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1
Wilson, Theodore A., Maurizio Angelillo, Alexandre Legrand, and André de Troyer. "Muscle kinematics for minimal work of breathing." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 554–60. http://dx.doi.org/10.1152/jappl.1999.87.2.554.
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A mathematical model was analyzed to obtain a quantitative and testable representation of the long-standing hypothesis that the respiratory muscles drive the chest wall along the trajectory for which the work of breathing is minimal. The respiratory system was modeled as a linear elastic system that can be expanded either by pressure applied at the airway opening (passive inflation) or by active forces in respiratory muscles (active inflation). The work of active expansion was calculated, and the distribution of muscle forces that produces a given lung expansion with minimal work was computed. The calculated expression for muscle force is complicated, but the corresponding kinematics of muscle shortening is simple: active inspiratory muscles shorten more during active inflation than during passive inflation, and the ratio of active to passive shortening is the same for all active muscles. In addition, the ratio of the minimal work done by respiratory muscles during active inflation to work required for passive inflation is the same as the ratio of active to passive muscle shortening. The minimal-work hypothesis was tested by measurement of the passive and active shortening of the internal intercostal muscles in the parasternal region of two interspaces in five supine anesthetized dogs. Fractional changes in muscle length were measured by sonomicrometry during passive inflation, during quiet breathing, and during forceful inspiratory efforts against a closed airway. Active muscle shortening during quiet breathing was, on average, 70% greater than passive shortening, but it was only weakly correlated with passive shortening. Active shortening inferred from the data for more forceful inspiratory efforts was ∼40% greater than passive shortening and was highly correlated with passive shortening. These data support the hypothesis that, during forceful inspiratory efforts, muscle activation is coordinated so as to expand the chest wall with minimal work.
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Suzuki, S., J. Suzuki, and T. Okubo. "Expiratory muscle fatigue in normal subjects." Journal of Applied Physiology 70, no. 6 (June 1, 1991): 2632–39. http://dx.doi.org/10.1152/jappl.1991.70.6.2632.
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We examined expiratory muscle fatigue during expiratory resistive loading in 11 normal subjects. Subjects breathed against expiratory resistances at their own breathing frequency and tidal volume until exhaustion or for 60 min. Respiratory muscle strength was assessed from both the maximum static expiratory and inspiratory mouth pressures (PEmax and PImax). At the lowest resistance, PEmax and PImax measured after completion of the expiratory loaded breathing were not different from control values. With higher resistance, both PEmax and PImax were decreased (P less than 0.05), and the decrease lasted for greater than or equal to 60 min. The electromyogram high-to-low frequency power ratio for the rectus abdominis muscle decreased progressively during loading (P less than 0.01), but the integrated EMG activity did not change during recovery. Transdiaphragmatic pressure during loading was increased 3.6-fold compared with control (P less than 0.05). These findings suggest that expiratory resistive loaded breathing induces muscle fatigue in both expiratory and inspiratory muscles. Fatigue of the expiratory muscles can be attributed directly to the high work load and that of the inspiratory muscles may be related to increased work due to shortened inspiratory time.
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McConnell, Alison K., and Michelle Lomax. "The influence of inspiratory muscle work history and specific inspiratory muscle training upon human limb muscle fatigue." Journal of Physiology 577, no. 1 (November 8, 2006): 445–57. http://dx.doi.org/10.1113/jphysiol.2006.117614.
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Yan, S., P. Sliwinski, A. P. Gauthier, I. Lichros, S. Zakynthinos, and P. T. Macklem. "Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2." Journal of Applied Physiology 75, no. 3 (September 1, 1993): 1371–77. http://dx.doi.org/10.1152/jappl.1993.75.3.1371.
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We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.
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Collett, P. W., and L. A. Engel. "Influence of lung volume on oxygen cost of resistive breathing." Journal of Applied Physiology 61, no. 1 (July 1, 1986): 16–24. http://dx.doi.org/10.1152/jappl.1986.61.1.16.
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We examined the relationship between the O2 cost of breathing (VO2 resp) and lung volume at constant load, ventilation, work rate, and pressure-time product in five trained normal subjects breathing through an inspiratory resistance at functional residual capacity (FRC) and when lung volume (VL) was increased to 37 +/- 2% (mean +/- SE) of inspiratory capacity (high VL). High VL was maintained using continuous positive airway pressure of 9 +/- 2 cmH2O and with the subjects coached to relax during expiration to minimize respiratory muscle activity. Six paired runs were performed in each subject at constant tidal volume (0.62 +/- 0.2 liters), frequency (23 +/- 1 breaths/min), inspiratory flow rate (0.45 +/- 0.1 l/s), and inspiratory muscle pressure (45 +/- 2% of maximum static pressure at FRC). VO2 resp increased from 109 +/- 15 ml/min at FRC by 41 +/- 11% at high VL (P less than 0.05). Thus the efficiency of breathing at high VL (3.9 +/- 0.2%) was less than that at FRC (5.2 +/- 0.3%, P less than 0.01). The decrease in inspiratory muscle efficiency at high VL may be due to changes in mechanical coupling, in the pattern of recruitment of the respiratory muscles, or in the intrinsic properties of the inspiratory muscles at shorter length. When the work of breathing at high VL was normalized for the decrease in maximum inspiratory muscle pressure with VL, efficiency at high VL (5.2 +/- 0.3%) did not differ from that at FRC (P less than 0.7), suggesting that the fall in efficiency may have been related to the fall in inspiratory muscle strength. During acute hyperinflation the decreased efficiency contributes to the increased O2 cost of breathing and may contribute to the diminished inspiratory muscle endurance.
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Van Hollebeke, Marine, Diego Poddighe, Tin Gojevic, Beatrix Clerckx, Jan Muller, Greet Hermans, Rik Gosselink, and Daniel Langer. "Measurement validity of an electronic training device to assess breathing characteristics during inspiratory muscle training in patients with weaning difficulties." PLOS ONE 16, no. 8 (August 26, 2021): e0255431. http://dx.doi.org/10.1371/journal.pone.0255431.
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Inspiratory muscle training (IMT) improves respiratory muscle function and might enhance weaning outcomes in patients with weaning difficulties. An electronic inspiratory loading device provides valid, automatically processed information on breathing characteristics during IMT sessions. Adherence to and quality of IMT, as reflected by work of breathing and power generated by inspiratory muscles, are related to improvements in inspiratory muscle function in patients with chronic obstructive pulmonary disease. The aim of this study was to investigate the validity of an electronic training device to assess and provide real-time feedback on breathing characteristics during inspiratory muscle training (IMT) in patient with weaning difficulties. Patients with weaning difficulties performed daily IMT sessions against a tapered flow-resistive load of approximately 30 to 50% of the patient’s maximal inspiratory pressure. Airflow and airway pressure measurements were simultaneously collected with the training device (POWERbreatheKH2, POWERbreathe International Ltd, UK) and a portable spirometer (reference device, Pocket-Spiro USB/BT100, M.E.C, Belgium). Breath by breath analysis of 1002 breaths of 27 training sessions (n = 13) against a mean load of 46±16% of the patient’s maximal inspiratory pressure were performed. Good to excellent agreement (Intraclass correlation coefficients: 0.73–0.97) was observed for all breathing characteristics. When individual differences were plotted against mean values of breaths recorded by both devices, small average biases were observed for all breathing characteristics. To conclude, the training device provides valid assessments of breathing characteristics to quantify inspiratory muscle effort (e.g. work of breathing and peak power) during IMT in patients with weaning difficulties. Availability of valid real-time data of breathing responses provided to both the physical therapist and the patient, can be clinically usefull to optimize the training stimulus. By adapting the external load based on the visual feedback of the training device, respiratory muscle work and power generation during IMT can be maximized during the training.
