Chemical and postural influence on scalene and diaphragmatic activation in humans

1991 ◽  
Vol 70 (2) ◽  
pp. 658-664 ◽  
Author(s):  
A. L. Xie ◽  
Y. Takasaki ◽  
J. Popkin ◽  
D. Orr ◽  
T. D. Bradley

The electromyographic activity of the diaphragm (EMGdi) and scalene muscle (EMGsc) was studied in the supine and upright positions, respectively, during hyperoxic progressive hypercapnic rebreathing (HCVR) in five healthy males. End-expiratory esophageal pressure (EEPes) was quantified on a breath-to-breath basis as a reflection of altered end-expiratory lung volume. There was no significant difference in the slopes of EMGdi, expressed as a percentage of maximum at total lung capacity vs. minute volume of ventilation (VI), between the supine and upright positions [0.79 +/- 0.05 (SE) vs. 0.92 +/- 0.17, respectively]. In contrast, the slope of the regression line relating EMGsc to VI was steeper in the upright than in the supine position (0.69 +/- 0.05 vs. 0.35 +/- 0.04, respectively; P less than 0.005). Positive EEPes at comparable VI at the ends of HCVRs were of greater magnitude upright than supine (3.27 +/- 0.68 vs. 4.35 +/- 0.60 cmH2O, respectively, P less than 0.001). We conclude that altering posture has a greater effect on scalene and expiratory muscle activity than on diaphragmatic activity during hypercapnic stimulation.

1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.


1999 ◽  
Vol 86 (5) ◽  
pp. 1663-1669 ◽  
Author(s):  
A. L. Perlman ◽  
P. M. Palmer ◽  
T. M. McCulloch ◽  
D. J. Vandaele

The durations and temporal relationships of electromyographic activity from the submental complex, superior pharyngeal constrictor, cricopharyngeus, thyroarytenoid, and interarytenoid muscles were examined during swallowing of saliva and of 5- and 10-ml water boluses. Bipolar, hooked-wire electrodes were inserted into all muscles except for the submental complex, which was studied with bipolar surface electrodes. Eight healthy, normal, subjects produced five swallows of each of three bolus volumes for a total of 120 swallows. The total duration of electromyographic activity during the pharyngeal stage of the swallow did not alter with bolus condition; however, specific muscles did show a volume-dependent change in electromyograph duration and time of firing. Submental muscle activity was longest for saliva swallows. The interarytenoid muscle showed a significant difference in duration between the saliva and 10-ml water bolus. Finally, the interval between the onset of laryngeal muscle activity (thyroarytenoid, interarytenoid) and of pharyngeal muscle firing patterns (superior pharyngeal constrictor onset, cricopharyngeus offset) decreased as bolus volume increased. The pattern of muscle activity associated with the swallow showed a high level of intrasubject agreement; the presence of somewhat different patterns among subjects indicated a degree of population variance.


1983 ◽  
Vol 54 (1) ◽  
pp. 152-158 ◽  
Author(s):  
D. Rodenstein ◽  
D. C. Stanescu

In acute induced asthma, plethysmographic total lung capacity (TLCm) was reported to increase and lung elastic recoil [Pst(L)] to decrease. The increase in TLC is spurious (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 939–954, 1982), so that the rapid loss in Pst(L) could be due to errors in lung volume. We studied seven asthmatic patients before and during an induced bronchospasm. TLC was derived simultaneously from mouth and esophageal pressure vs. plethysmographic volume plots (TLCm and TLCes, respectively). Before bronchospasm, TLCm and TLCes were similar. During bronchospasm average TLCm increased, from 7.30 +/- 1.34 (SD) to 8.12 +/- 1.49 liters (P less than 0.001), whereas TLCes did not (P greater than 0.60). Static pressure-volume curves, derived from TLCes (P-Ves), were superimposed on prechallenge curves or only slightly shifted to the left, whereas those derived from TLCm (P-Vm) showed a clear-cut parallel shift to the left. At 70% of control TLC there was no significant change in Pst(L) measured from P-Ves curves (7.3 +/- 3.1 cmH2O before bronchospasm; 6.7 +/- 2.3 cmH2O during bronchospasm, P greater than 0.10), whereas Pst(L) measured from P-Vm curves decreased from 7.3 +/- 3.1 to 5.1 +/- 2.4 cmH2O (P less than 0.01). No significant change in Pst(L) at TLC was observed during bronchospasm. We conclude that in our patients acute decrease in Pst(L) during induced asthma was artifactual, secondary to lung volume overestimation by body plethysmography.


