Effects of expiratory loading on respiration in humans

1980 ◽  
Vol 49 (4) ◽  
pp. 601-608 ◽  
Author(s):  
B. Gothe ◽  
N. S. Cherniack

We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.

1983 ◽  
Vol 55 (3) ◽  
pp. 929-934 ◽  
Author(s):  
T. M. Michiels ◽  
R. W. Light ◽  
C. K. Mahutte

The respiratory depressant effects of ethanol and their potential reversibility by naloxone were studied in 10 normal subjects. Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia without and with an inspiratory resistive load (13 cmH2O X 1(-1) X S) were measured. The resistive load detected with 50% probability (delta R50) and the exponent (n) in Stevens' psychophysical law for magnitude estimation of resistive loads were studied using standard psychophysical techniques. Each of these studies was performed before ethanol ingestion, after ethanol ingestion (1.5 ml/kg, by mouth), and then again after naloxone (0.8 mg iv). Ethanol increased delta R50 (P less than 0.05) and decreased n (P less than 0.05). Naloxone caused no further change in these parameters. The load compensation (Lc), defined as the ratio of loaded to unloaded response slopes, was not significantly changed after ethanol and naloxone. No correlation was found between the Lc and delta R50 or n. The ventilatory and P0.1 responses to hypercapnia and hypoxia with and without inspiratory resistive loading decreased after ethanol (P less than 0.05, hypercapnia; NS, hypoxia). After naloxone the hypercapnic ventilatory responses increased (P less than 0.05). This suggests that the respiratory depressant effects of ethanol may be mediated via endorphins.


1987 ◽  
Vol 62 (5) ◽  
pp. 2026-2030 ◽  
Author(s):  
C. G. Alex ◽  
R. M. Aronson ◽  
E. Onal ◽  
M. Lopata

To study the effects of continuous positive airway pressure (CPAP) on lung volume, and upper airway and respiratory muscle activity, we quantitated the CPAP-induced changes in diaphragmatic and genioglossal electromyograms, esophageal and transdiaphragmatic pressures (Pes and Pdi), and functional residual capacity (FRC) in six normal awake subjects in the supine position. CPAP resulted in increased FRC, increased peak and rate of rise of diaphragmatic activity (EMGdi and EMGdi/TI), decreased peak genioglossal activity (EMGge), decreased inspiratory time and inspiratory duty cycle (P less than 0.001 for all comparisons). Inspiratory changes in Pes and Pdi, as well as Pes/EMGdi and Pdi/EMGdi also decreased (P less than 0.001 for all comparisons), but mean inspiratory airflow for a given Pes increased (P less than 0.001) on CPAP. The increase in mean inspiratory airflow for a given Pes despite the decrease in upper airway muscle activity suggests that CPAP mechanically splints the upper airway. The changes in EMGge and EMGdi after CPAP application most likely reflect the effects of CPAP and the associated changes in respiratory system mechanics on the afferent input from receptors distributed throughout the intact respiratory system.


1991 ◽  
Vol 70 (1) ◽  
pp. 158-168 ◽  
Author(s):  
K. G. Henke ◽  
J. A. Dempsey ◽  
M. S. Badr ◽  
J. M. Kowitz ◽  
J. B. Skatrud

To investigate the response of inspiratory and expiratory muscles to naturally occurring inspiratory resistive loads in the absence of conscious control, five male "snorers" were studied during non-rapid-eye-movement (NREM) sleep with and without continuous positive airway pressure (CPAP). Diaphragm (EMGdi) and scalene (EMGsc) electromyographic activity were monitored with surface electrodes and abdominal EMG activity (EMGab) with wire electrodes. Subjects were studied in the following conditions: 1) awake, 2) stage 2 sleep, 3) stage 3/4 sleep, 4) CPAP during stage 3/4 sleep, 5) CPAP plus end-tidal CO2 pressure (PETCO2) isocapnic to stage 2 sleep, and 6) CPAP plus PETCO2 isocapnic to stage 3/4 sleep. Inspired pulmonary resistance (RL) at peak flow rate and PETCO2 increased in all stages of sleep. Activity of EMGdi, EMGsc, and EMGab increased significantly in stage 3/4 sleep. CPAP reduced RL at peak flow, increased tidal volume and expired ventilation, and reduced PETCO2. EMGdi and EMGsc were reduced, and EMGab was silenced. During CPAP, with CO2 added to make PETCO2 isocapnic to stage 3/4 sleep, EMGsc and EMGab increased, but EMGdi was augmented in only one-half of the trials. EMG activity in this condition, however, was only 75% (EMGsc) and 43% (EMGab) of the activity observed during eupneic breathing in stage 3/4 sleep when PETCO2 was equal but RL was much higher. We conclude that during NREM sleep 1) inspiratory and expiratory muscles respond to internal inspiratory resistive loads and the associated dynamic airway narrowing and turbulent flow developed throughout inspiration, 2) some of the augmentation of respiratory muscle activity is also due to the hypercapnia that accompanies loading, and 3) the abdominal muscles are the most sensitive to load and CO2 and the diaphragm is the least sensitive.