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Wheatley, S. West, SJ Cala, and LA Engel. "The effect of hyperinflation on respiratory muscle work in acute induced asthma." European Respiratory Journal 3, no. 6 (June 1, 1990): 625–32. http://dx.doi.org/10.1183/09031936.93.03060625.
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To examine the relationship between end-expiratory lung volume and respiratory muscle work during acute bronchoconstriction, we measured the work of breathing in nine asthmatic subjects, in whom bronchoconstriction was induced with histamine aerosol. When the forced expiratory volume in one second (FEV1) fell below 60% of the control value, work was measured at the spontaneously hyperinflated lung volume (VLS), at a volume equivalent to the control functional residual capacity (FRC) and at a volume 30% of vital capacity (VC) above the control FRC. Hyperinflation to VLS caused a 39% decrease in the total positive work per breath from 2.8 +/- 0.4 to 1.7 +/- 0.1 J, entirely due to a decrease in expiratory work per breath from 1.6 +/- 0.4 to 0.10 +/- 0.05 J. Inspiratory work did not change at any lung volume, because the increase in inspiratory elastic work due to hyperinflation was offset by the decrease in flow resistive work. Breathing above VLS did not alter the total positive muscle work, but did increase the negative work of the inspiratory muscles from 0.4 +/- 0.1 to 0.8 +/- 0.1 J.breath. We conclude that during induced asthma spontaneous hyperinflation minimizes the total respiratory muscle work and may constitute a mechanism for minimizing energy expenditure.
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Hsia, C. C., M. Ramanathan, J. L. Pean, and R. L. Johnson. "Respiratory muscle blood flow in exercising dogs after pneumonectomy." Journal of Applied Physiology 73, no. 1 (July 1, 1992): 240–47. http://dx.doi.org/10.1152/jappl.1992.73.1.240.
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In three foxhounds after left pneumonectomy, the relationships of ventilatory work and respiratory muscle (RM) blood flow to ventilation (VE) during steady-state exercise were examined. VE was measured using a specially constructed respiratory mask and a pneumotach; work of breathing was measured by the esophageal balloon technique. Blood flow to RM was measured by the radionuclide-labeled microsphere technique. Lung compliance after pneumonectomy was 55% of that before pneumonectomy; compliance of the thorax was unchanged. O2 uptake (VO2) of RM comprised only 5% of total body VO2 at exercise. At rest, inspiratory muscles received 62% and expiratory muscles 38% of the total O2 delivered to the RM (QO2RM). During exercise, inspiratory muscles received 59% and expiratory muscles 41% of total QO2RM. Blood flow per gram of muscle to the costal diaphragm was significantly higher than that to the crural diaphragm. The diaphragm, parasternals, and posterior cricoarytenoids were the most important inspiratory muscles, and internal intercostals and external obliques were the most important expiratory muscles for exercise. Up to a VE of 120 l/min through one lung, QO2RM constituted only a small fraction of total body VO2 during exercise and maximal vasodilation in the diaphragm was never approached.
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Ramsook, Andrew H., Yannick Molgat-Seon, Michele R. Schaeffer, Sabrina S. Wilkie, Pat G. Camp, W. Darlene Reid, Lee M. Romer, and Jordan A. Guenette. "Effects of inspiratory muscle training on respiratory muscle electromyography and dyspnea during exercise in healthy men." Journal of Applied Physiology 122, no. 5 (May 1, 2017): 1267–75. http://dx.doi.org/10.1152/japplphysiol.00046.2017.
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Inspiratory muscle training (IMT) has consistently been shown to reduce exertional dyspnea in health and disease; however, the physiological mechanisms remain poorly understood. A growing body of literature suggests that dyspnea intensity can be explained largely by an awareness of increased neural respiratory drive, as measured indirectly using diaphragmatic electromyography (EMGdi). Accordingly, we sought to determine whether improvements in dyspnea following IMT can be explained by decreases in inspiratory muscle electromyography (EMG) activity. Twenty-five young, healthy, recreationally active men completed a detailed familiarization visit followed by two maximal incremental cycle exercise tests separated by 5 wk of randomly assigned pressure threshold IMT or sham control (SC) training. The IMT group ( n = 12) performed 30 inspiratory efforts twice daily against a 30-repetition maximum intensity. The SC group ( n = 13) performed a daily bout of 60 inspiratory efforts against 10% maximal inspiratory pressure (MIP), with no weekly adjustments. Dyspnea intensity was measured throughout exercise using the modified 0–10 Borg scale. Sternocleidomastoid and scalene EMG was measured using surface electrodes, whereas EMGdi was measured using a multipair esophageal electrode catheter. IMT significantly improved MIP (pre: −138 ± 45 vs. post: −160 ± 43 cmH2O, P < 0.01), whereas the SC intervention did not. Dyspnea was significantly reduced at the highest equivalent work rate (pre: 7.6 ± 2.5 vs. post: 6.8 ± 2.9 Borg units, P < 0.05), but not in the SC group, with no between-group interaction effects. There were no significant differences in respiratory muscle EMG during exercise in either group. Improvements in dyspnea intensity ratings following IMT in healthy humans cannot be explained by changes in the electrical activity of the inspiratory muscles. NEW & NOTEWORTHY Exertional dyspnea intensity is thought to reflect an increased awareness of neural respiratory drive, which is measured indirectly using diaphragmatic electromyography (EMGdi). We examined the effects of inspiratory muscle training (IMT) on dyspnea, EMGdi, and EMG of accessory inspiratory muscles. IMT significantly reduced submaximal dyspnea intensity ratings but did not change EMG of any inspiratory muscles. Improvements in exertional dyspnea following IMT may be the result of nonphysiological factors or physiological adaptations unrelated to neural respiratory drive.
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Dodd, D. S., S. Kelly, P. W. Collett, and L. A. Engel. "Pressure-time product, work rate, and endurance during resistive breathing in humans." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1397–404. http://dx.doi.org/10.1152/jappl.1988.64.4.1397.
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We examined the effect of increasing work rate, without a corresponding increase in the pressure-time product, on energy cost and inspiratory muscle endurance (Tlim) in five normal subjects during inspiratory resistive breathing. Tidal volume, mean inspiratory mouth pressure, duty cycle, and hence the pressure-time product were kept constant, whereas work rate was varied by changing the frequency of breathing. There was a linear decrease in Tlim of -2.1 ± 0.5 s.J-1.min-1 (r = 0.87 ± 0.06) with increasing work rate. The data satisfied a model of energy balance during fatiguing runs (Monod and Scherrer. Ergonomics 8: 329-337, 1965) and were consistent with the hypothesis that the rate of energy supply, or respiratory muscle blood flow, is fixed when the pressure-time product is constant. Our results indicate that during inspiratory resistive breathing against fatiguing loads, work rate determines endurance independently of the pressure-time product. On the basis of the model, our results lead to estimates of respiratory muscle blood flow and available energy stores under the conditions of our experiment.
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Taylor, Nigel A. S., and James B. Morrison. "Static respiratory muscle work during immersion with positive and negative respiratory loading." Journal of Applied Physiology 87, no. 4 (October 1, 1999): 1397–403. http://dx.doi.org/10.1152/jappl.1999.87.4.1397.