1983 ◽  
Vol 54 (1) ◽  
pp. 37-44 ◽  
Author(s):  
T. D. Sweeney ◽  
J. D. Brain ◽  
S. LeMott

General anesthesia was used to produce nonventilated areas of the lung, and aerosol inhalation was used to locate these areas, assuming that no aerosol deposits in a nonventilated region. Male Syrian golden hamsters were anesthetized with pentobarbital sodium (90 mg/kg), which reduced respiratory frequency, tidal volume, minute volume, and O2 consumption to 61, 41, 24, and 36%, respectively, of the corresponding awake levels. Awake and anesthetized hamsters were exposed to the aerosol for 30 min; then the lungs were excised, dried at total lung capacity, sliced into sections, and dissected into pieces. Autoradiographs were made of slices, and the activity and weight of pieces were determined. The evenness index (EI), a measure of the uniformity of retention, was calculated for each piece. With complete uniformity of retention, all EI's would be 1.0. In awake animals, only 0.2% (by wt) of the lungs had little or no retention (EI's less than 0.20). More particles deposited in the apex than in the base of the lungs. General anesthesia for extended periods of time with no deep breaths alters ventilation and therefore the distribution of aerosol retention. Many regions of the lungs in the anesthetized animals received few or no particles (11.6% of lungs had EI less than 0.20); however, no consistent pattern was observed in the location of these areas from animal to animal. The apex-to-base gradient for retention in these animals was also reversed. Radioactive aerosols can be used as probes to indicate the extent and distribution of nonventilated areas in the lungs.


Author(s):  
Pat Tittiranonda ◽  
Bernard Martin ◽  
Stephen Burastero

This study examined the use of four different computer pointing devices on surface electromyographic activity of the index finger, forearm and shoulder/neck muscles among CAD operators in the workplace. Subjects were randomly assigned to use their own mouse, a trackball, a joystick mouse or an experimental mouse. Results showed that there was a statistically significant difference in muscle load for the upper trapezius, extensor indicis proprius, and extensor carpi ulnaris across pointing devices for CAD operations. The flexor digitorum superficialis muscle load remained relatively constant when all pointing devices were compared.


1995 ◽  
Vol 83 (4) ◽  
pp. 835-843. ◽  
Author(s):  
David O. Warner ◽  
Michael J. Joyner ◽  
Erik L. Ritman

