal position with this external abdominal pressure. In another four animals the twitch and pressure-frequency characteristics with the use of DPS were found to be reproducible over a 2-h period. We conclude that DPS is an effective method of diaphragmatic stimulation and should prove to be a valuable technique to study the diaphragm in long-term studies of small rodents.
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Beck, Jennifer, Christer Sinderby, Lars Lindström, and Alex Grassino. "Effects of lung volume on diaphragm EMG signal strength during voluntary contractions." Journal of Applied Physiology 85, no. 3 (September 1, 1998): 1123–34. http://dx.doi.org/10.1152/jappl.1998.85.3.1123.
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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.
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Cheeseman, M., and W. R. Revelette. "Phrenic afferent contribution to reflexes elicited by changes in diaphragm length." Journal of Applied Physiology 69, no. 2 (August 1, 1990): 640–47. http://dx.doi.org/10.1152/jappl.1990.69.2.640.
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Recent evidence from several laboratories suggests that activation of afferents in the diaphragm can reflexly affect inspiratory muscle activation. This study determined whether afferents in the diaphragm contribute to compensatory changes in phrenic motor drive when the operating length of the diaphragm is suddenly increased. Experiments were performed in six closed-chest pentothal-anesthetized cats. Length changes were measured using a pair of piezoelectric crystals implanted in the left crural diaphragm. The crural electromyogram (EMGdi) was measured by electrodes fixed to each crystal. The animal was suspended in a spinal frame, and a Plexiglas tube was fitted around the cat's abdomen. A balloon placed inside the tube was inflated during the expiratory phase to produce a mean increase of 17% in diaphragm length at functional residual capacity. Ten trials were performed in succession under the following conditions: intact, after bilateral vagotomy, after spinal section at C7, and after cervical dorsal rhizotomy. Peak integrated EMGdi (integral of EMGdi) and neural inspiratory time (nTI) were measured for the last control inspiration and the first after inflation. There was a significant reduction in the peak integral of EMGdi when the length of the diaphragm was increased for all conditions except after rhizotomy. Although not measured, it is likely that the tension developed by the diaphragm was also increased during abdominal compression. Results suggest that afferents sensitive to changes in the operating length and/or tension in the diaphragm contribute to compensatory alterations in phrenic motor drive.
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Fisher, Michael J., and Ravinder K. Mittal. "Effect of Intraesophageal Electrode Position on Signal Amplitude of the Crural Diaphragm Electromyogram." Neurogastroenterology & Motility 2, no. 3 (June 28, 2008): 184–89. http://dx.doi.org/10.1111/j.1365-2982.1990.tb00023.x.
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Newman, S. L., J. D. Road, and A. Grassino. "In vivo length and shortening of canine diaphragm with body postural change." Journal of Applied Physiology 60, no. 2 (February 1, 1986): 661–69. http://dx.doi.org/10.1152/jappl.1986.60.2.661.
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Using sonomicrometry, we measured the in vivo tidal shortening and velocity of shortening of the costal and crural segments of the diaphragm in the anesthetized dog in the supine, upright, tailup, prone, and lateral decubitus postures. When compared with the supine position, end-expiratory diaphragmatic length varied by less than 11% in all postures, except the upright. During spontaneous breathing, the tidal shortening and the velocity of shortening of the crural segment exceeded that of the costal segment in all postures except the upright and was maximal for both segments in the prone posture. We noted the phasic integrated electromyogram to increase as the end-expiratory length of the diaphragm shortened below and to decrease as the diaphragm lengthened above its optimal length. This study shows that the costal and crural segments have a different quantitative behavior with body posture and both segments show a compensation in neural drive to changes in resting length.
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Easton, P. A., M. Katagiri, T. M. Kieser, and R. S. Platt. "Postinspiratory activity of costal and crural diaphragm." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 582–89. http://dx.doi.org/10.1152/jappl.1999.87.2.582.