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Upright immersion imposes a pressure imbalance across the thorax. This study examined the effects of air-delivery pressure on inspiratory muscle work during upright immersion. Eight subjects performed respiratory pressure-volume relaxation maneuvers while seated in air (control) and during immersion. Hydrostatic, respiratory elastic (lung and chest wall), and resultant static respiratory muscle work components were computed. During immersion, the effects of four air-delivery pressures were evaluated: mouth pressure (uncompensated); the pressure at the lung centroid (Pl,c); and at Pl,c ±0.98 kPa. When breathing at pressures less than the Pl,c, subjects generally defended an expiratory reserve volume (ERV) greater than the immersed relaxation volume, minus residual volume, resulting in additional inspiratory muscle work. The resultant static inspiratory muscle work, computed over a 1-liter tidal volume above the ERV, increased from 0.23 J ⋅ l−1, when subjects were breathing at Pl,c, to 0.83 J ⋅ l−1 at Pl,c −0.98 kPa ( P < 0.05), and to 1.79 J ⋅ l−1 at mouth pressure ( P < 0.05). Under the control state, and during the above experimental conditions, static expiratory work was minimal. When breathing at Pl,c +0.98 kPa, subjects adopted an ERV less than the immersed relaxation volume, minus residual volume, resulting in 0.36 J ⋅ l−1 of expiratory muscle work. Thus static inspiratory muscle work varied with respiratory loading, whereas Pl,c air supply minimized this work during upright immersion, restoring lung-tissue, chest-wall, and static muscle work to levels obtained in the control state.
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Kawagoe, Y., S. Permutt, and H. E. Fessler. "Hyperinflation with intrinsic PEEP and respiratory muscle blood flow." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2440–48. http://dx.doi.org/10.1152/jappl.1994.77.5.2440.
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Increased end-expiratory lung volume and intrinsic positive end-expiratory pressure (PEEP) are common in obstructive lung disease, especially during exacerbations or exercise. This loads the respiratory muscles and may also stress the circulatory system, causing a reduction or redistribution of cardiac output. We measured the blood flow to respiratory muscles and systemic organs using colored microspheres in 10 spontaneously breathing anesthetized tracheotomized dogs. Flows during baseline breathing (BL) were compared with those during hyperinflation (HI) induced by a mechanical analogue of airway closure and with those during an inspiratory resistive load (IR) that produced an equivalent increase in inspiratory work and time-integrated transdiaphragmatic pressure. Cardiac output was unchanged during IR (3.19 +/- 0.27 l/min at BL, 3.09 +/- 0.34 l/min during IR) but was reduced during HI (2.14 +/- 0.29 l/min; P < 0.01). Among the organs studied, flow was unaltered by IR but decreased to the liver and pancreas and increased to the brain during HI. For the respiratory muscles, flow to the diaphragm increased during IR. However, despite a 1.9-fold increase in inspiratory work per minute and a 2.5-fold increase in integrated transdiaphragmatic pressure during HI, blood flow to the diaphragm was unchanged and flow to the scalenes and sternomastoid fell. The only respiratory muscle to which flow increased during HI was the transversus abdominis, an expiratory muscle. We conclude that the circulatory effects of hyperinflation in this model impair inspiratory muscle perfusion and speculate that this may contribute to respiratory muscle dysfunction in hyperinflated states.
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Laoutaris, Ioannis D., Stamatis Adamopoulos, Athanassios Manginas, Demosthenes B. Panagiotakos, Dennis V. Cokkinos, and Athanasios Dritsas. "Inspiratory work capacity is more severely depressed than inspiratory muscle strength in patients with heart failure: Novel applications for inspiratory muscle training." International Journal of Cardiology 221 (October 2016): 622–26. http://dx.doi.org/10.1016/j.ijcard.2016.07.102.
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Sliwinski, P., S. Yan, A. P. Gauthier, and P. T. Macklem. "Influence of global inspiratory muscle fatigue on breathing during exercise." Journal of Applied Physiology 80, no. 4 (April 1, 1996): 1270–78. http://dx.doi.org/10.1152/jappl.1996.80.4.1270.
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We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30, 60, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Esophageal and gastric pressures, anteroposterior displacement of the rib cage and abdomen, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. We conclude that the respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.
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Yamada, Y., M. Shigeta, K. Suwa, and K. Hanaoka. "Respiratory muscle pressure analysis in pressure-support ventilation." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2237–43. http://dx.doi.org/10.1152/jappl.1994.77.5.2237.
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The extent to which respiratory muscles are exerted during partially supported ventilation is difficult to differentiate, because these muscles and the ventilator work simultaneously to produce ventilation. We have developed a new method for determining the pressure developed by the respiratory muscles in partially supported ventilation. In seven patients on pressure-support ventilation (PSV), pressure, flow, and lung volume change were measured at the airway opening. Various PSV levels (0–15 cmH2O) were applied to each patient in random order. By utilizing a model of respiratory mechanics, we calculated the pressure developed by the respiratory muscles and the inspiratory work performed by the muscles from the measured parameters by use of the resistance and elastance of the respiratory system obtained during controlled ventilation. Increasing PSV from 0 to 15 cmH2O modulated the resultant breathing pattern, i.e., increasing tidal volume and decreasing respiratory rate. The respiratory muscle pressure, although less negative, had a shape that corresponded to the shape of airway occlusion pressure at each PSV level, and both pressures decreased concomitantly with increasing PSV. The respiratory muscle work progressively decreased with increasing PSV. This analysis enabled clear and continuous quantifications of the respiratory muscle force generation and inspiratory work during partially supported ventilation.
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Amann, Markus, David F. Pegelow, and Jerome A. Dempsey. "Effect of Inspiratory Muscle Work on Peripheral Locomotor Muscle Fatigue in Hypoxia." Medicine & Science in Sports & Exercise 38, Suppl 1 (November 2006): S15. http://dx.doi.org/10.1249/00005768-200611001-00060.
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Wolpat, Andiara, Francisco V. Lima, Fabiola M. Silva, Micheli Tochetto, Andressa de Freitas, Tatiane Grandi, Leonardo Rodrigues, et al. "Association between inspiratory muscle weakness and slowed oxygen uptake kinetics in patients with chronic obstructive pulmonary disease." Applied Physiology, Nutrition, and Metabolism 42, no. 12 (December 2017): 1239–46. http://dx.doi.org/10.1139/apnm-2016-0568.
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Patients with chronic obstructive pulmonary disease (COPD) may have poor inspiratory muscle function, which reduces minute and alveolar ventilation, leading to increased hypoxemia and slow pulmonary oxygen uptake kinetics. However, little is known about the effect of inspiratory muscle weakness (IMW) on oxygen uptake kinetics in patients with COPD. Thus, we tested the hypothesis that COPD patients with IMW have slowed oxygen uptake kinetics. An observational study was conducted that included COPD patients with moderate to severe airflow limitation and a history of intolerance to exercise. Participants were divided into 2 groups: (IMW+; n = 22) (IMW–; n = 23) of muscle weakness. The maximal inspiratory, expiratory, and sustained inspiratory strength as well as the maximal endurance of the inspiratory muscles were lower in IMW+ patients (36 ± 9.5 cm H2O; 52 ± 14 cm H2O; 20 ± 6.5 cm H2O; 94 ± 84 s, respectively) than in IMW– patients (88 ± 12 cm H2O; 97 ± 28 cm H2O; 82.5 ± 54 cm H2O; 559 ± 92 s, respectively; p < 0.05). Moreover, the 6-min walk test and peak oxygen uptake were reduced in the IMW+ patients. During the constant work test, oxygen uptake kinetics were slowed in the IMW+ compared with IMW– patients (88 ± 29 vs 61 ± 18 s, p < 0.05). Our findings demonstrate that inspiratory muscle weakness in COPD is associated with slowed oxygen uptake kinetics, and thus, reduced functional capacity.