Background The pattern of respiratory muscle use during halothane-induced anesthesia differs markedly among species breathing quietly. In humans, halothane accentuates phasic activity in rib cage and abdominal expiratory muscles, whereas activity in the parasternal intercostal muscles is abolished. In contrast, halothane abolishes phasic expiratory muscle activity during quiet breathing in dogs, but parasternal muscle activity is maintained. Respiratory muscle responses to CO2 rebreathing were measured in halothane-anesthetized dogs to determine if species differences present during quiet breathing persist over a wide range of central respiratory drive. Methods Chronic electromyogram electrodes were implanted in three expiratory agonists (the triangularis sterni, transversus abdominis, and external oblique muscles) and three inspiratory agonists (the parasternal intercostal muscle, costal and crural diaphragm) of six mongrel dogs. After a 1-month recovery period, the dogs were anesthetized in the supine position with halothane. The rebreathing response was determined by Read's method during anesthesia with stable 1 and 2 minimum alveolar end-tidal concentrations of halothane. CO2 concentrations were measured in the rebreathing bag using an infrared analyzer. Chest wall motion was measured by fast three-dimensional computed tomographic scanning. Results Halothane concentration did not significantly affect the slope of the relationship between minute ventilation (VE) and PCO2 (0.34 +/- 0.04 [M +/- SE] and 0.28 +/- 0.05 l.min-1.mmHg-1 during 1 and 2 minimum alveolar concentration anesthesia, respectively). However, 2 minimum alveolar concentration anesthesia did significantly decrease the calculated VE at a PCO2 of 60 mmHg (from 7.4 +/- 1.2 to 4.0 +/- 0.6 l.min-1), indicating a rightward shift in the response relationship. No electromyographic activity was observed in any expiratory muscle before rebreathing. Rebreathing produced electromyographic activity in at least one expiratory muscle in only two dogs. Rebreathing significantly increased electromyographic activity in all inspiratory agonists. Rebreathing significantly increased inspiratory thoracic volume change (delta Vth), with percentage of delta Vth attributed to outward rib cage displacement increasing over the course of rebreathing during 1 minimum alveolar concentration anesthesia (from 33 +/- 6% to 48 +/- 2% of delta Vth). Conclusions Rebreathing did not produce expiratory muscle activation in most dogs, demonstrating that the suppression of expiratory muscle activity observed at rest persists at high levels of ventilatory drive. Other features of the rebreathing response also differed significantly from previous reports in halothane-anesthetized humans, including (1) an increase in the rib cage contribution to tidal volume during the course of rebreathing, (2) recruitment of parasternal intercostal activity by rebreathing, (3) differences in the response of ventilatory timing, and (4) the lack of effect of anesthetic depth on the slope of the ventilatory response. These marked species differences are further evidence that the dog is not a suitable model to study anesthetic effects on the activation of human respiratory muscles.


1985 ◽  
Vol 59 (6) ◽  
pp. 1849-1854 ◽  
Author(s):  
I. G. Brown ◽  
P. A. McClean ◽  
P. M. Webster ◽  
V. Hoffstein ◽  
N. Zamel

There is conflicting evidence in the literature regarding tissue pressure in the neck. We studied esophageal pressure along cervical and intrathoracic esophageal segments in six healthy men to determine extramural pressure for the cervical and intrathoracic airways. A balloon catheter system with a 1.5-cm-long balloon was used to measure intraesophageal pressures. It was positioned at 2-cm intervals, starting 10 cm above the cardiac sphincter and ending at the cricopharyngeal sphincter. We found that esophageal pressures became more negative as the balloon catheter moved from intrathoracic to cervical segments, until the level of the cricopharyngeal sphincter was reached. At total lung capacity, esophageal pressures were -10.5 +/- 2.9 (SE) cmH2O in the lower esophagus, -18.9 +/- 3.0 just within the thorax, and -21.3 +/- 2.73 within 2 cm of the cricopharyngeal sphincter. The variation in mouth minus esophageal pressure with lung volume was similar in cervical and thoracic segments. We conclude that the subatmospheric tissue pressure applied to the posterior membrane of the cervical trachea results in part from transmission of apical pleural pressure into the neck. Transmural pressure for cervical and thoracic tracheal segments is therefore similar.


1993 ◽  
Vol 75 (5) ◽  
pp. 2234-2238 ◽  
Author(s):  
A. Xie ◽  
Y. Takasaki ◽  
T. D. Bradley

We measured electromyographic activity of the diaphragm (EMGdi) and scalene (EMGsc) during isocapnic progressive hypoxic ventilatory responses in five normal males in the supine and upright seated positions. The slope of the regression line relating EMGdi expressed as a percentage of maximum to percent fall in arterial oxyhemoglobin saturation was 93% steeper upright than supine (P < 0.005), whereas the slope of EMGdi activity to minute volume of ventilation was 73% higher upright than supine (P < 0.05). In addition, the slope of EMGsc activity relative to percent fall in arterial oxyhemoglobin saturation and minute ventilation was greater upright than supine (151%, P < 0.001 and 61%, P = 0.056, respectively). Greater EMGsc activity upright than supine was similar to findings during hypercapnic rebreathing. However, the greater EMGdi activity upright than supine stands in contrast to hypercapnic rebreathing where it was previously shown that EMGdi activity was not affected by a change in body position. We conclude that during hypoxic ventilatory responses both EMGdi and EMGsc activities are more pronounced upright than supine. Diaphragmatic activation during progressive hypoxia in response to a change in body position is different from that seen during progressive hypercapnia.


