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1
el-Manshawi, A., K. J. Killian, E. Summers, and N. L. Jones. "Breathlessness during exercise with and without resistive loading." Journal of Applied Physiology 61, no. 3 (September 1, 1986): 896–905. http://dx.doi.org/10.1152/jappl.1986.61.3.896.
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The purpose of this study was to quantify the intensity of breathlessness associated with exercise and respiratory resistive loading, with the specific purpose of isolating the quantitative contributions of inspiratory pressure, length, velocity, and frequency of inspiratory muscle shortening and duty cycle to breathlessness. The intensity of inspiratory pressure was quantified by measurement of estimated esophageal pressure (Pes = pressure at the mouth plus lung pressure), the extent of shortening by tidal volume (VT), and the velocity of shortening by inspiratory flow rate (VI). Six normal subjects underwent five incremental (100 kpm X min-1 X min-1) exercise tests on a cycle ergometer to maximum capacity. The first and last test were unloaded and the intervening tests were performed with external added resistances of 33, 57, and 73 cm H2O X l-1 X s in random order. The resistances were selected to provide a range of pressures, tidal volumes, flow rates, and patterns of breathing. At rest and at the end of each minute during exercise the subjects estimated the intensity of breathlessness (psi) by selecting a number ranging from 0 to 10 (Borg rating scale, 0 indicating no appreciable breathlessness and 10 the maximum tolerable sensation). Breathlessness was significantly and independently related to Pes (P less than 0.0001), VI (P less than 0.0001), frequency of breathing (fb) (P less than 0.01), and duty cycle [ratio of inspiratory duration to total breath duration (TI/TT)] (P less than 0.01): psi = 0.11 Pes + 0.61 VI + 1.99 TI/TT + 0.04 fb - 2.60 (r = 0.83). The results suggest that peak pressure (tension), VI (velocity of inspiratory muscle shortening), TI/TT, and fb contribute independently and collectively to breathlessness. The perception of respiratory muscle effort is ideally suited to subserve this sensation. The neurophysiological mechanism purported is a conscious awareness of the intensity of the outgoing motor command by means of corollary discharge within the central nervous system.
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Tarasiuk, A., S. M. Scharf, and M. J. Miller. "Effect of chronic resistive loading on inspiratory muscles in rats." Journal of Applied Physiology 70, no. 1 (January 1, 1991): 216–22. http://dx.doi.org/10.1152/jappl.1991.70.1.216.
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The development of animal models of respiratory muscle training would be useful in studying the physiological effects of training. Hence, we studied the effects of chronic resistive loading (CRL) for 5 wk on mass, composition, and mechanics of inspiratory muscles in laboratory rats. CRL was produced by means of a tracheal cannula (loaded animals) and results were compared with sham-operated controls. Acutely, upper airway obstruction led to a doubling of inspiratory pleural pressure excursion and 25% decrease in respiratory rate. We observed no changes in lung pressure-volume curves, nor in the geometry of the respiratory system in loaded compared with control animals. Muscle mass normalized for body mass increased in the diaphragm (DI) and the wet weight-to-dry weight ratio increased in the sternomastoid (SM) in loaded compared with control animals. Loaded animals demonstrated a decrease in ether extractable (fat) content of the DI and SM muscles but not the gastrocnemius. For the DI there was no change in length at which active tension was maximal (Lo), but there was an increase in maximum tension at lengths close to Lo in loaded compared with control rats. Endurance did not change, although twitch tensions remained higher in loaded compared with control rats. We conclude that 1) alteration of inspiratory muscle structure and function occurs in rats with CRL; 2) the DI and SM demonstrate different adaptive responses to CRL; and 3) although maximum tension increases, endurance does not.
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Davenport, P. W., D. J. Dalziel, B. Webb, J. R. Bellah, and C. J. Vierck. "Inspiratory resistive load detection in conscious dogs." Journal of Applied Physiology 70, no. 3 (March 1, 1991): 1284–89. http://dx.doi.org/10.1152/jappl.1991.70.3.1284.
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The physiological mechanisms mediating the detection of mechanical loads are unknown. This is, in part, due to the lack of an animal model of load detection that could be used to investigate specific sensory systems. We used American Foxhounds with tracheal stomata to behaviorally condition the detection of inspiratory occlusion and graded resistive loads. The resistive loads were presented with a loading manifold connected to the inspiratory port of a non-rebreathing valve. The dogs signaled detection of the load by lifting their front paw off a lever. Inspiratory occlusion was used as the initial training stimulus, and the dogs could reliably respond within the first or second inspiratory effort to 100% of the occlusion presentations after 13 trials. Graded resistances that spanned the 50% detection threshold were then presented. The detection threshold resistances (delta R50) were 0.96 and 1.70 cmH2O.l-1.s. Ratios of delta R50 to background resistance were 0.15 and 0.30. The near-threshold resistive loads did not significantly change expired PCO2 or breathing patterns. These results demonstrate that dogs can be conditioned to reliably and specifically signal the detection of graded inspiratory mechanical loads. Inspiration through the tracheal stoma excludes afferents in the upper extrathoracic trachea, larynx, pharynx, nasal passages, and mouth from mediating load detection in these dogs. It is unknown which remaining afferents (vagal or respiratory muscle) are responsible for load detection.
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Kosch, P. C., P. W. Davenport, J. A. Wozniak, and A. R. Stark. "Reflex control of inspiratory duration in newborn infants." Journal of Applied Physiology 60, no. 6 (June 1, 1986): 2007–14. http://dx.doi.org/10.1152/jappl.1986.60.6.2007.
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We applied graded resistive and elastic loads and total airway occlusions to single inspirations in six full-term healthy infants on days 2–3 of life to investigate the effect on neural and mechanical inspiratory duration (TI). The infants breathed through a face mask and pneumotachograph, and flow, volume, airway pressure, and diaphragm electromyogram (EMG) were recorded. Loads were applied to the inspiratory outlet of a two-way respiratory valve using a manifold system. Application of all loads resulted in inspired volumes decreased from control (P less than 0.001), and changes were progressive with increasing loads. TI measured from the pattern of the diaphragm EMG (TIEMG) was prolonged from control by application of all elastic and resistive loads and by total airway occlusions, resulting in a single curvilinear relationship between inspired volume and TIEMG that was independent of inspired volume trajectory. In contrast, when TI was measured from the pattern of airflow, the effect of loading on the mechanical time constant of the respiratory system resulted in different inspired volume-TI relationships for elastic and resistive loads. Mechanical and neural inspired volume and duration of the following unloaded inspiration were unchanged from control values. These findings indicate that neural inspiratory timing in infants depends on magnitude of phasic volume change during inspiration. They are consistent with the hypothesis that termination of inspiration is accomplished by an “off-switch” mechanism and that inspired volume determines the level of vagally mediated inspiratory inhibition to trigger this mechanism.
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Puddy, A., G. Giesbrecht, R. Sanii, and M. Younes. "Mechanism of detection of resistive loads in conscious humans." Journal of Applied Physiology 72, no. 6 (June 1, 1992): 2267–70. http://dx.doi.org/10.1152/jappl.1992.72.6.2267.
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Conscious humans easily detect loads applied to the respiratory system. Resistive loads as small as 0.5 cmH2O.l-1.s can be detected. Previous work suggested that afferent information from the chest wall served as the primary source of information for load detection, but the evidence for this was not convincing, and we recently reported that the chest wall was a relatively poor detector for applied elastic loads. Using the same setup of a loading device and body cast, we sought resistive load detection thresholds under three conditions: 1) loading of the total respiratory system, 2) loading such that the chest wall was protected from the load but airway and intrathoracic pressures experienced negative pressure in proportion to inspiratory flow, and 3) loading of the chest wall alone with no alteration of airway or intrathoracic pressure. The threshold for detection for the three types of load application in seven normal subjects was 1.17 +/- 0.33, 1.68 +/- 0.45, and 6.3 +/- 1.38 (SE) cmH2O.l-1.s for total respiratory system, chest wall protected, and chest wall alone, respectively. We conclude that the active chest wall is a less potent source of information for detection of applied resistive loads than structures affected by negative airway and intrathoracic pressure, a finding similar to that previously reported for elastic load detection.