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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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Boriek, Aladin M., Joseph R. Rodarte, and Theodore A. Wilson. "Ratio of active to passive muscle shortening in the canine diaphragm." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 561–66. http://dx.doi.org/10.1152/jappl.1999.87.2.561.
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Active and passive shortening of muscle bundles in the canine diaphragm were measured with the objective of testing a consequence of the minimal-work hypothesis: namely, that the ratio of active to passive shortening is the same for all active muscles. Lengths of six muscle bundles in the costal diaphragm and two muscle bundles in the crural diaphragm of each of four bred-for-research beagle dogs were measured by the radiopaque marker technique during the following maneuvers: a passive deflation maneuver from total lung capacity to functional residual capacity, quiet breathing, and forceful inspiratory efforts against an occluded airway at different lung volumes. Shortening per liter increase in lung volume was, on average, 70% greater during quiet breathing than during passive inflation in the prone posture and 40% greater in the supine posture. For the prone posture, the ratio of active to passive shortening was larger in the ventral and midcostal diaphragm than at the dorsal end of the costal diaphragm. For both postures, active shortening during quiet breathing was poorly correlated with passive shortening. However, shortening during forceful inspiratory efforts was highly correlated with passive shortening. The average ratios of active to passive shortening were 1.23 ± 0.02 and 1.32 ± 0.03 for the prone and supine postures, respectively. These data, taken together with the data reported in the companion paper (T. A. Wilson, M. Angelillo, A. Legrand, and A. De Troyer, J. Appl. Physiol. 87: 554-560, 1999), support the hypothesis that, during forceful inspiratory efforts, the inspiratory muscles drive the chest wall along the minimal-work trajectory.
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Jeruc Tanšek, Monika, Andrej Švent, and Alan Kacin. "Effects of inspiratory muscle training on physical performance during backpack carrying." Annales Kinesiologiae 13, no. 1 (December 30, 2022): 5–21. http://dx.doi.org/10.35469/ak.2022.335.
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Purpose: Restricting chest movement when carrying a loaded backpack reduces efficiency and increases the work of the respiratory muscles. The aim of the present study was to investigate the effects of six weeks of inspiratory muscle training (IMT) on respiratory muscle strength and endurance and on physical performance when carrying a load. Methods: Twenty male (age: 32.2 ± 3.4 years) members of the Special Operations Unit of the Slovenian Army volunteered to participate. The experimental group (n=10) trained their respiratory muscles for six weeks against an incremental inspiratory resistance with a breathing apparatus. The placebo group (n=10) performed the same IMT protocol but with a sham inspiratory resistance. Assessment of the subjects before and after IMT included measurements of the maximal inspiratory and expiratory pressures, heart rate measurements, and ratings of perceived physical and respiratory exertion before and after a 60-min walk test with a 25-kg backpack. Results: After six weeks of IMT, the maximum inspiratory pressure measured before and after the 60-minute walk test increased significantly (p < 0.001) in the experimental group by 47 ± 13% and 58 ± 20%, respectively. Inspiratory fatigue was also significantly lower in the experimental group. No changes were observed in the heart rate and the rating of perceived exertion during the walking test. In the placebo group, no significant changes were observed in the measured parameters after IMT.Conclusion: Six weeks of IMT with progressive breathing resistance improves strength and reduces fatigue of the respiratory muscles. Individuals who perform tasks that require them to carry a heavy backpack for extended periods of time may benefit from IMT.
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Clanton, T. L., G. F. Dixon, J. Drake, and J. E. Gadek. "Effects of breathing pattern on inspiratory muscle endurance in humans." Journal of Applied Physiology 59, no. 6 (December 1, 1985): 1834–41. http://dx.doi.org/10.1152/jappl.1985.59.6.1834.
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Endurance of the inspiratory muscles was measured in normal volunteers using a threshold resistance that produced a relatively constant mouth-pressure load, independent of inspiratory flow rate (VTI). Breathing pattern was controlled by visual feedback from an oscilloscope. Endurance was measured as the length of time (Tlim) a target VTI could be maintained with maximum effort. Effects of changes in breathing pattern on Tlim were compared with control measurements made the same day. Increases in VTI or in duty cycle (inspiratory time/total period) shortened Tlim, whereas decreases lengthened Tlim. However, effects of changes in VTI were less than equivalent changes in tidal volume produced by alterations in duty cycle. Furthermore, when two breathing pattern changes were altered simultaneously to keep the rate of external inspiratory work (Winsp) constant, significant effects due to changes in duty cycle were still observed. In conclusion, 1) both VTI and duty cycle have significant effects on measurements of inspiratory muscle endurance and 2) the effects of VTI are less than the effects of duty cycle for the same Winsp.
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Croix, Claudette M., Barbara J. Morgan, Thomas J. Wetter, and Jerome A. Dempsey. "Fatiguing inspiratory muscle work causes reflex sympathetic activation in humans." Journal of Physiology 529, no. 2 (December 2000): 493–504. http://dx.doi.org/10.1111/j.1469-7793.2000.00493.x.
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Langer, Daniel, Casey Ciavaglia, Azmy Faisal, Katherine A. Webb, J. Alberto Neder, Rik Gosselink, Sauwaluk Dacha, Marko Topalovic, Anna Ivanova, and Denis E. O’Donnell. "Inspiratory muscle training reduces diaphragm activation and dyspnea during exercise in COPD." Journal of Applied Physiology 125, no. 2 (August 1, 2018): 381–92. http://dx.doi.org/10.1152/japplphysiol.01078.2017.
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Among patients with chronic obstructive pulmonary disease (COPD), those with the lowest maximal inspiratory pressures experience greater breathing discomfort (dyspnea) during exercise. In such individuals, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. Therefore, we aimed to identify physiological mechanisms of improvement in dyspnea and exercise endurance following inspiratory muscle training (IMT) in patients with COPD and low maximal inspiratory pressure (Pimax). The effects of 8 wk of controlled IMT on respiratory muscle function, dyspnea, respiratory mechanics, and diaphragm electromyography (EMGdi) during constant work rate cycle exercise were evaluated in patients with activity-related dyspnea (baseline dyspnea index <9). Subjects were randomized to either IMT or a sham training control group ( n = 10 each). Twenty subjects (FEV1 = 47 ± 19% predicted; Pimax = −59 ± 14 cmH2O; cycle ergometer peak work rate = 47 ± 21% predicted) completed the study; groups had comparable baseline lung function, respiratory muscle strength, activity-related dyspnea, and exercise capacity. IMT, compared with control, was associated with greater increases in inspiratory muscle strength and endurance, with attendant improvements in exertional dyspnea and exercise endurance time (all P < 0.05). After IMT, EMGdi expressed relative to its maximum (EMGdi/EMGdimax) decreased ( P < 0.05) with no significant change in ventilation, tidal inspiratory pressures, breathing pattern, or operating lung volumes during exercise. In conclusion, IMT improved inspiratory muscle strength and endurance in mechanically compromised patients with COPD and low Pimax. The attendant reduction in EMGdi/EMGdimax helped explain the decrease in perceived respiratory discomfort despite sustained high ventilation and intrinsic mechanical loading over a longer exercise duration. NEW & NOTEWORTHY In patients with COPD and low maximal inspiratory pressures, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. This study showed that 8 wk of home-based, partially supervised IMT improved respiratory muscle strength and endurance, dyspnea, and exercise endurance. Dyspnea relief occurred in conjunction with a reduced activation of the diaphragm relative to maximum in the absence of significant changes in ventilation, breathing pattern, and operating lung volumes.