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Because the first stage of expiration or “postinspiration” is an active neurorespiratory event, we expect some persistence of diaphragm electromyogram (EMG) after the cessation of inspiratory airflow, as postinspiratory inspiratory activity (PIIA). The costal and crural segments of the mammalian diaphragm have different mechanical and proprioceptive characteristics, so postinspiratory activity of these two portions may be different. In six canines, we implanted chronically EMG electrodes and sonomicrometer transducers and then sampled EMG activity and length of costal and crural diaphragm segments at 4 kHz, 10.2 days after implantation during wakeful, resting breathing. Costal and crural EMG were reviewed on-screen, and duration of PIIA was calculated for each breath. Crural PIIA was present in nearly every breath, with mean duration 16% of expiratory time, compared with costal PIIA with duration −2.6% of expiratory time ( P < 0.002). A linear regression model of crural centroid frequency vs. length, which was computed during the active shortening of inspiration, did not accurately predict crural EMG centroid frequency values at equivalent length during the controlled relaxation of postinspiration. This difference in activation of crural diaphragm in inspiration and postinspiration is consistent with a different pattern of motor unit recruitment during PIIA.
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Smith, C. A., D. M. Ainsworth, K. S. Henderson, and J. A. Dempsey. "Differential timing of respiratory muscles in response to chemical stimuli in awake dogs." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 392–99. http://dx.doi.org/10.1152/jappl.1989.66.1.392.
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We assessed changes in respiratory muscle timing in response to hyperpnea and shortened inspiratory and expiratory times caused by chemoreceptor stimuli in six awake dogs. Durations of postinspiratory inspiratory activity of costal and crural diaphragm (PIIA), the delay in diaphragm electromyogram (EMG) after the initiation of inspiratory airflow, postexpiratory expiratory activity of the transversus abdominis (PEEA), and the delay of abdominal expiratory muscle activity after the initiation of expiratory airflow were measured. In control, four out of six dogs showed PIIA [8–10% of expiratory time (TE)]; all showed delay of diaphragm [19% of inspiratory time (TI)], delay of abdominal muscle activation (21% of TE), and PEEA (24% of TI). Hypercapnia decreased PIIA (4–9% of TE), maintained diaphragm delay at near control values (23% of TI), increased PEEA (36% of TI), eliminated delay of abdominal muscle activation (4% of TE), and decreased end-expiratory lung volume (EELV). Hypocapnic hypoxia increased PIIA (24–25% of TE), eliminated diaphragm delay (3% of TI), eliminated PEEA (3% of TI), reduced delay of abdominal muscle activation (14% of TE), and increased EELV. Most of these effects of hypoxic hypocapnia vs. hypercapnia on the within-breath EMG timing parameters corresponded to differences in the magnitude of expiratory muscle activation. These changes exerted significant influences on flow rates and EELV.
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Katagiri, M., R. N. Young, R. S. Platt, T. M. Kieser, and P. A. Easton. "Respiratory muscle compensation for unilateral or bilateral hemidiaphragm paralysis in awake canines." Journal of Applied Physiology 77, no. 4 (October 1, 1994): 1972–82. http://dx.doi.org/10.1152/jappl.1994.77.4.1972.
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In humans and some animals, the surviving respiratory muscles are able to compensate fully for unilateral, and partially for bilateral, hemidiaphragm paralysis. To examine differential activity of individual respiratory muscles after unilateral or bilateral diaphragm paralysis, length and electromyogram (EMG) of left costal and crural diaphragm segments, parasternal intercostal, and transversus abdominis were measured directly in five awake canines after implantation with sonomicrometry transducers and bipolar EMG electrodes under three conditions: during normal breathing (NOFRZ), after infusion of local anesthetic (bupivacaine) through a cervical phrenic nerve cuff to induce reversible contralateral hemidiaphragm (CNFRZ), and after bilateral diaphragm (BIFRZ) paralysis. From NOFRZ to CNFRZ, costal, crural, parasternal, and transversus abdominis increased shortening and EMG activity to compensate for contralateral diaphragm paralysis, but the increase in activity was not equivalent for each muscle. With BIFRZ, parasternal and transversus abdominis showed further increases in activity, coordinated between both inspiration and expiration. Normalized intrabreath profiles revealed dynamic differences in development of muscle activity within each breath as paralysis worsened. Review of simultaneous muscle activities showed coordinated interactions among the compensating muscles: passive shortening of transversus, and lengthening of costal and crural, coincided with increased active inspiratory shortening of parasternal. We conclude that an integrated strategy of respiratory muscle compensation for unilateral or bilateral diaphragm paralysis occurs among chest wall, abdominal, and diaphragm segmental muscles, with relative contributions of individual muscles adjusted according to the degree of diaphragm dysfunction.