6
Brancatisano, T. P., D. S. Dodd, P. W. Collett, and L. A. Engel. "Effect of expiratory loading on glottic dimensions in humans." Journal of Applied Physiology 58, no. 2 (February 1, 1985): 605–11. http://dx.doi.org/10.1152/jappl.1985.58.2.605.
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We examined the effects of external mechanical loading on glottic dimensions in 13 normal subjects. When flow-resistive loads of 7, 27, and 48 cmH2O X l-1 X s, measured at 0.2 l/s, were applied during expiration, glottic width at the mid-tidal volume point in expiration (dge) was 2.3 +/- 12, 37.9 +/- 7.5, and 38.3 +/- 8.9% (means +/- SE) less than the control dge, respectively. Simultaneously, mouth pressure (Pm) increased by 2.5 +/- 4, 3.0 +/- 0.4, and 4.6 +/- 0.6 cmH2O, respectively. When subjects were switched from a resistance to a positive end-expiratory pressure at comparable values of Pm, both dge and expiratory flow returned to control values, whereas the level of hyperinflation remained constant. Glottic width during inspiration (unloaded) did not change on any of the resistive loads. There was a slight inverse relationship between the ratio of expiratory to inspiratory glottic width and the ratio of expiratory to inspiratory duration. Our results show noncompensatory glottic narrowing when subjects breathe against an expiratory resistance and suggest that the glottic dimensions are influenced by the time course of lung emptying during expiration. We speculate that the glottic constriction is related to the increased activity of expiratory medullary neurons during loaded expiration and, by increasing the internal impedance of the respiratory system, may have a stabilizing function.
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Mengeot, P. M., J. H. Bates, and J. G. Martin. "Effect of mechanical loading on displacements of chest wall during breathing in humans." Journal of Applied Physiology 58, no. 2 (February 1, 1985): 477–84. http://dx.doi.org/10.1152/jappl.1985.58.2.477.
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Using a respiratory inductive plethysmograph (Respitrace) we studied thoracoabdominal movements in eight normal subjects during inspiratory resistive (Res) and elastic (El) loading. The magnitude of loads was chosen so as to produce a fall in inspiratory mouth pressure of 20 cmH2O. The contribution of rib cage (RC) to tidal volume (VT) increased significantly from 68% during quiet breathing (QB) to 74% during El and 78% during Res. VT and breathing frequency did not change significantly. During loading a phase lag was present on inspiration so that the abdomen led the rib cage. However, outward movement of the abdomen ceased in the latter part of inspiration, and the RC became the sole contributor to VT. These observations suggest greater recruitment of the inspiratory musculature of the RC than the diaphragm during loading, although changes in the mechanical properties of the chest wall may also have contributed. Indeed, an increase in abdominal end-expiratory and end-inspiratory pressures was observed in five out of six subjects, indicating abdominal muscle recruitment which may account for part of the reduction in abdominal excursion. Both Res and El increased the rate of emptying of the respiratory system during the ensuing unloaded expiration as a result of a reduction in rib cage expiratory-braking mechanisms. The time course of abdominal displacements during expiration was unaffected by loading.
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Fernandes, Andréia K., Bruna Ziegler, Glauco L. Konzen, Paulo R. S. Sanches, André F. Müller, Rosemary P. Pereira, and Paulo de Tarso R. Dalcin. "Repeatability of the Evaluation of Perception of Dyspnea in Normal Subjects Assessed Through Inspiratory Resistive Loads." Open Respiratory Medicine Journal 8, no. 1 (December 26, 2014): 41–47. http://dx.doi.org/10.2174/1874306401408010041.
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Purpose: Study the repeatability of the evaluation of the perception of dyspnea using an inspiratory resistive loading system in healthy subjects. Methods: We designed a cross sectional study conducted in individuals aged 18 years and older. Perception of dyspnea was assessed using an inspiratory resistive load system. Dyspnea was assessed during ventilation at rest and at increasing resistive loads (0.6, 6.7, 15, 25, 46.7, 67, 78 and returning to 0.6 cm H2O/L/s). After breathing in at each level of resistive load for two minutes, the subject rated the dyspnea using the Borg scale. Subjects were tested twice (intervals from 2 to 7 days). Results: Testing included 16 Caucasian individuals (8 male and 8 female, mean age: 36 years). The median scores for dyspnea rating in the first test were 0 at resting ventilation and 0, 2, 3, 4, 5, 7, 7 and 1 point, respectively, with increasing loads. The median scores in the second test were 0 at resting and 0, 0, 2, 2, 3, 4, 4 and 0.5 points, respectively. The intra-class correlation coefficient was 0.57, 0.80, 0.74, 0.80, 0.83, 0.86, 0.91, and 0.92 for each resistive load, respectively. In a generalized linear model analysis, there was a statistically significant difference between the levels of resistive loads (p<0.001) and between tests (p=0.003). Dyspnea scores were significantly lower in the second test. Conclusion: The agreement between the two tests of the perception of dyspnea was only moderate and dyspnea scores were lower in the second test. These findings suggest a learning effect or an effect that could be at least partly attributed to desensitization of dyspnea sensation in the brain.
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Kosch, P. C., P. W. Davenport, J. A. Wozniak, and A. R. Stark. "Reflex control of expiratory duration in newborn infants." Journal of Applied Physiology 58, no. 2 (February 1, 1985): 575–81. http://dx.doi.org/10.1152/jappl.1985.58.2.575.
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We investigated the effect on expiratory duration (TE) of application of graded resistive and elastic loads and total airway occlusions to single expirations in 9 full-term healthy infants studied on the 2nd or 3rd day of life. The infants breathed through a face mask and pneumotachograph, and flow, volume, airway pressure, and diaphragm electromyogram (EMG) were recorded. Loads were applied to the expiratory outlet of a two-way respiratory valve using a manifold system. Application of all loads resulted in expired volumes (VE) decreased from control (P less than 0.05), and changes were progressive with increasing loads. As VE became smaller, end-expiratory volume (EEV) became greater. TE, measured either from the pattern of airflow or airway pressure, or from diaphragm EMG activity, progressively increased with increasing loads and was greatest with total occlusions (P less than 0.05, compared with control). Resistive loading resulted in a greater accumulated VE history than elastic loading to the same EEV. For equivalent changes in EEV, TE was more prolonged with resistive than with elastic loading. Expiratory loading did not change the inspiratory duration determined from the diaphragm EMG activity of the breath immediately following each loaded expiration. These findings in infants are consistent with an integrative neural mechanism that modulates TE in response to the accumulated VE history, including both EEV and rate of lung deflation.
10
Mortola, Jacopo P., Anne Marie Lauzon, and Brian Mott. "Expiratory flow pattern and respiratory mechanics." Canadian Journal of Physiology and Pharmacology 65, no. 6 (June 1, 1987): 1142–45. http://dx.doi.org/10.1139/y87-180.
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During resting breathing, expiration is characterized by the narrowing of the vocal folds which, by increasing the expiratory resistance, raises mean lung volume and airway pressure. This is even more pronounced in the neonatal period, during which expirations with short complete airway closure are commonly occurring. We asked to which extent differences in expiratory flow pattern may modify the inspiratory impedance of the respiratory system. To this aim, newborn puppies, piglets, and adult rats were anesthetized, paralyzed, and ventilated with different expiratory patterns, (a) no expiratory load, (b) expiratory resistive load, and (c) end-inspiratory pause. The stroke volume of the ventilator and inspiratory and expiratory times were maintained constant, and the loads were adjusted in such a way that inflation always started from the resting volume of the respiratory system. After 1 min of each ventilatory pattern, mean inspiratory impedance and compliance of lung and respiratory system were measured. The values were unchanged or minimally altered by changing the type of ventilation. We conclude that the expiratory laryngeal loading is not primarily aimed to decrease the work of breathing. It is conceivable that the expiratory pattern is oriented to increase and control mean airway pressure in the regulation of pulmonary fluid reabsorption, distribution of ventilation, and diffusion of gases.
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Orr, R. S., A. S. Jordan, P. Catcheside, N. A. Saunders, and R. D. McEvoy. "Sustained isocapnic hypoxia suppresses the perception of the magnitude of inspiratory resistive loads." Journal of Applied Physiology 89, no. 1 (July 1, 2000): 47–55. http://dx.doi.org/10.1152/jappl.2000.89.1.47.