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Moawd, Samah A., Alshimaa R. Azab, Saud M. Alrawaili, and Walid Kamal Abdelbasset. "Inspiratory Muscle Training in Obstructive Sleep Apnea Associating Diabetic Peripheral Neuropathy: A Randomized Control Study." BioMed Research International 2020 (June 12, 2020): 1–8. http://dx.doi.org/10.1155/2020/5036585.
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Objective. This work is aimed at assessing the effects of inspiratory muscle training on lung functions, inspiratory muscle strength, and aerobic capacity in diabetic peripheral neuropathy (DPN) patients with obstructive sleep apnea (OSA). Methods. A randomized control study was performed on 55 patients diagnosed with DPN and OSA. They were assigned to the training group (IMT, n=28) and placebo training group (P-IMT, n=27). Inspiratory muscle strength, lung functions, and aerobic capacity were evaluated before and after 12 weeks postintervention. An electronic inspiratory muscle trainer was conducted, 30 min a session, three times a week for 12 consecutive weeks. Results. From seventy-four patients, 55 have completed the study program. A significant improvement was observed in inspiratory muscle strength (p<0.05) in the IMT group while no changes were observed in the P-IMT group (p>0.05). No changes were observed in the lung function in the two groups (p>0.05). Also, VO2max and VCO2max changed significantly after training in the IMT group (p<0.05) while no changes were observed in the P-IMT group (p>0.05). Other cardiopulmonary exercise tests did not show any significant change in both groups (p>0.05). Conclusions. Based on the outcomes of the study, it was found that inspiratory muscle training improves inspiratory muscle strength and aerobic capacity without a notable effect on lung functions for diabetic patients suffering from DPN and OSA.
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Ríos-Castro, Francisco, Felipe González-Seguel, and Jorge Molina. "Respiratory drive, inspiratory effort, and work of breathing: review of definitions and non-invasive monitoring tools for intensive care ventilators during pandemic times." Medwave 22, no. 03 (April 29, 2022): e002550-e002550. http://dx.doi.org/10.5867/medwave.2022.03.002550.
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Technological advances in mechanical ventilation have been essential to increasing the survival rate in intensive care units. Usually, patients needing mechanical ventilation use controlled ventilation to override the patient’s respiratory muscles and favor lung protection. Weaning from mechanical ventilation implies a transition towards spontaneous breathing, mainly using assisted mechanical ventilation. In this transition, the challenge for clinicians is to avoid under and over assistance and minimize excessive respiratory effort and iatrogenic diaphragmatic and lung damage. Esophageal balloon monitoring allows objective measurements of respiratory muscle activity in real time, but there are still limitations to its routine application in intensive care unit patients using mechanical ventilation. Like the esophageal balloon, respiratory muscle electromyography and diaphragmatic ultrasound are minimally invasive tools requiring specific training that monitor respiratory muscle activity. Particularly during the coronavirus disease pandemic, non invasive tools available on mechanical ventilators to monitor respiratory drive, inspiratory effort, and work of breathing have been extended to individualize mechanical ventilation based on patient’s needs. This review aims to identify the conceptual definitions of respiratory drive, inspiratory effort, and work of breathing and to identify non invasive maneuvers available on intensive care ventilators to measure these parameters. The literature highlights that although respiratory drive, inspiratory effort, and work of breathing are intuitive concepts, even distinguished authors disagree on their definitions.
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Chaunchaiyakul, Rungchai, Herb Groeller, John R. Clarke, and Nigel A. S. Taylor. "The impact of aging and habitual physical activity on static respiratory work at rest and during exercise." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 6 (December 2004): L1098—L1106. http://dx.doi.org/10.1152/ajplung.00399.2003.
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We investigated the effects of aging on the elastic properties of lung tissue and the chest wall, simultaneously quantifying the contribution of each component to static inspiratory muscle work in resting and exercising adults. We further evaluated the interaction of aging and habitual physical activity on respiratory mechanics. Static lung volumes and elastic properties of the lung and chest wall (pressure-volume relaxation maneuvers) in 29 chronically sedentary and 29 habitually active subjects, grouped by age, were investigated: young (Y, 20–30 years), middle-aged (M, 40–50 years), and older (O, >60 years). Using static pressure-volume data, we computed the elastic work of breathing (joules per liter, J·l−1), including inspiratory muscle work, over resting and exercising tidal volume excursions. Elastic work of the lung (Y = 0.79 ± 0.05; M = 0.47 ± 0.05; O = 0.43 ± 0.05 J·l−1) and chest wall (Y = −0.49 ± 0.06; M = −0.12 ± 0.07; O = 0.04 ± 0.05 J·l−1 ) changed significantly with age ( P < 0.05). With aging, a parallel displacement of the chest wall pressure-volume curve resulted in a shift from energy being stored primarily during expiration to energy storage during inspiration, and driving expiration, both at rest and during exercise. Although deviating significantly from young adults, this did not significantly elevate static inspiratory muscle work but resulted in a redistribution of the tissues on which this work was performed and the phase of the respiratory cycle in which it occurred. Nevertheless, static inspiratory muscle work remained similar across age groups, at rest and during exercise, and habitual physical activity failed to influence these changes.
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Clague, J. E., J. Carter, M. G. Pearson, and P. M. A. Calverley. "Physiological Determinants of Inspiratory Effort Sensation during CO2 Rebreathing in Normal Subjects." Clinical Science 85, no. 5 (November 1, 1993): 637–42. http://dx.doi.org/10.1042/cs0850637.
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1. The physiological basis of inspiratory effort sensation remains uncertain. Previous studies have suggested that pleural pressure, rather than inspiratory muscle fatigue, is the principal determinant of inspiratory effort sensation. However, only a limited range of inspiratory flows and breathing patterns have been examined. We suspected that inspiratory effort sensation was related to the inspiratory muscle tension-time index developed whatever the breathing pattern or load, and that this might explain the additional rise in sensation seen with hypercapnia. 2. To investigate this we measured hypercapnic re-breathing responses in seven normal subjects (six males, age range 21–38 years) with and without an inspiratory resistive load of 10 cm H2O. Pleural and transdiaphragmatic pressures, mouth occlusion pressure and breathing pattern were measured. Diaphragmatic and ribcage tension-time indices were calculated from these data. Inspiratory effort sensation was recorded using a Borg scale at 30s intervals during each rebreathing run. 3. Breathing pattern and inspiratory pressure partitioning were unrelated to changes in inspiratory effort sensation during hypercapnia. Tension-time indices reached pre-fatiguing levels during both free breathing and inspiratory resistive loading. 4. Stepwise multiple regression analysis using pooled mechanical, chemical and breathing pattern variables showed that pleural pressure was more closely related to inspiratory effort sensation than was transdiaphragmatic pressure. When converted to tension-time indices, ribcage tension-time index was the major determinant of inspiratory effort sensation during loaded rebreathing, but partial pressure of CO2 was an important independent variable, whereas during unloaded rebreathing partial pressure of CO2 was the most important determinant of inspiratory effort sensation. 5. These results suggest that the pattern of inspiratory pressure partitioning and inspiratory flow rate have little influence on inspiratory effort sensation during CO2 stimulated breathing. The close association between inspiratory effort sensation and ribcage tension-time index, an index of inspiratory muscle work, suggests that inspiratory effort sensation may forewarn of potential inspiratory muscle fatigue. Changes in PaCO2 have a small independent effect on respiratory perception.