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Ward, M. E., D. Eidelman, D. G. Stubbing, F. Bellemare, and P. T. Macklem. "Respiratory sensation and pattern of respiratory muscle activation during diaphragm fatigue." Journal of Applied Physiology 65, no. 5 (November 1, 1988): 2181–89. http://dx.doi.org/10.1152/jappl.1988.65.5.2181.
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We have examined the relationship between respiratory effort sensation (modified Borg scale) and amplitude of the integrated surface electromyogram of the diaphragm (Edi, esophageal electrode), rib cage muscles (Erc), and sternomastoid muscle (Esm) during the development of diaphragm fatigue in five normal subjects. Three conditions were studied: run A: transdiaphragmatic pressure (Pdi), 65% Pdimax; esophageal pressure (Pes), 60% Pesmax; run B: Pdi, 50% Pdimax; Pes, 60% Pesmax; and run C: Pdi, 50% Pdimax; Pes, 20% Pesmax. During all runs there was a progressive rise in sensation, which was greater in runs A and B than in run C (P less than 0.05, analysis of variance). There was no difference between runs A and B. At the end of run C subjects did not report a maximal Borg score despite their inability to generate the target Pdi. The increase in sensory score with fatigue correlated highly with Esm/Esmmax and with Erc/Ercmax. There was no correlation between sensory score and Edi/Edimax. We conclude that the increase in respiratory effort sensation that accompanies diaphragm fatigue is not due to perception of increased diaphragmatic activation. It may reflect increased overall respiratory motor output not directed to the diaphragm.
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Beck, Jennifer, Christer Sinderby, Lars Lindström, and Alex Grassino. "Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration." Journal of Applied Physiology 82, no. 2 (February 1, 1997): 520–30. http://dx.doi.org/10.1152/jappl.1997.82.2.520.
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Beck, Jennifer, Christer Sinderby, Lars Lindström, and Alex Grassino. Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration. J. Appl. Physiol. 82(2): 520–530, 1997.—The effect of chest wall configuration on the diaphragm electromyogram (EMGdi) was evaluated in five healthy subjects with an esophageal electrode for both interference pattern EMGdi (voluntary contractions) and electrically evoked diaphragm compound muscle action potentials (CMAPs). Diaphragm CMAPs (both unilateral and bilateral) were evaluated for the baseline-to-peak amplitude (Ampl), the time from the onset of the CMAP to first peak (T1), root mean square (RMS), and center frequency (CF) values of the CMAP power spectrum. CF values from the interference pattern EMGdi power spectrum were also calculated. For CMAPs obtained at an electrode position least influenced by variations induced by electrode positioning, Ampl increased with diaphragm shortening from functional residual capacity (FRC) to total lung capacity (TLC) by 101 and 98% (unilateral and bilateral, respectively). Bilateral CMAP RMS values increased 116% from FRC to TLC. CMAP T1 values decreased with diaphragm shortening from FRC to TLC by 1.1 and 2.1 ms for the unilateral and bilateral stimulations, respectively, and CF increased for the bilateral diaphragm CMAPs with diaphragm shortening. CF values from the interference pattern EMGdi did not show any consistent change with chest wall configuration. Thus CF values of the interference pattern EMGdi obtained with an esophageal electrode can be considered reliable for physiological interpretation, at any diaphragm length (if electrode positioning and signal contamination are controlled for), contrary to the diaphragm CMAPs, which are sensitive to changes in chest wall configuration. It is speculated that the different results (over the effects of chest wall configuration on interference pattern EMGdi and diaphragm CMAPs) may be because of summation properties of the signals and how these influence the EMG power spectrum.
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Road, J., R. Vahi, P. del Rio, and A. Grassino. "In vivo contractile properties of fatigued diaphragm." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 471–78. http://dx.doi.org/10.1152/jappl.1987.63.2.471.
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The effects of fatigue on diaphragmatic contractility in vivo are unknown. In this study we used sonomicrometry to examine the velocity of shortening and lengthening and the amount of shortening in the fresh and fatigued canine hemidiaphragm (8 dogs) including the force generated. Fatigue was produced by epiphrenic stimulation of the left phrenic nerve; the right hemidiaphragm acted as the control. We found that 1) hemidiaphragmatic fatigue caused an increase in frequency with reduced tidal volume; 2) fatigue resulted in a near complete cessation of tidal shortening during spontaneous breathing; 3) there was an initial decrease in central activation (electromyogram) to the fatigued hemidiaphragm, an indication of central fatigue; 4) force-frequency curves showed a considerable and prolonged loss of the amount of shortening, velocity, and force generated by the fatigued hemidiaphragm during supramaximal stimulation, an indication of peripheral fatigue; and 5) during spontaneous breathing in the fatigued hemidiaphragm, tidal shortening remained reduced for up to 3 h, whereas in the right right hemidiaphragm tidal shortening and electromyographic activity did not change. We conclude that fatigue of a hemidiaphragm alters the spontaneous breathing pattern and produces profound modifications in its contractile properties without altering contralateral hemidiaphragmatic performance.