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The sensation of increased respiratory resistance or effort is likely to be important for the initiation of alerting or arousal responses, particularly in sleep. Hypoxia, through its central nervous system-depressant effects, may decrease the perceived magnitude of respiratory loads. To examine this, we measured the effect of isocapnic hypoxia on the ability of 10 normal, awake males (mean age = 24.0 ± 1.8 yr) to magnitude-scale five externally applied inspiratory resistive loads (mean values from 7.5 to 54.4 cmH2O · l−1 · s). Each subject scaled the loads during 37 min of isocapnic hypoxia (inspired O2 fraction = 0.09, arterial O2 saturation of ∼80%) and during 37 min of normoxia, using the method of open magnitude numerical scaling. Results were normalized by modulus equalization to allow between-subject comparisons. With the use of peak inspiratory pressure (PIP) as the measure of load stimulus magnitude, the perception of load magnitude (Ψ) increased linearly with load and, averaged for all loaded breaths, was significantly lower during hypoxia than during normoxia (20.1 ± 0.9 and 23.9 ± 1.3 arbitrary units, respectively; P = 0.048). Ψ declined with time during hypoxia ( P = 0.007) but not during normoxia ( P= 0.361). Our result is remarkable because PIP was higher at all times during hypoxia than during normoxia, and previous studies have shown that an elevation in PIP results in increased Ψ. We conclude that sustained isocapnic hypoxia causes a progressive suppression of the perception of the magnitude of inspiratory resistive loads in normal subjects and could, therefore, impair alerting or arousal responses to respiratory loading.
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Petrozzino, J. J., A. T. Scardella, J. K. Li, N. Krawciw, N. H. Edelman, and T. V. Santiago. "Effect of naloxone on spectral shifts of the diaphragm EMG during inspiratory loading." Journal of Applied Physiology 68, no. 4 (April 1, 1990): 1376–85. http://dx.doi.org/10.1152/jappl.1990.68.4.1376.
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Shifts in the power spectrum of the diaphragm EMG to lower frequencies may occur in the presence of fatiguing inspiratory flow-resistive loads (IRL). However, such a shift of the centroid frequency (fc) could follow a reduction in central output through a differential reduction in end-inspiratory high-frequency power (HFP). In unanesthetized goats, we tested the hypothesis that activation of the endogenous opioid system by IRL would differentially reduce central respiratory output, causing a reduction in fc. IRL was imposed for 180 min after which naloxone (0.1 mg/kg, NLX) was given. fc was computed from the power spectral density estimated by the Welch method. IRL reduced fc from 148.0 +/- 9.8 (SE) Hz at base line to 141.1 +/- 8.9 Hz or to 95.5 +/- 1.3% of base line by 180 min (both P less than 0.05). NLX increased fc to 148.9 +/- 9.9 Hz or to 100.6 +/- 1.1% of base line (both P less than 0.05). The decline in fc during IRL was found to be the result of a reduction in HFP, predominantly toward the end of inspiration. The reversibility of this fc shift with NLX suggests a central mechanism consequent to elaboration of endogenous opioids and not a peripheral (muscular) event consequent to muscle fatigue.
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Akiyama, Y., R. E. Garcia, L. J. Prochaska, and A. R. Bazzy. "Effect of chronic respiratory loading on the subunit composition of cytochrome c oxidase in the diaphragm." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 3 (September 1, 1994): L350—L355. http://dx.doi.org/10.1152/ajplung.1994.267.3.l350.
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To elucidate in the diaphragm, 1) whether chronic inspiratory loading increases the amount of cytochrome c oxidase (COX) subunit proteins, and 2) how well the regulation of mitochondrially and nuclearly coded COX subunits is coordinated, we have trained six adult sheep with inspiratory flow-resistive loads for 3 h/day for 3 wk. Six other sheep served as controls. Proteins from crude muscle homogenates were separated using sodium dodecyl sulfate polyacrylamide gel electrophoresis, immunoblotted, and reacted with polyclonal rabbit anti-bovine COX antibodies. A mitochondrially coded subunit (II) and nuclearly coded subunits (IV and VII) reacted with anti-COX antibodies and were quantified with laser densitometry using purified COX as a standard. In the costal diaphragm and for the equivalent amount of muscle homogenate protein, the integrated optical densities (IOD) for subunits II, IV, and VII were significantly greater in the trained sheep than in the controls. Similarly, the IOD for subunits II and VII were significantly greater in the trained than in the controls in the crural diaphragm. There were no differences between the two groups in the quadriceps, a muscle that was used as an untrained, internal control muscle. The ratios of the IOD for each of the two nuclearly coded subunits to that for mitochondrially coded subunit II were not different between the two groups. These data suggest that chronic inspiratory loading increases both mitochondrially and nuclearly coded COX subunits in the diaphragm and that the subunits coded by the two genetic systems are coordinately regulated.
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Onal, E., D. L. Burrows, R. H. Hart, and M. Lopata. "Induction of periodic breathing during sleep causes upper airway obstruction in humans." Journal of Applied Physiology 61, no. 4 (October 1, 1986): 1438–43. http://dx.doi.org/10.1152/jappl.1986.61.4.1438.
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To test the hypothesis that occlusive apneas result from sleep-induced periodic breathing in association with some degree of upper airway compromise, periodic breathing was induced during non-rapid-eye-movement (NREM) sleep by administering hypoxic gas mixtures with and without applied external inspiratory resistance (9 cmH2O X l-1 X s) in five normal male volunteers. In addition to standard polysomnography for sleep staging and respiratory pattern monitoring, esophageal pressure, tidal volume (VT), and airflow were measured via an esophageal catheter and pneumotachograph, respectively, with the latter attached to a tight-fitting face mask, allowing calculation of total pulmonary system resistance (Rp). During stage I/II NREM sleep minimal period breathing was evident in two of the subjects; however, in four subjects during hypoxia and/or relief from hypoxia, with and without added resistance, pronounced periodic breathing developed with waxing and waning of VT, sometimes with apneic phases. Resistive loading without hypoxia did not cause periodicity. At the nadir of periodic changes in VT, Rp was usually at its highest and there was a significant linear relationship between Rp and 1/VT, indicating the development of obstructive hypopneas. In one subject without added resistance and in the same subject and in another during resistive loading, upper airway obstruction at the nadir of the periodic fluctuations in VT was observed. We conclude that periodic breathing resulting in periodic diminution of upper airway muscle activity is associated with increased upper airway resistance that predisposes upper airways to collapse.
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Poon, C. S., S. A. Ward, and B. J. Whipp. "Influence of inspiratory assistance on ventilatory control during moderate exercise." Journal of Applied Physiology 62, no. 2 (February 1, 1987): 551–60. http://dx.doi.org/10.1152/jappl.1987.62.2.551.
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In five healthy subjects, we studied the effects of controlled mechanical unloading of the respiratory system on ventilatory control during moderate exercise, utilizing a modified positive-pressure ventilator (IEEE Trans. Biomed. Eng. BME-33: 361–365, 1986). We were especially interested in whether isocapnia was maintained when a portion of the normal ventilatory response to constant-load cycling was subserved by the ventilator. The mechanical unloading was achieved by “assisting” airflow throughout inspiration in a constant proportion to instantaneous flow. Two modest degrees of assistance (A1 = 1.5 and A2 = 3.0 cmH2O X l-1 X s) were imposed. The assistance caused minute ventilation (VE) to increase immediately (inspiratory time shortening and tidal volume rising) and end-tidal PCO2 (PETCO2) to fall. Some 10–15 s later, inspiratory occlusion pressure (P100) decreased, and in the new steady-state VE and PETCO2 were virtually restored to their control exercise levels. The modest residual hyperventilation [delta PETCO2 = -0.9 Torr (A1) and -1.6 Torr (A2)], which was not significant statistically, contrasted markedly with the much larger increase predicted for VE had there been no compensatory reduction in ventilatory drive (as evidenced by the fall in P100). Consistent with earlier studies utilizing resistive loading (J. Appl. Physiol. 35: 361–366, 1973 and Acta Physiol. Scand. 120: 557–565, 1984), these observations suggest that ventilatory drive during moderate exercise is controlled to compensate for modest changes in respiratory-mechanical load, so that VE is preserved at a level appropriate to metabolic rate or nearly so.