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Bersten, A. D., A. J. Rutten, and A. E. Vedig. "Efficacy of Pressure Support in Compensating for Apparatus Work." Anaesthesia and Intensive Care 21, no. 1 (February 1993): 67–71. http://dx.doi.org/10.1177/0310057x9302100116.
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Breathing through an endotracheal tube, connector, and ventilator demand valve imposes an added load on the respiratory muscles. As respiratory muscle fatigue is thought to be a frequent cause of ventilator dependence, we sought to examine the efficacy of five different ventilators in reducing this imposed work through the application of pressure support ventilation. Using a model of spontaneous breathing, we examined the apparatus work imposed by the Servo 900-C, Puritan Bennett 7200a, Engstrom Erica, Drager EV-A or Hamilton Veolar ventilators, a size 7.0 and 8.0 mm endotracheal tube, and inspiratory flow rates of 40 and 60 l/min. Pressure support of 0, 5, 10, 15, 20 and 30 cm H2O was tested at each experimental condition. Apparatus work was greater with increased inspiratory flow rate and decreased endotracheal tube size, and was lowest for the Servo 900-C and Puritan Bennett 7200a ventilators. Apparatus work fell in a curvilinear fashion when pressure support was applied, with no major difference noted between the five ventilators tested. At an inspiratory flow rate of 40 l/min, a pressure support of 5 and 8 cm H2O compensated for apparatus work through size 8.0 and 7.0 endotracheal tubes and the Servo 900-C and Puritan Bennett 7200a ventilators. However, the maximum negative pressure was greater for the Servo 900-C. The added work of breathing through endotracheal tubes and ventilator demand valves may be compensated for by the application of pressure support. The level of pressure support required depends on inspiratory flow rate, endotracheal tube size, and type of ventilator.
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Yan, Sheng, and Jason H. T. Bates. "Breathing responses to small inspiratory threshold loads in humans." Journal of Applied Physiology 86, no. 3 (March 1, 1999): 874–80. http://dx.doi.org/10.1152/jappl.1999.86.3.874.
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To investiage the effect of inspiratory threshold load (ITL) on breathing, all previous work studied loads that were much greater than would be encountered under pathophysiological conditions. We hypothesized that mild ITL from 2.5 to 20 cmH2O is sufficient to modify control and sensation of breathing. The study was performed in healthy subjects. The results demonstrated that with mild ITL 1) inspiratory difficulty sensation could be perceived at an ITL of 2.5 cmH2O; 2) tidal volume increased without change in breathing frequency, resulting in hyperpnea; and 3) although additional time was required for inspiratory pressure to attain the threshold before inspiratory flow was initiated, the total inspiratory muscle contraction time remained constant. This resulted in shortening of the available time for inspiratory flow, so that the tidal volume was maintained or increased by significant increase in mean inspiratory flow. On the basis of computer simulation, we conclude that the mild ITL is sufficient to increase breathing sensation and alter breathing control, presumably aiming at maintaining a certain level of ventilation but minimizing the energy consumption of the inspiratory muscles.
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Sheel, A. William, P. Alexander Derchak, David F. Pegelow, and Jerome A. Dempsey. "Threshold effects of respiratory muscle work on limb vascular resistance." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 5 (May 1, 2002): H1732—H1738. http://dx.doi.org/10.1152/ajpheart.00798.2001.
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The purpose of this study was to determine whether the human diaphragm, like limb muscle, has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction. We used Doppler ultrasound techniques to quantify leg blood flow (QL) and utilized the changes in mouth twitch pressure (ΔPMT) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue. Six healthy male subjects performed four randomly assigned trials of identical duration (8 ± 2 min) and breathing pattern [20 breaths/min and time spent on inspiration during the duty cycle (time spent on inspiration/total time of one breathing cycle) was 0.4] during which they inspired primarily with the diaphragm. For trials 1- 3, inspiratory resistance and effort was gradually increased [30, 40, and 50% maximal inspiratory pressure (MIP)], diaphragm fatigue did not occur, and QL, limb vascular resistance (LVR), and mean arterial pressure remained unchanged from control ( P > 0.05). The fourth trial utilized the same breathing pattern with 60% MIP and caused diaphragm fatigue, as shown by a 30 ± 12% reduction in PMT with bilateral phrenic nerve stimulation. During the fatigue trial, QL and LVR were unchanged from baseline at minute 1, but LVR rose 36% and QL fell 25% at minute 2 and by 52% and 30%, respectively, during the final minutes of the trial. Both LVR and QL returned to control within 30 s of recovery. In summary, voluntary increases in inspiratory muscle effort, in the absence of fatigue, had no effect on LVR and QL, whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in QL. We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm, which reaches its threshold for activation during fatiguing contractions.
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Mizuno, M. "Human respiratory muscles: fibre morphology and capillary supply." European Respiratory Journal 4, no. 5 (May 1, 1991): 587–601. http://dx.doi.org/10.1183/09031936.93.04050587.
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In man the diaphragm (DIA) and abdominal muscles comprise approximately 50% slow-twitch (ST) fibres, whereas a higher proportion (60%) is found in intercostal muscles and the scalenes. All respiratory muscles show an equal distribution of fast-twitch (FTa and b) fibres with the exception of the expiratory intercostal muscles which have few FTb fibres. The inspiratory muscles have a uniformly small fibre size, in contrast to the expiratory intercostal muscle fibres which are large. The fibre size of the inspiratory muscles is maintained with ageing, whereas that of the expiratory intercostal muscles appears to be reduced after the age of 50 yrs. Capillary supply is most abundant in the expiratory muscles followed by DIA and the inspiratory intercostal muscles. In patients with chronic obstructive pulmonary disease (COPD) it is unknown whether a reduction in fibre size of the thoracic respiratory muscles is caused by extreme use due to increased ventilatory work, or by disuse due to an increased involvement of the extrathoracic respiratory muscles. Histochemical characteristics suggest that, in normal humans, the load on the inspiratory muscles is relatively small during contractions, whereas the expiratory intercostal muscles are exposed to severe continuous activity with a heavy load.
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Romer, Lee M., Andrew T. Lovering, Hans C. Haverkamp, David F. Pegelow, and Jerome A. Dempsey. "Effect of inspiratory muscle work on peripheral fatigue of locomotor muscles in healthy humans." Journal of Physiology 571, no. 2 (February 17, 2006): 425–39. http://dx.doi.org/10.1113/jphysiol.2005.099697.
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Eastwood, P. R., D. R. Hillman, and K. E. Finucane. "Ventilatory responses to inspiratory threshold loading and role of muscle fatigue in task failure." Journal of Applied Physiology 76, no. 1 (January 1, 1994): 185–95. http://dx.doi.org/10.1152/jappl.1994.76.1.185.