1982 ◽  
Vol 52 (3) ◽  
pp. 748-756 ◽  
Author(s):  
K. Axen

Load compensation in 29 cervical cord-injured men was inferred from the difference between actual first-breath responses to graded elastic and resistive loads and those calculated assuming identical respiratory muscle pressure (Pmus) wave forms in the unloaded and loaded states (i.e., the passive prediction). At every load, respiratory frequency (f) and tidal volume (VT) responses from different individuals formed a continuum ranging from a weak VT defense coupled with an increased f to a strong VT defense coupled with a decreased f. Individual VT responses ranged from values smaller than the passive prediction to values exceeding control, suggesting that phrenic motoneuron output was not constant but decreased in some subjects and increased in others. In support of this hypothesis, 1) individual VT responses varied with inspiratory duration (TI; P less than 0.01); 2) TI responses indicated some subjects prematurely terminated their phrenic motoneuron output, whereas others prolonged it; 3) VT/TI responses suggested that some subjects modified the discharge frequency of their phrenic output; and 4) rib cage instability contributed insignificantly to these responses. These findings, which are similar to those reported for normal men, indicate that 1) afferent pathways from the rib cage and intercostal muscles are not required for the initiation of a range of ventilatory responses to loads; and 2) afferent pathways from the mouth, lung, and/or diaphragm are sufficient, by themselves, to modulate the duration, intensity, and timing of the phrenic discharge during the first loaded breath.


1991 ◽  
Vol 71 (5) ◽  
pp. 1941-1948 ◽  
Author(s):  
M. Ramonatxo ◽  
J. Mercier ◽  
R. Cohendy ◽  
C. Prefaut

In healthy subjects, we compared the effects of an expiratory (ERL) and an inspiratory (IRL) resistive load (6 cmH2O.l-1.s) with no added resistive load on the pattern of respiratory muscle recruitment during exercise. Fifteen male subjects performed three exercise tests at 40% of maximum O2 uptake: 1) with no-added-resistive load (control), 2) with ERL, and 3) with IRL. In all subjects, we measured breathing pattern and mouth occlusion pressure (P0.1) from the 3rd min of exercise, in 10 subjects O2 uptake (VO2), CO2 output (VCO2), and respiratory exchange ratio (R), and in 5 subjects we measured gastric (Pga), pleural (Ppl), and transdiaphragmatic (Pdi) pressures. Both ERL and IRL induced a high increase of P0.1 and a decrease of minute ventilation. ERL induced a prolongation of expiratory time with a reduction of inspiratory time (TI), mean expiratory flow, and ratio of inspiratory to total time of the respiratory cycle (TI/TT). IRL induced a prolongation of TI with a decrease of mean inspiratory flow and an increase of tidal volume and TI/TT. With ERL, in two subjects, Pga increased and Ppl decreased more during inspiration than during control suggesting that the diaphragm was the most active muscle. In one subject, the increases of Ppl and Pga were weak; thus Pdi increased very little. In the two other subjects, Ppl decreased more during inspiration but Pga also decreased, leading to a decrease of Pdi. This suggests a recruitment of abdominal muscles during expiration and of accessory and intercostal muscles during inspiration. With IRL, in all subjects, Ppl again decreased more, Pga began to decrease until 40% of TI and then increased.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 60 (5) ◽  
pp. 1471-1481 ◽  
Author(s):  
V. Im Hof ◽  
P. West ◽  
M. Younes

Tidal volume (VT) is usually preserved when conscious humans are made to breathe against an inspiratory resistance. To identify the neural changes responsible for VT compensation we calculated the respiratory driving pressure waveform during steady-state unloaded and loaded breathing (delta R = 8.5 cmH2O X 1(-1) X s) in eight conscious normal subjects. Driving pressure (DP) was calculated according to the method of Younes et al. (J. Appl. Physiol. 51: 963–989, 1981), which provides the equivalent of occlusion pressure at functional residual capacity throughout the breath. VT during resistance breathing was 108% of unloaded VT, as opposed to a predicted value of 82% of control in the absence of neural compensation. Compensation was accomplished through three changes in the DP waveform: 1) peak amplitude increased (+/- 23%), 2) the duration of the rising phase increased (+42%); and 3) the rising phase became more concave to the time axis. There were no changes in the relative decay rate of inspiratory pressure during expiration, in the shape of the declining phase of DP, or in end-expiratory lung volume.