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Harms, Craig A., Thomas J. Wetter, Steven R. McClaran, David F. Pegelow, Glenn A. Nickele, William B. Nelson, Peter Hanson, and Jerome A. Dempsey. "Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise." Journal of Applied Physiology 85, no. 2 (August 1, 1998): 609–18. http://dx.doi.org/10.1152/jappl.1998.85.2.609.
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We have recently demonstrated that changes in the work of breathing during maximal exercise affect leg blood flow and leg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Pegelow, G. A. Nickele, W. B. Nelson, and J. A. Dempsey. J. Appl. Physiol. 82: 1573–1583, 1997). Our present study examined the effects of changes in the work of breathing on cardiac output (CO) during maximal exercise. Eight male cyclists [maximal O2 consumption (V˙o 2 max): 62 ± 5 ml ⋅ kg−1 ⋅ min−1] performed repeated 2.5-min bouts of cycle exercise atV˙o 2 max. Inspiratory muscle work was either 1) at control levels [inspiratory esophageal pressure (Pes): −27.8 ± 0.6 cmH2O], 2) reduced via a proportional-assist ventilator (Pes: −16.3 ± 0.5 cmH2O), or 3) increased via resistive loads (Pes: −35.6 ± 0.8 cmH2O). O2 contents measured in arterial and mixed venous blood were used to calculate CO via the direct Fick method. Stroke volume, CO, and pulmonary O2 consumption (V˙o 2) were not different ( P > 0.05) between control and loaded trials atV˙o 2 max but were lower (−8, −9, and −7%, respectively) than control with inspiratory muscle unloading atV˙o 2 max. The arterial-mixed venous O2difference was unchanged with unloading or loading. We combined these findings with our recent study to show that the respiratory muscle work normally expended during maximal exercise has two significant effects on the cardiovascular system: 1) up to 14–16% of the CO is directed to the respiratory muscles; and 2) local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.
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Akiyama, Y., M. Nishimura, S. Kobayashi, A. Yoshioka, M. Yamamoto, K. Miyamoto, and Y. Kawakami. "Effects of naloxone on the sensation of dyspnea during acute respiratory stress in normal adults." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 590–95. http://dx.doi.org/10.1152/jappl.1993.74.2.590.
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To clarify whether endogenous opioids modulate the dyspnea intensity and, if so, by what mechanism they act on it, we examined 12 healthy male volunteers aged 19–27 yr for ventilatory and peak mouth pressure (Pm) responses to hypoxic progressive hypercapnia with inspiratory flow-resistive loading after the intravenous infusion of 3 mg of naloxone or saline. The intensity of dyspnea was simultaneously assessed by visual analogue scaling every 15 s. Naloxone administration increased both ventilatory and Pm responses to hypoxic progressive hypercapnia (P < 0.05 for both). The increase in dyspnea intensity for a given increase in end-tidal PCO2 was significantly greater after naloxone infusion than after saline (P < 0.05). However, there were no differences in the increase in dyspnea intensity for a given increase in minute ventilation or Pm. These results suggest that the endogenous opioid system suppresses the respiratory output under a strong, acute respiratory stress in normal adults and that this system may relieve the dyspnea sensation secondary to the suppression of the brain stem respiratory center without specific effects on the processing of respiratory sensations in the higher brain.
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Mador, M. J., and F. A. Acevedo. "Effect of inspiratory muscle fatigue on breathing pattern during inspiratory resistive loading." Journal of Applied Physiology 70, no. 4 (April 1, 1991): 1627–32. http://dx.doi.org/10.1152/jappl.1991.70.4.1627.
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The purpose of this study was to determine whether induction of either inspiratory muscle fatigue (expt 1) or diaphragmatic fatigue (expt 2) would alter the breathing pattern response to large inspiratory resistive loads. In particular, we wondered whether induction of fatigue would result in rapid shallow breathing during inspiratory resistive loading. The breathing pattern during inspiratory resistive loading was measured for 5 min in the absence of fatigue (control) and immediately after induction of either inspiratory muscle fatigue or diaphragmatic fatigue. Data were separately analyzed for the 1st and 5th min of resistive loading to distinguish between immediate and sustained effects. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating a predetermined fraction of either the maximal mouth pressure or maximal transdiaphragmatic pressure until they could no longer reach the target pressure. Compared with control, there were no significant alterations in breathing pattern after induction of fatigue during either the 1st or 5th min of resistive loading, regardless of whether fatigue was induced in the majority of the inspiratory muscles or just in the diaphragm. We conclude that the development of inspiratory muscle fatigue does not alter the breathing pattern response to large inspiratory resistive loads.
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Hudgel, D. W., M. Mulholland, and C. Hendricks. "Neuromuscular and mechanical responses to inspiratory resistive loading during sleep." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 603–8. http://dx.doi.org/10.1152/jappl.1987.63.2.603.
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The purposes of this study were 1) to characterize the immediate inspiratory muscle and ventilation responses to inspiratory resistive loading during sleep in humans and 2) to determine whether upper airway caliber was compromised in the presence of a resistive load. Ventilation variables, chest wall, and upper airway inspiratory muscle electromyograms (EMG), and upper airway resistance were measured for two breaths immediately preceding and immediately following six applications of an inspiratory resistive load of 15 cmH2O.l–1 X s during wakefulness and stage 2 sleep. During wakefulness, chest wall inspiratory peak EMG activity increased 40 +/- 15% (SE), and inspiratory time increased 20 +/- 5%. Therefore, the rate of rise of chest wall EMG increased 14 +/- 10.9% (NS). Upper airway inspiratory muscle activity changed in an inconsistent fashion with application of the load. Tidal volume decreased 16 +/- 6%, and upper airway resistance increased 141 +/- 23% above pre-load levels. During sleep, there was no significant chest wall or upper airway inspiratory muscle or timing responses to loading. Tidal volume decreased 40 +/- 7% and upper airway resistance increased 188 +/- 52%, changes greater than those observed during wakefulness. We conclude that 1) the immediate inspiratory muscle and timing responses observed during inspiratory resistive loading in wakefulness were absent during sleep, 2) there was inadequate activation of upper airway inspiratory muscle activity to compensate for the increased upper airway inspiratory subatmospheric pressure present during loading, and 3) the alteration in upper airway mechanics during resistive loading was greater during sleep than wakefulness.
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Ringel, E. R., S. H. Loring, J. Mead, and R. H. Ingram. "Chest wall distortion during resistive inspiratory loading." Journal of Applied Physiology 58, no. 5 (May 1, 1985): 1646–53. http://dx.doi.org/10.1152/jappl.1985.58.5.1646.
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We studied six (1 naive and 5 experienced) subjects breathing with added inspiratory resistive loads while we recorded chest wall motion (anteroposterior rib cage, anteroposterior abdomen, and lateral rib cage) and tidal volumes. In the five experienced subjects, transdiaphragmatic and pleural pressures, and electromyographs of the sternocleidomastoid and abdominal muscles were also measured. Subjects inspired against the resistor spontaneously and then with specific instructions to reach a target pleural or transdiaphragmatic pressure or to maximize selected electromyographic activities. Depending on the instructions, a wide variety of patterns of inspiratory motion resulted. Although the forces leading to a more elliptical or circular configuration of the chest wall can be identified, it is difficult to analyze or predict the configurational results based on insertional and pressure-related contributions of a few individual respiratory muscles. Although overall chest wall respiratory motion cannot be readily inferred from the electromyographic and pressure data we recorded, it is clear that responses to loading can vary substantially within and between individuals. Undoubtedly, the underlying mechanism for the distortional changes with loading are complex and perhaps many are behavioral rather than automatic and/or compensatory.
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Zin, W. A., P. K. Behrakis, S. C. Luijendijk, B. D. Higgs, A. Baydur, A. Boddener, and J. Milic-Emili. "Immediate response to resistive loading in anesthetized humans." Journal of Applied Physiology 60, no. 2 (February 1, 1986): 506–12. http://dx.doi.org/10.1152/jappl.1986.60.2.506.