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Hendricks, J. C., and L. R. Kline. "Differential activation within costal diaphragm during rapid-eye-movement sleep in cats." Journal of Applied Physiology 70, no. 3 (March 1, 1991): 1194–200. http://dx.doi.org/10.1152/jappl.1991.70.3.1194.
Full textAbstract:
Simultaneous recordings of the diaphragmatic electromyogram (EMG) were made from two separate regions of the costal diaphragm in six normal cats. The diaphragmatic activities were always synchronous and the amplitudes and rates of rise were similar during slow-wave sleep. In contrast, during natural rapid-eye-movement (REM) sleep, different activity was often present in the two leads. These differences were in the time of onset and offset, as well as in the amplitude and spike patterns, and occurred in approximately 5-20% of the diaphragmatic bursts averaged over the entire REM sleep period. With respect to eye movement density, the rate of differential activation was higher during periods of high density (26%) than in the absence of eye movements (1%) in the four animals for which these data were available. Differential activation of portions of the costal diaphragm is apparently a normal event of REM sleep. This could result from descending state-specific phasic neuronal activity that bypasses the medullary respiratory generator. Differential activation of portions of the diaphragm could contribute to disordered ventilation during REM sleep.
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Road, J. D., and A. M. Leevers. "Effect of lung inflation on diaphragmatic shortening." Journal of Applied Physiology 65, no. 6 (December 1, 1988): 2383–89. http://dx.doi.org/10.1152/jappl.1988.65.6.2383.
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The effect of lung inflation on chest wall mechanics was studied in 11 vagotomized pentobarbital sodium-anesthetized dogs. Diaphragmatic shortening (percent change from initial length at functional residual capacity, %LFRC) and transdiaphragmatic pressure swings (delta Pdi) were compared with control values over a range of positive-pressure breathing that produced a maximum increase in lung volume to 40% of inspiratory capacity. There was no change in the electromyogram of the diaphragm or parasternal intercostals during positive-pressure breathing. delta Pdi and tidal volume (VT) fell to 52 +/- 3.3 and 42.5 +/- 5% (SE) of control. This was associated with a reduction in the initial resting length of 13 +/- 1.9 and 21 +/- 2.2%LFRC (SE) in the costal and crural diaphragms, respectively. Tidal diaphragmatic shortening, however, decreased to 66 +/- 7 and 57 +/- 7 and the mean velocity decreased to 78 +/- 10 and 63 +/- 8% (SE) of control for the costal and crural diaphragms, respectively. We conclude that the reduction in diaphragmatic shortening is the main determinant of the reduced delta Pdi and VT during lung inflation and relate this to what is currently known about diaphragmatic contractile properties.
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Smith, C. A., D. M. Ainsworth, K. S. Henderson, and J. A. Dempsey. "Differential responses of expiratory muscles to chemical stimuli in awake dogs." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 384–91. http://dx.doi.org/10.1152/jappl.1989.66.1.384.
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We assessed respiratory muscle response patterns to chemoreceptor stimuli (hypercapnia, hypoxia, normocapnic hypoxia, almitrine, and almitrine + CO2) in six awake dogs. Mean electromyogram (EMG) activities were measured in the crural (CR) diaphragm, triangularis sterni (TS), and transversus abdominis (TA). Hypercapnia and normocapnic hypoxia caused mild to marked hyperpnea [2–5 times control inspiratory flow (VI)] and increased activity in CR diaphragm, TS, and TA. When hypocapnia was permitted to develop during hypoxia and almitrine-induced moderate hyperpnea, CR diaphragm activity increased, whereas TS and TA activities usually did not change or were reduced below control. Over time in hypercapnia, CR diaphragm, TS, and TA were augmented and maintained at these levels over many minutes; with hypoxic hyperventilation CR diaphragm, TS, and TA were first augmented but then CR diaphragm remained augmented while TS and, less consistently, TA were inhibited over time. Marked hyperpnea (4–5 times control) due to carotid body stimulation increased TA and TS EMG activity despite an accompanying hypocapnia. We conclude that in the intact awake dog 1) carotid body stimulation augments the activity of both inspiratory and expiratory muscles; 2) hypocapnia overrides the augmenting effect of carotid body stimulation on expiratory muscles during moderate hyperpnea, usually resulting in either no change or inhibition; 3) at higher levels of hyperpnea both chemoreceptor stimulation and stimulatory effects secondary to a high ventilatory output favor expiratory muscle activation; these effects override any inhibitory effects of a coincident hypocapnia; and 4) expiratory muscles of the rib cage/abdomen may be augmented/inhibited independently of one another.