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To examine respiratory muscle recruitment pattern during inspiratory loading and role of fatigue in limiting endurance, we studied seven normal subjects on 17 +/- 6 days during breathing against progressive inspiratory threshold load. Threshold pressure (Pth) was progressively increased 14 +/- 5 cmH2O every 2 min until voluntary cessation (task failure). Subjects could adopt any breathing pattern. Tidal volume (VT), chest wall motion, end-tidal PCO2, and arterial O2 saturation were measured. At moderate loads [50–75% of maximum Pth (Pthmax)], inspiratory time (TI) decreased and VT/TI and expiratory time increased, increasing time for recovery of muscles between inspirations. At high loads (> 75% Pthmax), VT/TI decreased, which, with progressive decrease in end-expiratory lung volume (EELV) throughout, increased potential for inspiratory force development. Progressive hypoxia and hypercapnia occurred at higher work loads. Immediately after task failure all subjects could recover at high loads and still reachieve initial Pthmax on reimposition of progressive loading. Respiratory pressures were measured in subgroup of three subjects: transdiaphragmatic pressure response to 0.1-ms bilateral supramaximal phrenic nerve stimulation at end expiration initially increased with increasing load/decreasing EELV, consistent with increasing mechanical advantage of diaphragm, but decreased at highest loads, suggesting diaphragm fatigue. Full recovery had not occurred at 30 min after task failure. We demonstrated that progressive threshold loading is associated with systematic changes in breathing pattern that act to optimize muscle strength and increase endurance. Task failure occurred when these compensatory mechanisms were maximal. Inspiratory muscles appeared relatively resistant to fatigue, which was late but persistent.
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Formiga, Magno F., Isabel Vital, Gisel Urdaneta, Kira Balestrini, Lawrence P. Cahalin, and Michael A. Campos. "The BODE index and inspiratory muscle performance in COPD: Clinical findings and implications." SAGE Open Medicine 6 (January 2018): 205031211881901. http://dx.doi.org/10.1177/2050312118819015.
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Objectives: The Test of Incremental Respiratory Endurance is a novel testing method that provides a unique examination of one’s inspiratory muscle strength, work and endurance. Little is known about the relationship between inspiratory muscle performance and mortality risk in obstructive lung disease. We examined the relationship between the Test of Incremental Respiratory Endurance measures and the Body-mass index, airflow Obstruction, Dyspnea and Exercise index in chronic obstructive pulmonary disease. Methods: In all, 70 males with mild-to-very severe chronic obstructive pulmonary disease (mean ± standard deviation of 70.2 ± 5.9 years) underwent measurements of body-mass index, spirometry, dyspnea and a 6-min walk test from which the Body-mass index, airflow Obstruction, Dyspnea and Exercise score was calculated. The Test of Incremental Respiratory Endurance provided measures of maximal inspiratory pressure, sustained maximal inspiratory pressure and inspiratory duration. Results: All Test of Incremental Respiratory Endurance parameters inversely correlated with the Body-mass index, airflow Obstruction, Dyspnea and Exercise score: maximal inspiratory pressure (r = −0.355, p = 0.00), sustained maximal inspiratory pressure (r = −0.426, p = 0.00) and ID (r = −0.278, p = 0.02), with sustained maximal inspiratory pressure displaying the highest correlation. Independent significant correlations were also observed between the sustained maximal inspiratory pressure and all Body-mass index, airflow Obstruction, Dyspnea and Exercise score components, except for body-mass index. Finally, sustained maximal inspiratory pressure was significantly different among the Body-mass index, airflow Obstruction, Dyspnea and Exercise index quartiles. Discussion: The significant association between the Body-mass index, airflow Obstruction, Dyspnea and Exercise score and inspiratory muscle performance, in particular sustained maximal inspiratory pressure, suggests that these measures may have a potential prognostic value in the evaluation of chronic obstructive pulmonary disease.
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Carra, J., R. Candau, S. Keslacy, F. Giolbas, F. Borrani, G. P. Millet, A. Varray, and M. Ramonatxo. "Addition of inspiratory resistance increases the amplitude of the slow component of O2 uptake kinetics." Journal of Applied Physiology 94, no. 6 (June 1, 2003): 2448–55. http://dx.doi.org/10.1152/japplphysiol.00493.2002.
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The contribution of respiratory muscle work to the development of the O2consumption (V˙o 2) slow component is a point of controversy because it has been shown that the increased ventilation in hypoxia is not associated with a concomitant increase inV˙o 2 slow component. The first purpose of this study was thus to test the hypothesis of a direct relationship between respiratory muscle work andV˙o 2 slow component by manipulating inspiratory resistance. Because the conditions for aV˙o 2 slow component specific to respiratory muscle can be reached during intense exercise, the second purpose was to determine whether respiratory muscles behave like limb muscles during heavy exercise. Ten trained subjects performed two 8-min constant-load heavy cycling exercises with and without a threshold valve in random order. V˙o 2 was measured breath by breath by using a fast gas exchange analyzer, and the V˙o 2 response was modeled after removal of the cardiodynamic phase by using two monoexponential functions. As anticipated, when total work was slightly increased with loaded inspiratory resistance, slight increases in baseV˙o 2, the primary phase amplitude, and peak V˙o 2 were noted (14.2%, P < 0.01; 3.5%, P > 0.05; and 8.3%, P < 0.01, respectively). The bootstrap method revealed small coefficients of variation for the model parameter, including the slow-component amplitude and delay (15 and 19%, respectively), indicating an accurate determination for this critical parameter. The amplitude of the V˙o 2 slow component displayed a 27% increase from 8.1 ± 3.6 to 10.3 ± 3.4 ml · min−1 · kg−1( P < 0.01) with the addition of inspiratory resistance. Taken together, this increase and the lack of any differences in minute volume and ventilatory parameters between the two experimental conditions suggest the occurrence of aV˙o 2 slow component specific to the respiratory muscles in loaded condition.
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Krishnan, Bharath S., Trevor Zintel, Colm McParland, and Charles G. Gallagher. "Evolution of inspiratory and expiratory muscle pressures during endurance exercise." Journal of Applied Physiology 88, no. 1 (January 1, 2000): 234–45. http://dx.doi.org/10.1152/jappl.2000.88.1.234.
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We investigated the relationship between minute ventilation (V˙e) and net respiratory muscle pressure (Pmus) throughout the breathing cycle [Total Pmus = mean Pmus, i (inspiratory) + mean Pmus, e(expiratory)] in six normal subjects performing constant-work heavy exercise (CWHE, at ∼80% maximum) to exhaustion on a cycle ergometer. Pmus was calculated as the sum of chest wall pressure (elastic + resistive) and pleural pressure, and all mean Pmus variables were averaged over the total breath duration. Pmus, i was also expressed as a fraction of volume-matched, flow-corrected dynamic capacity of the inspiratory muscles ([Formula: see text]).V˙e increased significantly from 3 min to the end of CWHE and was the result of a significantly linear increase in Total Pmus (Δ = 43 ± 9% from 3 min to end exercise, P < 0.005) in all subjects ( r = 0.81–0.99). Although mean Pmus, i during inspiratory flow increased significantly (Δ = 35 ± 10%), postinspiratory Pmus, i fell (Δ = −54 ± 10%) and postexpiratory expiratory activity was negligible or absent throughout CWHE. There was a greater increase in mean Pmus, e (Δ = 168 ± 48%), which served to increaseV˙e throughout CWHE. In five of six subjects, there were significant linear relationships betweenV˙eand mean Pmus, i( r = 0.50–0.97) and mean Pmus, e( r = 0.82–0.93) during CWHE. The subjects generated a wide range of Pmus, i/[Formula: see text]values (25–80%), and mean Pmus, i/[Formula: see text]increased significantly (Δ = 42 ± 16%) and in a linear fashion ( r = 0.69–0.99) withV˙ethroughout CWHE. The progressive increase inV˙e during CWHE is due to 1) a linear increase in Total Pmus, 2) a linear increase in inspiratory muscle load, and 3) a progressive fall in postinspiratory inspiratory activity. We conclude that the relationship between respiratory muscle pressure andV˙e during exercise is linear and not curvilinear.