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In eight spontaneously breathing anesthetized subjects (halothane: approximately 1 minimal alveolar concn; 70% N2O-30% O2), we determined 1) the inspiratory driving pressure by analysis of the pressure developed at the airway opening (Poao) during inspiratory efforts against airways occluded at end expiration; 2) the active inspiratory impedance; and 3) the immediate (first loaded breath) response to added inspiratory resistive loads (delta R). Based on these data we made model predictions of the immediate tidal volume response to delta R. Such predictions closely fitted the experimental results. The present investigation indicates that 1) in halothane-anesthetized humans the shape of the Poao wave differs from that in anesthetized animals, 2) the immediate response to delta R is not associated with appreciable changes in intensity, shape, and timing of inspiratory neural drive but depends mainly on intrinsic (nonneural) mechanisms; 3) the flow-dependent resistance of endotracheal tubes must be taken into account in studies dealing with increased neuromuscular drive in intubated subjects; and 4) in anesthetized humans Poao reflects the driving pressure available to produce the breathing movements.
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Duara, S., S. Abbasi, T. H. Shaffer, and W. W. Fox. "Preterm infants: ventilation and P100 changes with CO2 and inspiratory resistive loading." Journal of Applied Physiology 58, no. 6 (June 1, 1985): 1982–87. http://dx.doi.org/10.1152/jappl.1985.58.6.1982.
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The ventilatory effects of inspiratory flow-resistive loading and increased chemical drive were measured in ten neonates during progressive hypercapnia in control and loaded states. Hypercapnia (mean increase PCO2 = 15–20) resulted from inspiring 8% CO2 in room air and inspiratory loading by a flow-resistive load = 100 cmH2O X l-1) X s. Hypercapnia produced an increase in group minute ventilation secondary to increasing tidal volumes and breathing frequencies. Loading shifted the minute ventilation-CO2 response to the right, and slopes decreased significantly (P less than 0.05) consequent to a significant decrease in the frequency-CO2 slopes (P less than 0.05), which became negative in four of the ten subjects. Mouth pressure measured at 100 ms after onset of inspiratory effort (P100) occlusion pressure-CO2 slopes measured in five subjects showed no significant increase with load application. Resistive loading produced significant increases in inspiratory time (P less than 0.02) and the inspiratory time/total breath time ratio (P less than 0.01). Airway occlusion elicited the Hering-Breuer reflex, with a significant increase in inspiratory time-to-total breath time ratio (P less than 0.01). The results show that the inspiratory resistive load produced ventilatory compromise in newborns and insufficient compensatory augmentation of central drive.
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Chonan, T., M. D. Altose, and N. S. Cherniack. "Effects of expiratory resistive loading on the sensation of dyspnea." Journal of Applied Physiology 69, no. 1 (July 1, 1990): 91–95. http://dx.doi.org/10.1152/jappl.1990.69.1.91.
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To determine whether an increase in expiratory motor output accentuates the sensation of dyspnea (difficulty in breathing), the following experiments were undertaken. Ten normal subjects, in a series of 2-min trials, breathed freely (level I) or maintained a target tidal volume equal to (level II) or twice the control (level III) at a breathing frequency of 15/min (similar to the control frequency) with an inspiratory load, an expiratory load, and without loads under hyperoxic normocapnia. In tests at levels II and III, end-expiratory lung volume was maintained at functional residual capacity. A linear resistance of 25 cmH2O.1(-1).s was used for both inspiratory and expiratory loading; peak mouth pressure (Pm) was measured, and the intensity of dyspnea (psi) was assessed with a visual analog scale. The sensation of dyspnea increased significantly with the magnitude of expiratory Pm during expiratory loading (level II: Pm = 9.4 +/- 1.5 (SE) cmH2O, psi = 1.26 +/- 0.35; level III: Pm = 20.3 +/- 2.8 cmH2O, psi = 2.22 +/- 0.48) and with inspiratory Pm during inspiratory loading (level II: Pm = 9.7 +/- 1.2 cmH2O, psi = 1.35 +/- 0.38; level III: Pm = 23.9 +/- 3.0 cmH2O, psi = 2.69 +/- 0.60). However, at each level of breathing, neither the intensity of dyspnea nor the magnitude of peak Pm during loading was different between inspiratory and expiratory loading. The augmentation of dyspnea during expiratory loading was not explained simply by increases in inspiratory activity. The results indicate that heightened expiratory as well as inspiratory motor output causes comparable increases in the sensation of difficulty in breathing.
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Gallagher, Charles G., and Magdy Younes. "Closing volume after inspiratory resistive loading to fatigue." Respiration Physiology 68, no. 2 (May 1987): 137–44. http://dx.doi.org/10.1016/s0034-5687(87)80001-4.
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Cala, S. J., P. Wilcox, J. Edyvean, M. Rynn, and L. A. Engel. "Oxygen cost of inspiratory loading: resistive vs. elastic." Journal of Applied Physiology 70, no. 5 (May 1, 1991): 1983–90. http://dx.doi.org/10.1152/jappl.1991.70.5.1983.
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We measured the O2 cost of breathing (VO2resp) against external inspiratory elastic (E) and resistive loads (R) when end-expiratory lung volume, tidal volume, breathing frequency, work rate, and pressure-time product were matched in each of six pairs of runs in six subjects. During E, peak inspiratory mouth pressure was 65.7 +/- 1.8% (SD) of the maximum at functional residual capacity. However, during resistive runs, peak inspiratory mouth pressure was 41.1 +/- 2.8% of the maximum at functional residual capacity. In 36 paired runs, where both work rate and pressure-time product were within 10%, VO2resp for E was less than for R (81 and 96 ml/min, respectively; P less than 0.01). During loaded and unloaded breathing with the same tidal volume, we measured the changes in anteroposterior diameter of the lower rib cage in five subjects. In four subjects we also recorded the electromyograms of several fixator and stabilizing muscles. During E and R, the change in anteroposterior diameter of the lower rib cage was -116 +/- 5 and -45 +/- 4% (SE), respectively, of the unloaded value (P less than 0.01), indicating greater deformation during E. Although the peak electromyographic activity was 72 +/- 16% greater during E (P less than 0.01), there was no difference between the loads for area under the electromyogram time curve (P greater than 0.05). However, the time to 50% peak activity was less during R (P less than 0.02). We conclude that, even when work rate and pressure-time product are matched, VO2resp during R is greater than that during E. This difference may be due to preferential recruitment of faster and less efficient muscle fibers.
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Janssens, Stefan, Eric Derom, Johan Vanhaecke, and Marc Decramer. "Theophylline Increases Oxygen Consumption During Inspiratory Resistive Loading." American Journal of Respiratory and Critical Care Medicine 151, no. 4 (April 1995): 1000–1005. http://dx.doi.org/10.1164/ajrccm/151.4.1000.
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Iscoe, Steve. "Phrenic motoneuron discharge during sustained inspiratory resistive loading." Journal of Applied Physiology 81, no. 5 (November 1, 1996): 2260–66. http://dx.doi.org/10.1152/jappl.1996.81.5.2260.
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Iscoe, Steve. Phrenic motoneuron discharge during sustained inspiratory resistive loading. J. Appl. Physiol. 81(5): 2260–2266, 1996.—I determined whether prolonged inspiratory resistive loading (IRL) affects phrenic motoneuron discharge, independent of changes in chemical drive. In seven decerebrate spontaneously breathing cats, the discharge patterns of eight phrenic motoneurons from filaments of one phrenic nerve were monitored, along with the global activity of the contralateral phrenic nerve, transdiaphragmatic pressure, and fractional end-tidal CO2 levels. Discharge patterns during hyperoxic CO2 rebreathing and breathing against an IRL (2,500–4,000 cmH2O ⋅ l−1 ⋅ s) were compared. During IRL, transdiaphragmatic pressure increased and then either plateaued or decreased. At the highest fractional end-tidal CO2 common to both runs, instantaneous discharge frequencies in six motoneurons were greater during sustained IRL than during rebreathing, when compared at the same time after the onset of inspiration. These increased discharge frequencies suggest the presence of a load-induced nonchemical drive to phrenic motoneurons from unidentified source(s).
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Janssens, S., E. Derom, J. Vanhaecke, and M. Decramer. "Theophylline increases oxygen consumption during inspiratory resistive loading." American Journal of Respiratory and Critical Care Medicine 151, no. 4 (April 1995): 1000–1005. http://dx.doi.org/10.1164/ajrccm.151.4.7697222.
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Bolser, Donald C., and Paul W. Davenport. "Volume-timing relationships during cough and resistive loading in the cat." Journal of Applied Physiology 89, no. 2 (August 1, 2000): 785–90. http://dx.doi.org/10.1152/jappl.2000.89.2.785.