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Forster, H. V., B. K. Erickson, T. F. Lowry, L. G. Pan, M. J. Korducki, and A. L. Forster. "Effect of helium-induced ventilatory unloading on breathing and diaphragm EMG in awake ponies." Journal of Applied Physiology 77, no. 1 (July 1, 1994): 452–62. http://dx.doi.org/10.1152/jappl.1994.77.1.452.
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Two questions were addressed in this study: 1) Does respiratory resistive unloading (inspired O2 fraction = 0.21, inspired He fraction = 0.79) elicit a compensatory reduction in stimulation of the diaphragm? 2) Do diaphragm and lung afferents contribute to compensatory responses to unloading? Ten intact (I), five diaphragm-deafferented (DD), four hilar nerve-denervated (HND), and seven DD+HND adult ponies were studied at rest and during mild and moderate treadmill exercise. During steady-state unloading at rest, duration of the diaphragm electromyogram (EMGdi) was less (P < 0.05) than control in I ponies, but there were no additional significant changes in breathing or blood gases. Unloading during mild and moderate exercise increased (P < 0.05) pulmonary ventilation in all groups, and this response did not differ (P > 0.05) among the groups. With unloading during exercise, arterial PCO2 was within 1 Torr of control except in the DD+HND ponies, which were 1–2 Torr hypocapnic (P < 0.05). During exercise, the duration and rate of rise of the EMGdi were reduced (P < 0.05) below control, beginning at about the third unloaded breath. The decrease in rate of rise was usually not sustained, inasmuch as there was a gradual return toward control over 2 min of unloading. There were no consistent group differences in these EMGdi responses. We conclude that resistive unloading during mild and moderate exercise in ponies results in a transient reduction in neural drive to the diaphragm that is not critically dependent on diaphragm and pulmonary afferents.
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Navarrete-Opazo, A., and G. S. Mitchell. "Recruitment and plasticity in diaphragm, intercostal, and abdominal muscles in unanesthetized rats." Journal of Applied Physiology 117, no. 2 (July 15, 2014): 180–88. http://dx.doi.org/10.1152/japplphysiol.00130.2014.
Full textAbstract:
Although rats are a frequent model for studies of plasticity in respiratory motor control, the relative capacity of rat accessory respiratory muscles to express plasticity is not well known, particularly in unanesthetized animals. Here, we characterized external intercostal (T2, T4, T5, T6, T7, T8, T9 EIC) and abdominal muscle (external oblique and rectus abdominis) electromyogram (EMG) activity in unanesthetized rats via radiotelemetry during normoxia (Nx: 21% O2) and following acute intermittent hypoxia (AIH: 10 × 5-min, 10.5% O2; 5-min intervals). Diaphragm and T2–T5 EIC EMG activity, and ventilation were also assessed during maximal chemoreceptor stimulation (MCS: 7% CO2, 10.5% O2) and sustained hypoxia (SH: 10.5% O2). In Nx, T2 EIC exhibits prominent inspiratory activity, whereas T4, T5, T6, and T7 EIC inspiratory activity decreases in a caudal direction. T8 and T9 EIC and abdominal muscles show only tonic or sporadic activity, without consistent respiratory activity. MCS increases diaphragm and T2 EIC EMG amplitude and tidal volume more than SH (0.94 ± 0.10 vs. 0.68 ± 0.05 ml/100 g; P < 0.001). Following AIH, T2 EIC EMG amplitude remained above baseline for more than 60 min post-AIH (i.e., EIC long-term facilitation, LTF), and was greater than diaphragm LTF (41.5 ± 1.3% vs. 19.1 ± 2.0% baseline; P < 0.001). We conclude that 1) diaphragm and rostral T2–T5 EIC muscles exhibit inspiratory activity during Nx; 2) MCS elicits greater ventilatory, diaphragm, and rostral T2–T5 EIC muscle activity vs. SH; and 3) AIH induces greater rostral EIC LTF than diaphragm LTF.