1995 ◽  
Vol 82 (1) ◽  
pp. 6-19 ◽  
Author(s):  
David O. Warner ◽  
Mark A. Warner ◽  
Erik L. Ritman

Background Data concerning chest wall configuration and the activities of the major respiratory muscles that determine this configuration during anesthesia in humans are limited. The aim of this study was to determine the effects of halothane anesthesia on respiratory muscle activity and chest wall shape and motion during spontaneous breathing. Methods Six human subjects were studied while awake and during 1 MAC halothane anesthesia. Respiratory muscle activity was measured using fine-wire electromyography electrodes. Chest wall configuration was determined using images of the thorax obtained by three-dimensional fast computed tomography. Tidal changes in gas volume were measured by integrating respiratory gas flow, and the functional residual capacity was measured by a nitrogen dilution technique. Results While awake, ribcage expansion was responsible for 25 +/- 4% (mean +/- SE) of the total change in thoracic volume (delta Vth) during inspiration. Phasic inspiratory activity was regularly present in the diaphragm and parasternal intercostal muscles. Halothane anesthesia (1 MAC) abolished activity in the parasternal intercostal muscles and increased phasic expiratory activity in the abdominal muscles and lateral ribcage muscles. However, halothane did not significantly change the ribcage contribution to delta Vth (18 +/- 4%). Intrathoracic blood volume, measured by comparing changes in total thoracic volume and gas volume, increased significantly during inspiration both while awake and while anesthetized (by approximately 20% of delta Vth, P < 0.05). Halothane anesthesia significantly reduced the functional residual capacity (by 258 +/- 78 ml), primarily via an inward motion of the end-expiratory position of the ribcage. Although the diaphragm consistently changed shape, with a cephalad displacement of posterior regions and a caudad displacement of anterior regions, the diaphragm did not consistently contribute to the reduction in the functional residual capacity. Halothane anesthesia consistently increased the curvature of the thoracic spine measured in the saggital plane. Conclusions The authors conclude that (1) ribcage expansion is relatively well preserved during halothane anesthesia despite the loss of parasternal intercostal muscle activity; (2) an inward displacement of the ribcage accounts for most of the decrease in functional residual capacity caused by halothane anesthesia, accompanied by changes in diaphragm shape that may be related to motion of its insertions on the thoracoabdominal wall; and (3) changes in intrathoracic blood volume constitute a significant fraction of delta Vth during tidal breathing.


1959 ◽  
Vol 14 (3) ◽  
pp. 279-283 ◽  
Author(s):  
William A. Spencer ◽  
Carlos Vallbona

A method is described for the reproduction of the natural inspiratory capacity in healthy subjects utilizing a pressure breathing device capable of delivering high inflow rates at low pressures (1.3 l/sec. at 5 cm of water in the delivery system). A highly significant correlation was found between natural inspiratory capacity and the estimation of inspiratory capacity carried out in this manner in healthy subjects. The reliability of this method in cooperative individuals suggested applicability in patients with respiratory muscle paralysis when maximum natural inspiration is impossible. In poliomyelitis subjects with respiratory muscle paralysis the values of estimated inspiratory capacity were significantly reduced below those found in health. The degree of reduction was not directly related to the diminution of natural inspiratory capacity or to the maximum volume changes that could be produced by means of tank respirator assistance at comparable peak transthoracic pressures. Measurement of inspiratory capacity with this technique together with the determination of functional residual capacity makes it practical to estimate the total lung capacity and thus describe the lung compartments in such subjects. Submitted on June 10, 1958


1980 ◽  
Vol 59 (6) ◽  
pp. 493-495 ◽  
Author(s):  
K. J. Killian ◽  
C. K. Mahutte ◽  
E. J. M. Campbell

1. By using standard psychophysical techniques resistive load detection was estimated in five normal subjects during spontaneous breathing and during passive ventilation in a Drinker respirator. 2. During assisted ventilation a gross deterioration in resistive load detection occurred. 3. The findings imply that active respiratory muscle contraction plays an essential role in the detection of added resistive loads.


1981 ◽  
Vol 50 (1) ◽  
pp. 162-164 ◽  
Author(s):  
N. K. Burki

To examine the effects of continuously added background inspiratory loads on the difference thresholds for resistive (delta R50) and elastic load detection (delta E50), 12 healthy subjects were studied. The results showed that, whereas the addition of a constant background elastic load significantly altered delta R50, the addition of a constant background resistive load did not significantly affect delta E 50. These results can be explained on the basis that the addition of a constant elastic load alters the total sensory information a midbreath, where resistive load detection occurs, but the addition of a constant resistive load does not affect elastic load detection, which occurs at the end of the breath where flow-dependent information is minimal.


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