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The relationship between pulmonary volume-related feedback and inspiratory (CTi) and expiratory (CTe) phase durations during cough was determined. Cough was produced in anesthetized cats by mechanical stimulation of the intrathoracic tracheal lumen. During eupnea, the animals were exposed to single-breath inspiratory and expiratory resistive loads. Cough was associated with large increases in inspiratory volume (Vi) and expiratory volume (Ve) but no change in phase durations compared with eupnea. There was no relationship between Viand CTi during coughing. A linear relationship with a negative slope existed between Vi and eupneic inspiratory time during control and inspiratory resistive loading trials. There was no relationship between Ve and CTe during all coughs. However, when the first cough in a series or a single cough was analyzed, the Ve/CTe relationship had a positive slope. A linear relationship with a negative slope existed between Ve and eupneic expiratory time during control and expiratory resistive loading trials. These results support separate ventilatory pattern regulation during cough that does not include modulation of phase durations by pulmonary volume-related feedback.
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Jones, G. L., K. J. Killian, E. Summers, and N. L. Jones. "Inspiratory muscle forces and endurance in maximum resistive loading." Journal of Applied Physiology 58, no. 5 (May 1, 1985): 1608–15. http://dx.doi.org/10.1152/jappl.1985.58.5.1608.
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The ability of the respiratory muscles to sustain ventilation against increasing inspiratory resistive loads was measured in 10 normal subjects. All subjects reached a maximum rating of perceived respiratory effort and at maximum resistance showed signs of respiratory failure (CO2 retention, O2 desaturation, and rib cage and abdominal paradox). The maximum resistance achieved varied widely (range 73–660 cmH2O X l-1 X s). The increase in O2 uptake (delta Vo2) associated with loading was linearly related to the integrated mouth pressure (IMP): delta Vo2 = 0.028 X IMP + 19 ml/min (r = 0.88, P less than 0.001). Maximum delta Vo2 was 142 ml/min +/- SD 68 ml/min. There were significant (P less than 0.05) relationships between the maximum voluntary inspiratory pressure against an occluded airway (MIP) and both maximum IMP (r = 0.80) and maximum delta Vo2 (r = 0.76). In five subjects, three imposed breathing patterns were used to examine the effect of different patterns of respiratory muscle force deployment. Increasing inspiratory duration (TI) from 1.5 to 3.0 and 6.0 s, at the same frequency of breathing (5.5 breaths/min) reduced peak inspiratory pressure and increased the maximum resistance tolerated (190, 269, and 366 cmH2O X l-1 X s, respectively) and maximum IMP (2043, 2473, and 2913 cmH2O X s X min-1, but the effect on maximum delta Vo2 was less consistent (166, 237, and 180 ml/min). The ventilatory endurance capacity and the maximum O2 uptake of the respiratory muscles are related to the strength of the inspiratory muscles, but are also modified through the pattern of force deployment.
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Road, J., S. Osborne, and A. Cairns. "Phrenic motoneuron firing rates during brief inspiratory resistive loads." Journal of Applied Physiology 79, no. 5 (November 1, 1995): 1540–45. http://dx.doi.org/10.1152/jappl.1995.79.5.1540.
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The neural activation of the diaphragm during quiet and vigorously stimulated breathing has been hypothesized to be submaximal. In this study, we measured phrenic motoneuron firing rates during brief progressively increasing inspiratory resistive loads in anesthetized rabbits. We recorded activity in 68 phrenic motoneurons in 17 rabbits. We found that 40 of these axons were active during quiet breathing. Twenty-seven axons were silent during quiet breathing but began to fire as inspiratory loading progressed. The level of drive reflected by transdiaphragmatic pressure where silent phrenic motoneurons were recruited ranged from 5 to 45 cmH2O. Silent motoneurons showed significantly higher average rates of firing and significantly greater increases in firing rate as loading progressed (P < 0.01). The firing rate of both active and silent axons tended to plateau as rates approached 70–80 Hz. All motoneurons except for one, which may have been an afferent, were activated by inspiratory resistive loading. Inspiratory resistive loading activated phrenic motoneurons at high rates, and our results did not support the presence of significant numbers of unrecruited motoneurons.
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Wanke, T., H. Lahrmann, D. Formanek, B. Zwick, M. Merkle, and H. Zwick. "The effect of opioids on inspiratory muscle fatigue during inspiratory resistive loading." Clinical Physiology 13, no. 4 (July 1993): 349–60. http://dx.doi.org/10.1111/j.1475-097x.1993.tb00335.x.
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O'Donnell, D. E., R. Sanii, and M. Younes. "External mechanical loading in conscious humans: role of upper airway mechanoreceptors." Journal of Applied Physiology 65, no. 2 (August 1, 1988): 541–48. http://dx.doi.org/10.1152/jappl.1988.65.2.541.
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To determine whether upper airway mechanoreceptors partly subserve the ventilatory response to external mechanical loading in conscious humans, we studied 11 laryngectomized subjects. The oropharynx (OP) or tracheostomy was selectively loaded (in random order) by attaching the mouth or tracheal tube to a special pressure-generating apparatus, and steady-state ventilatory responses were recorded. Phasic negative pressure changes generated at the OP to simulate inspiratory resistive loading, expiratory resistive unloading, and elastic loading resulted in trivial prolongation of inspiratory duration by 12, 9, and 4%, respectively; other ventilatory variables were not significantly altered. Phasic positive pressure changes at the OP that simulated inspiratory resistive unloading and expiratory resistive loading had little effect on breathing pattern. When the above loads were applied via the tracheostomy, using pressures of similar magnitude, ventilatory responses were qualitatively similar and quantitatively not significantly different from those of normal healthy controls. The results suggest that the OP does not make an important contribution to ventilatory responses during external mechanical loading in conscious humans. Loading responses to conventional mechanical loads are preserved in the absence of afferent information from the upper airways.
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Clague, J. E., J. Carter, M. G. Pearson, and P. M. A. Calverley. "Effect of Sustained Inspiratory Loading on Respiratory Sensation and Co2 Responsiveness in Normal Humans." Clinical Science 91, no. 4 (October 1, 1996): 513–18. http://dx.doi.org/10.1042/cs0910513.
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1. To examine the effects of sustained resistive loading on the relationship between inspiratory effort sensation and respiratory drive (P0.1) and to determine if the change in CO2 responsiveness after sustained loading is accompanied by altered effort perception, hypercapnic responses were measured before, immediately after and 15 min after sustained resistive loading in seven subjects (six men, one woman). Sustained resistive loading was set to exceed a diaphragm tension—time index of 0.2. 2. Mean time to task failure during sustained loading was 17.7 min (range 12.5–22.5 min). The mean inspiratory effort sensation score rose from 3.4 (SEM 0.8) to 8.1 (0.8), whereas P0.1 fell from 29.5 (3.6) to 18.1 (3.6)cmH2O. 3. Immediately after loading the slopes of the ventilatory and sensory responses to CO2 fell (ventilatory response: before loading 16.7 (2.4)1 min−1 kPa−1, immediately after loading 7.88 (2.18) 1 min−1 kPa−1; sensory response: before loading 1.95 (0.38)units/kPa; immediately after loading 1.12 (0.38) units/kPa; P < 0.05. Changes reverted to preloading levels by 15 min. 4. Sustained loading can lead to a dissociation between respiratory drive, as reflected by P0.1, and inspiratory effort sensation, and this disturbance can persist once the load is removed. Impaired sensory perception may be the primary determinant of the change in CO2 responsiveness seen after sustained resistive loading.
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Wiegand, L., C. W. Zwillich, and D. P. White. "Sleep and the ventilatory response to resistive loading in normal men." Journal of Applied Physiology 64, no. 3 (March 1, 1988): 1186–95. http://dx.doi.org/10.1152/jappl.1988.64.3.1186.