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Mittal, R. K., M. Fisher, R. W. McCallum, D. F. Rochester, J. Dent, and J. Sluss. "Human lower esophageal sphincter pressure response to increased intra-abdominal pressure." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 4 (April 1, 1990): G624—G630. http://dx.doi.org/10.1152/ajpgi.1990.258.4.g624.
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We studied the effects of increased intra-abdominal pressure on the lower esophageal sphincter (LES) pressure in 15 healthy subjects. The role of the diaphragm in the genesis of LES pressure during increased intra-abdominal pressure was determined by measuring diaphragm electromyogram (EMG). The latter was recorded using bipolar intraesophageal platinum electrodes that were placed on the nonpressure sensing surface of the sleeve device. We also measured the LES pressure response to increased intra-abdominal pressure during inhibition of the smooth muscles of the LES by intravenous atropine (12 micrograms/kg). Straight-leg raising and abdominal compression were used to increase intra-abdominal pressure. Our results show that the increase in LES pressure during straight-leg raising is greater than the increase in gastric pressure. During abdominal compression, the rate of LES pressure increase is faster than that of the gastric pressure, suggesting an active contraction at the esophagogastric junction. The increase in LES pressure during periods of increased intra-abdominal pressure is associated with a tonic contraction of the crural diaphragm as demonstrated by EMG recording. Atropine inhibited the resting LES pressure by 50-70% in each subject but had no effect either on the peak LES pressure attained during increased intra-abdominal pressure or tonic crural diaphragm EMG. We conclude that 1) there is an active contraction at the esophagogastric junction during periods of increased intra-abdominal pressure and 2) tonic contraction of the crural diaphragm is a mechanism for this LES pressure response.
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Ikegami, Tetsunori, Michael Ji, Naoyuki Fujimura, Jenny V. Suneby Jagers, Teresa M. Kieser, and Paul A. Easton. "Costal and crural diaphragm function during sustained hypoxia in awake canines." Journal of Applied Physiology 126, no. 4 (April 1, 2019): 1117–28. http://dx.doi.org/10.1152/japplphysiol.00242.2018.
Full textAbstract:
In humans and other mammals, isocapnic hypoxia sustained for 20–60 min exhibits a biphasic ventilation pattern: initial increase followed by a significant ventilatory decline (“roll-off”) to a lesser intermediate plateau. During sustained hypoxia, the mechanical action and activity of the diaphragm have not been studied; thus we assessed diaphragm function in response to hypoxic breathing. Thirteen spontaneously breathing awake canines were exposed to moderate levels of sustained isocapnic hypoxia lasting 20–25 min (80 ± 2% pulse oximeter oxygen saturation). Breathing pattern and changes in muscle length and electromyogram (EMG) activity of the costal and crural diaphragm were continuously recorded. Mean tidal shortening and EMG activity of the costal and crural diaphragm exhibited an overall biphasic pattern, with initial brisk increase followed by a significant decline ( P < 0.01). Although costal and crural shortening did not differ significantly with sustained hypoxia, this equivalence in segmental shortening occurred despite distinct and differing EMG activities of the costal and crural segments. Specifically, initial hypoxia elicited a greater costal EMG activity compared with crural ( P < 0.05), whereas sustained hypoxia resulted in a lesser crural EMG decline/attenuation than costal ( P < 0.05). We conclude that sustained isocapnic hypoxia elicits a biphasic response in both ventilation and diaphragmatic function and there is clear differential activation and contribution of the two diaphragmatic segments. This different diaphragm segmental action is consistent with greater neural activation of costal diaphragm during initial hypoxia, then preferential sparing of crural activation as hypoxia is sustained. NEW & NOTEWORTHY In humans and other mammals, during isocapnic hypoxia sustained for 20–60 min ventilation exhibits a biphasic pattern: initial increase followed by significant ventilatory decline (“roll-off”). During sustained hypoxia, the function of the diaphragm is unknown. This study demonstrates that the diaphragm reveals a biphasic action during the time-dependent hypoxic “roll-off” in ventilation. These results also highlight that the two diaphragm segments, costal and crural, show differing, distinctive contributions to diaphragm function during sustained hypoxia.