2010 ◽  
Vol 109 (1) ◽  
pp. 87-94 ◽  
Author(s):  
N. P. S. Murray ◽  
D. K. McKenzie ◽  
S. C. Gandevia ◽  
J. E. Butler

The reflex mechanism of the short-latency inhibitory reflex to transient loading of human inspiratory muscles is unresolved. Muscle afferents mediate this reflex, but they may act via pontomedullary inspiratory centers, other bulbar networks, or spinal circuits. We hypothesized that altered chemical drive to breathe would alter the initial inhibitory reflex if the neural pathways involve inspiratory medullary centers. Inspiration was transiently loaded in 11 subjects during spontaneous hypercapnic hyperpnea and matched voluntary hyperventilation. Electromyographic activity was recorded bilaterally from scalene muscles with surface electrodes. The latencies of the initial inhibitory response (IR) onset (32 ± 0.7 and 38 ± 1 ms for spontaneous and voluntary conditions respectively, P < 0.001) and subsequent excitatory response (ER) onset (80 ± 2.9 and 78 ± 2.6 ms, respectively, P = 0.46) and the normalized sizes of IR (65 ± 2 and 67 ± 3%, respectively, P = 0.50) and ER (51 ± 8 and 69 ± 6%, respectively, P = 0.005) were measured. Mean end-tidal Pco2 was 43 ± 1.5 Torr with dead space ventilation and was 14 ± 0.6 Torr with matched voluntary hyperventilation ( P < 0.001). A mean minute volume >30 liters was achieved in both conditions. The absence of significant difference in the size of the IR suggested that the IR reflex arc does not transit the brain stem inspiratory centers and that the reflex may be integrated at a spinal level. In voluntary hyperventilation, an initial excitation occurred more frequently and, consequently, the IR onset latency was significantly longer. The size of the later ER was also greater during voluntary hyperventilation, which is consistent with it being mediated via longer, presumably cortical, pathways, which are influenced by voluntary drive.


1996 ◽  
Vol 81 (4) ◽  
pp. 1471-1476 ◽  
Author(s):  
Shaoping Zhang ◽  
Vicki Garbutt ◽  
John T. McBride

Zhang, Shaoping, Vicki Garbutt, and John T. McBride.Strain-induced growth of the immature lung. J. Appl. Physiol. 81(4): 1471–1476, 1996.—To investigate the relationship between strain and postnatal lung growth, two groups of weanling ferrets were tracheotomized: the study group was exposed for 2 wk to a continuous positive airway pressure (CPAP) of 6 cmH2O and the other group was exposed to atmospheric pressure (control). Total lung capacity after 2 wk was ∼40% higher in the CPAP-exposed animals than in the control animals ( n = 19 for the control group and 18 for the study group; P < 0.01). CPAP exposure was also associated with increases in lung weight and total lung protein and DNA contents. Lung recoil, measured in a subgroup of animals, was characterized by air-filled and saline-filled static expiratory pressure-volume curves. Neither in the air-filled lungs nor in the saline-filled lungs was there a significant difference between CPAP-exposed and control animals in lung recoil at equal fractions of total lung capacity. These data indicate that mechanical strain was associated with an acceleration of lung growth in immature ferrets. The preservation of volume-corrected lung recoil and the expected contribution of surface forces and tissue forces to lung recoil in CPAP-exposed animals suggest that this response did not involve simple lung distension but included a remodeling of the lung parenchyma.


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