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Since upper airway resistance is known to increase during sleep, inadequate resistive load compensation may contribute to the normal decline in sleeping ventilation. We determined the acute and sustained (4 min) ventilatory response to a range of external inspiratory resistive loads (4, 8, 12, and 25 cmH2O.l-1.s) during wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep in seven normal men. We found that minute ventilation (VI) was well maintained with acute and sustained resistive loading during wakefulness. Immediate adjustments in ventilatory timing (prolongation of inspiratory duration) provided full compensation for airflow reduction. In marked contrast, resistive load application during NREM sleep invariably produced a significant (P less than 0.05) reduction in VI with progressively larger resistive loads producing progressively greater ventilatory decrements. This decline in ventilation was a product of a falling inspiratory flow rate with inadequate prolongation of inspiratory duration (TI). The largest decrements in ventilation occurred immediately after load application followed by partial ventilatory recovery, which occurred over time in concert with rising PCO2 and augmented ventilatory effort (as reflected by P0.1 or mouth occlusion pressure). Similar observations were made during REM sleep, although the responses were less consistent and fewer data were obtained. These observations support the hypothesis that poor load compensation for increased upper airway resistance contributes to the hypoventilation characteristic of normal sleep.
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Insalaco, G., S. T. Kuna, B. M. Costanza, G. Catania, F. Cibella, and V. Bellia. "Thyroarytenoid muscle activity during loaded and nonloaded breathing in adult humans." Journal of Applied Physiology 70, no. 6 (June 1, 1991): 2410–16. http://dx.doi.org/10.1152/jappl.1991.70.6.2410.
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Previous fiber-optic studies in humans have demonstrated narrowing of the glottic aperture in expiration during application of expiratory resistive loads. Nine healthy subjects were studied to determine the effect of expiratory resistive loads on the electromyographic activity of the thyroarytenoid (TA) muscle, a vocal cord adductor. Four of the nine subjects also underwent the application of inspiratory resistive loads and voluntary prolongation of either inspiratory (TI) or expiratory (TE) time. TA activity was recorded by intramuscular hooked-wire electrodes. During quiet breathing in all subjects, the TA was phasically active on expiration and often tonically active throughout the respiratory cycle. TA expiratory activity progressively increased with increasing levels of expiratory load. Inspiratory loads resulted in increased TA "inspiratory" activity. Voluntary prolongation of TE to times similar to those reached during loaded breathing induced increases in TA expiratory activity similar to those reached during the loaded state. Voluntary prolongation of TI was associated with an increase in TA inspiratory activity. Similar increases in TI during inspiratory loading or voluntary conditions were associated with comparable increases in TA inspiratory activity in three of the four subjects. In conclusion, increased activation of TA during the application of expiratory resistive loads implies that the reported narrowing of glottic aperture during expiratory loading is an active phenomenon. Changes in activation of the TA with resistive loads appear to be related to changes in respiratory pattern.
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Aldrich, T. K., and D. Appel. "Diaphragm fatigue induced by inspiratory resistive loading in spontaneously breathing rabbits." Journal of Applied Physiology 59, no. 5 (November 1, 1985): 1527–32. http://dx.doi.org/10.1152/jappl.1985.59.5.1527.
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Diaphragmatic contractility was assessed in spontaneously breathing ketamine-anesthetized rabbits by measuring the strength of diaphragmatic contraction in response to bilateral supramaximal phrenic nerve stimulation at frequencies between 10 and 100 Hz. During 10–180 min of inspiratory resistive loading, contractility decreased by approximately 40%, and hypoxemia and both respiratory and lactic acidosis developed. After 10 min of recovery, both the response to high-frequency stimulation (100 Hz) and the arterial PO2 and PCO2 returned to base-line levels, whereas metabolic acidosis and reduced response to low-frequency stimulation (10–20 Hz) persisted. Similar levels of hypoxemia and respiratory acidosis in the absence of inspiratory resistive loading did not alter diaphragmatic contractility. We conclude that in anesthetized rabbits excessive inspiratory resistive loading results in partially reversible diaphragm fatigue of the high- and low-frequency types, accompanied by hypoventilation and lactic acidosis.
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Hlavac, Michael C., Peter G. Catcheside, Amanda Adams, Danny J. Eckert, and R. Doug McEvoy. "The effects of hypoxia on load compensation during sustained incremental resistive loading in patients with obstructive sleep apnea." Journal of Applied Physiology 103, no. 1 (July 2007): 234–39. http://dx.doi.org/10.1152/japplphysiol.01618.2005.
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Inspiratory load compensation is impaired in patients with obstructive sleep apnea (OSA), a condition characterized by hypoxia during sleep. We sought to compare the effects of sustained hypoxia on ventilation during inspiratory resistive loading in OSA patients and matched controls. Ten OSA patients and 10 controls received 30 min of isocapnic hypoxia (arterial oxygen saturation 80%) and normoxia in random order. Following the gas period, subjects were administered six incremental 2-min inspiratory resistive loads while breathing room air. Ventilation was measured throughout the loading period. In both patients and controls, there was a significant increase in inspiratory time with increasing load ( P = 0.006 and 0.003, respectively), accompanied by a significant fall in peak inspiratory flow ( P = 0.006 and P < 0.001, respectively). The result was a significant fall in minute ventilation in both groups with increasing load ( P = 0.003 and P < 0.001, respectively). There was no difference between the two groups for these parameters. The only difference between the two groups was a transient increase in tidal volume in controls ( P = 0.02) but not in OSA patients ( P = 0.57) during loading. Following hypoxia, there was a significant increase in minute ventilation during loading in both groups ( P < 0.001). These results suggest that ventilation during incremental resistive loading is preserved in OSA patients and that it appears relatively impervious to the effects of hypoxia.
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Cala, S. J., J. Edyvean, and L. A. Engel. "Chest wall and trunk muscle activity during inspiratory loading." Journal of Applied Physiology 73, no. 6 (December 1, 1992): 2373–81. http://dx.doi.org/10.1152/jappl.1992.73.6.2373.
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We measured the electromyographic (EMG) activity in four chest wall and trunk (CWT) muscles, the erector spinae, latissimus dorsi, pectoralis major, and trapezius, together with the parasternal, in four normal subjects during graded inspiratory efforts against an occlusion in both upright and seated postures. We also measured CWT EMGs in six seated subjects during inspiratory resistive loading at high and low tidal volumes [1,280 +/- 80 (SE) and 920 +/- 60 ml, respectively]. With one exception, CWT EMG increased as a function of inspiratory pressure generated (Pmus) at all lung volumes in both postures, with no systematic difference in recruitment between CWT and parasternal muscles as a function of Pmus. At any given lung volume there was no consistent difference in CWT EMG at a given Pmus between the two postures (P > 0.09). However, at a given Pmus during both graded inspiratory efforts and inspiratory resistive loading, EMGs of all muscles increased with lung volume, with greater volume dependence in the upright posture (P < 0.02). The results suggest that during inspiratory efforts, CWT muscles contribute to the generation of inspiratory pressure. The CWT muscles may act as fixators opposing deflationary forces transmitted to the vertebral column by rib cage articulations, a function that may be less effective at high lung volumes if the direction of the muscular insertions is altered disadvantageously.
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LAVIETES, MARC H, CARLOS W SANCHEZ, LANA A TIERSKY, NEIL S CHERNIACK, and BENJAMIN H NATELSON. "Psychological Profile and Ventilatory Response to Inspiratory Resistive Loading." American Journal of Respiratory and Critical Care Medicine 161, no. 3 (March 2000): 737–44. http://dx.doi.org/10.1164/ajrccm.161.3.9810075.
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Peters, Carli M., Joseph F. Welch, Paolo B. Dominelli, Yannick Molgat-Seon, Lee M. Romer, Donald C. McKenzie, and A. William Sheel. "Effect of Inspiratory Resistive Loading on Expiratory Muscle Fatigue." Medicine & Science in Sports & Exercise 48 (May 2016): 455. http://dx.doi.org/10.1249/01.mss.0000486368.44633.04.
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Hershenson, M. B., Y. Kikuchi, G. E. Tzelepis, and F. D. McCool. "Preferential fatigue of the rib cage muscles during inspiratory resistive loaded ventilation." Journal of Applied Physiology 66, no. 2 (February 1, 1989): 750–54. http://dx.doi.org/10.1152/jappl.1989.66.2.750.
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Because the inspiratory rib cage muscles are recruited during inspiratory resistive loaded breathing, we hypothesized that such loading would preferentially fatigue the rib cage muscles. We measured the pressure developed by the inspiratory rib cage muscles during maximal static inspiratory maneuvers (Pinsp) and the pressure developed by the diaphragm during maximal static open-glottis expulsive maneuvers (Pdimax) in four human subjects, both before and after fatigue induced by an inspiratory resistive loaded breathing task. Tasks consisted of maintaining a target esophageal pressure, breathing frequency, and duty cycle for 3–5 min, after which the subjects maintained the highest esophageal pressure possible for an additional 5 min. After loading, Pinsp decreased in all subjects [control, -128 +/- 14 (SD) cmH2O; with fatigue, -102 +/- 18 cmH2O; P less than 0.001, paired t test]. Pdimax was unchanged (control, -192 +/- 23 cmH2O; fatigue, -195 +/- 27 cmH2O). These data suggest that 1) inability to sustain the target during loading resulted from fatigue of the inspiratory rib cage muscles, not diaphragm, and 2) simultaneous measurement of Pinsp and Pdimax may be useful in partitioning muscle fatigue into rib cage and diaphragmatic components.
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Yanagisawa, Y., and Y. Matsuo. "Effect of inspiratory resistive loading in inspiratory muscle training on hyoid muscle activity." Physiotherapy 101 (May 2015): e1681-e1682. http://dx.doi.org/10.1016/j.physio.2015.03.085.
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Clague, J. E., J. Carter, M. G. Pearson, and P. M. A. Calverley. "Relationship between inspiratory drive and perceived inspiratory effort in normal man." Clinical Science 78, no. 5 (May 1, 1990): 493–96. http://dx.doi.org/10.1042/cs0780493.
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1. To examine the relationship between the inspiratory effort sensation (IES) and respiratory drive as reflected by mouth occlusion pressure (P0.1) we have studied loaded and unloaded ventilatory responses to CO2 in 12 normal subjects. 2. The individual coefficient of variation of the effort sensation response to CO2 (IES/Pco2) between replicate studies was 21% and was similar to the variability of the ventilatory response (VE/Pco2) (18%) and the occlusion pressure response (P0.1/Pco2) (22%). 3. IES was well correlated with P0.1 (r >0.9) for both free-breathing and loaded runs. 4. Resistive loading reduced the ventilatory response to hypercapnia from 19.3 1 min−1 kPa−1 (sd 7.5) to 12.6 1 min−1 kPa−1 (sd 3.9) (P <0.01). IES and P0.1 responses increased with resistive loading from 2.28 (sd 0.9) to 3.15 (sd 1.1) units/kPa and 2.8 (sd 1.2) to 3.73 (sd 1.5) cmH2O/kPa, respectively (P <0.01). 5. Experimentally induced changes in Pco2 and respiratory impedance were accompanied by increases in IES and P0.1. We found no evidence that CO2 increased IES independently of its effect on respiratory drive.
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Clague, J. E., J. Carter, M. G. Pearson, and P. M. Calverley. "Effort sensation, chemoresponsiveness, and breathing pattern during inspiratory resistive loading." Journal of Applied Physiology 73, no. 2 (August 1, 1992): 440–45. http://dx.doi.org/10.1152/jappl.1992.73.2.440.
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Although inspiratory resistive loading (IRL) reduces the ventilatory response to CO2 (VE/PCO2) and increases the sensation of inspiratory effort (IES), there are few data about the converse situation: whether CO2 responsiveness influences sustained load compensation and whether awareness of respiratory effort modifies this behavior. We studied 12 normal men during CO2 rebreathing while free breathing and with a 10-cmH2O.l-1.s IRL and compared these data with 5 min of resting breathing with and without the IRL. Breathing pattern, end-tidal PCO2, IES, and mouth occlusion pressure (P0.1) were recorded. Free-breathing VE/PCO2 was inversely related to an index of effort perception (IES/VE; r = -0.63, P less than 0.05), and the reduction in VE/PCO2 produced by IRL was related to the initial free-breathing VE/PCO2 (r = 0.87, P less than 0.01). IRL produced variable increases in inspiratory duration (TI), IES, and P0.1 at rest, and the change in tidal volume correlated with both VE/PCO2 (r = 0.63, P less than 0.05) and IES/VE (r = -0.69, P less than 0.05), this latter index also predicting the changes in TI with loading (r = -0.83, P less than 0.01). These data suggest that in normal subjects perception of inspiratory effort can modify free-breathing CO2 responsiveness and is as important as CO2 sensitivity in determining the response to short-term resistive loading. Individuals with good perception choose a small-tidal volume and short-TI breathing pattern during loading, possibly to minimize the discomfort of breathing.
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McKenzie, D. K., G. M. Allen, J. E. Butler, and S. C. Gandevia. "Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects." Journal of Applied Physiology 82, no. 6 (June 1, 1997): 2011–19. http://dx.doi.org/10.1152/jappl.1997.82.6.2011.
Full textAbstract:
McKenzie, D. K., G. M. Allen, J. E. Butler, and S. C. Gandevia. Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects. J. Appl. Physiol. 82(6): 2011–2019, 1997.—Task failure during inspiratory resistive loading is thought to be accompanied by substantial peripheral fatigue of the inspiratory muscles. Six healthy subjects performed eight resistive breathing trials with loads of 35, 50, 75 and 90% of maximal inspiratory pressure (MIP) with and without supplemental oxygen. MIP measured before, after, and at every minute during the trial increased slightly during the trials, even when corrected for lung volume (e.g., for 24 trials breathing air, 12.5% increase, P < 0.05). In some trials, task failure occurred before 20 min (end point of trial), and in these trials there was an increase in end-tidal[Formula: see text]( P < 0.01), despite the absence of peripheral muscle fatigue. In four subjects (6 trials with task failure), there was no decline in twitch amplitude with bilateral phrenic stimulation or in voluntary activation of the diaphragm, even though end-tidal [Formula: see text] rose by 1.6 ± 0.9%. These results suggest that hypoventilation, CO2 retention, and ultimate task failure during resistive breathing are not simply dependent on impaired force-generating capacity of the diaphragm or impaired voluntary activation of the diaphragm.
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Thompson, William H., Paula Carvalho, James P. Souza, and Nirmal B. Charan. "Effect of expiratory resistive loading on the noninvasive tension-time index in COPD." Journal of Applied Physiology 89, no. 5 (November 1, 2000): 2007–14. http://dx.doi.org/10.1152/jappl.2000.89.5.2007.
Full textAbstract:
Expiratory resistive loading (ERL) is used by chronic obstructive pulmonary disease (COPD) patients to improve respiratory function. We, therefore, used a noninvasive tension-time index of the inspiratory muscles (TTmus =P̄i/Pi max × Ti/Tt, where P̄i is mean inspiratory pressure estimated from the mouth occlusion pressure, Pi max is maximal inspiratory pressure, Ti is inspiratory time, and Tt is total respiratory cycle time) to better define the effect of ERL on COPD patients. To accomplish this, we measured airway pressures, mouth occlusion pressure, respiratory cycle flow rates, and functional residual capacity (FRC) in 14 COPD patients and 10 normal subjects with and without the application of ERL. TTmus was then calculated and found to drop in both COPD and normal subjects ( P < 0.05). The decline in TTmus in both groups resulted solely from a prolongation of expiratory time with ERL ( P < 0.001 for COPD, P < 0.05 for normal subjects). In contrast to the COPD patients, normal subjects had an elevation in P̄i and FRC, thus minimizing the decline in TTmus. In conclusion, ERL reduces the potential for inspiratory muscle fatigue in COPD by reducing Ti/Tt without affecting FRC andP̄i.
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Abbrecht, Peter H., Krishnan R. Rajagopal, and Richard R. Kyle. "Expiratory Muscle Recruitment during Inspiratory Flow-resistive Loading and Exercise." American Review of Respiratory Disease 144, no. 1 (July 1991): 113–20. http://dx.doi.org/10.1164/ajrccm/144.1.113.
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JIANG, TIAN-XI, W. DARLENE REID, and JEREMY D ROAD. "Free Radical Scavengers and Diaphragm Injury Following Inspiratory Resistive Loading." American Journal of Respiratory and Critical Care Medicine 164, no. 7 (October 2001): 1288–94. http://dx.doi.org/10.1164/ajrccm.164.7.2005081.
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Gething, A. D. "Inspiratory resistive loading improves cycling capacity: a placebo controlled trial." British Journal of Sports Medicine 38, no. 6 (December 1, 2004): 730–36. http://dx.doi.org/10.1136/bjsm.2003.007518.
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