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Krupnick, Alexander S., Jianliang Zhu, Taitan Nguyen, Daniel Kreisel, Keki R. Balsara, Edward B. Lankford, Charles C. Clark, Sanford Levine, Hansell H. Stedman, and Joseph B. Shrager. "Inspiratory loading does not accelerate dystrophy inmdx mouse diaphragm: implications for regenerative therapy." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 411–19. http://dx.doi.org/10.1152/japplphysiol.00689.2002.
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Since the finding that the mdx mouse diaphragm, in contrast to limb muscles, undergoes progressive degeneration analogous to that seen in Duchenne muscular dystrophy, the relationship between the workload on a muscle and the pathogenesis of dystrophy has remained controversial. We increased the work performed by the mdx mouse diaphragm in vivo by tracheal banding and evaluated the progression of dystrophic changes in that muscle. Despite the establishment of dramatically increased respiratory workload and accelerated myofiber damage documented by Evans blue dye, no change in the pace of progression of dystrophy was seen in banded animals vs. unbanded, sham-operated controls. At the completion of the study, more centrally nucleated fibers were evident in the diaphragms of banded mdx mice than in sham-operated mdx controls, indicating that myofiber regeneration increases to meet the demands of the work-induced damage. These data suggest that there is untapped regenerative capacity in dystrophin-deficient muscle and validates experimental efforts aimed at augmenting regeneration within skeletal muscle as a therapeutic strategy in the treatment of dystrophinopathies.
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Nunes Júnior, Adauto de Oliveira, Marina Andrade Donzeli, Suraya Gomes Novais Shimano, Nuno Miguel Lopes de Oliveira, Gualberto Ruas, and Dernival Bertoncello. "EFFECTS OF HIGH-INTENSITY INSPIRATORY MUSCLE TRAINING IN RUGBY PLAYERS." Revista Brasileira de Medicina do Esporte 24, no. 3 (May 2018): 216–19. http://dx.doi.org/10.1590/1517-869220182403166216.
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ABSTRACT Introduction: Rugby is a sport characterized by high and low intensity motor action. Therefore, the respiratory muscles need adequate work to maintain sustained effective breathing. Objective: To analyze the effects of high-intensity inspiratory muscle training (IMT) in amateur rugby players from the city of Uberaba, Minas Gerais, Brazil. Methods: This is a clinical study in which 20 amateur players underwent a pulmonary function test, respiratory muscle strength and physical capacity assessment. The participants were divided into two groups: 10 volunteers in the IMT group (G1) and 10 in the control group (G2). All the assessments were carried out before and after 12 weeks of IMT. Results: No significant changes were observed in the pulmonary function test. However, maximal voluntary ventilation, maximal inspiratory pressure, maximal expiratory pressure and distance increased significantly after IMT. Conclusion: IMT had beneficial effects on amateur rugby players. Level of evidence I; Therapeutic studies - Investigation of treatment results.
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Poon, C. S., S. L. Lin, and O. B. Knudson. "Optimization character of inspiratory neural drive." Journal of Applied Physiology 72, no. 5 (May 1, 1992): 2005–17. http://dx.doi.org/10.1152/jappl.1992.72.5.2005.
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A previous optimal chemical-mechanical model (C.-S. Poon. J. Appl. Physiol. 62: 2447–2459, 1987) suggested that the normal ventilatory responses to CO2 and exercise inputs and mechanical loading can be predicted by the minimization of a controller objective function consisting of the total chemical and mechanical costs of breathing. In this study the model was generalized to include a description of the inspiratory neuromuscular drive as the control output. With a mechanical work rate index for both inspiration and expiration, the general optimization model accurately reproduced the observed responses in the waveshape of inspiratory drive, breathing pattern, and total ventilation under differing conditions of CO2 inhalation, exercise, and inspiratory/expiratory mechanical loads. The simulation results are in general agreement with a wide range of respiratory phenomena, including exercise hyperpnea, CO2 chemoreflex, and post-inspiratory (postinflow) inspiratory activity, as well as respiratory neural compensations for mechanical loading, respiratory muscle fatigue, and muscle weakness.
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Coast, J. R., R. A. Jensen, S. S. Cassidy, M. Ramanathan, and R. L. Johnson. "Cardiac output and O2 consumption during inspiratory threshold loaded breathing." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1624–28. http://dx.doi.org/10.1152/jappl.1988.64.4.1624.
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In this study, noninvasive measurements of cardiac output and O2 consumption were performed to estimate the blood flow to and efficiency of the respiratory muscles that are used in elevated inspiratory work loads. Five subjects were studied for 4.5 min at a respiratory rate of 18 breaths/min and a duty cycle of 0.5. Studies were performed at rest without added respiratory loads and at elevated inspiratory work loads with the use of an inspiratory valve that permitted flow only when a threshold pressure was maintained. Cardiac output and O2 consumption were calculated using a rebreathing technique. Respiratory muscle blood flow and O2 consumption were estimated as the difference between resting and loaded breathing. Work of breathing was calculated by integrating the product of mouth pressure and volume. Increases in cardiac output and O2 consumption in response of 4.5 min loaded breathing averaged 1.84 l/min and 108 ml/min, respectively. No increases were seen in response to 20-s loaded breathing. In a separate series of experiments on four subjects, though, cardiac output increased for the first 2 min then leveled off. These results indicate that the increase in cardiac output was a metabolic effect of the increased work load and was not caused primarily by the influence of the highly negative intrathoracic pressure on venous return. Efficiency of the respiratory muscles during inspiratory threshold loading averaged 5.9%, which was similar to measurements of efficiency of respiratory muscles using whole-body O2 consumption that have been reported previously in humans and in dogs.
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Faghy, Mark. "A review of Inspiratory muscle training. When and why does it work?" Japanese Journal of Physical Fitness and Sports Medicine 68, no. 1 (2019): 3–5. http://dx.doi.org/10.7600/jspfsm.68.3.
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Bachasson, Damien, Martin Dres, Marie-Cécile Niérat, Jean-Luc Gennisson, Jean-Yves Hogrel, Jonne Doorduin, and Thomas Similowski. "Diaphragm shear modulus reflects transdiaphragmatic pressure during isovolumetric inspiratory efforts and ventilation against inspiratory loading." Journal of Applied Physiology 126, no. 3 (March 1, 2019): 699–707. http://dx.doi.org/10.1152/japplphysiol.01060.2018.
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The reference method for the assessment of diaphragm function relies on the measurement of transdiaphragmatic pressure (Pdi). Local muscle stiffness measured using ultrafast shear wave elastography (SWE) provides reliable estimates of muscle force in locomotor muscles. This study aimed at investigating whether SWE could be used as a surrogate of Pdi to evaluate diaphragm function. Fifteen healthy volunteers underwent a randomized stepwise inspiratory loading protocol of 0–60% of maximal isovolumetric inspiratory pressure during closed-airways maneuvers and 0–50% during ventilation against an external inspiratory threshold load. During all tasks, Pdi was measured and SWE was used to assess shear modulus of the right hemidiaphragm (SMdi) at the zone of apposition. Pearson correlation coefficients ( r) and repeated-measures correlation coefficients ( R) were computed to determine within-individual and overall relationships between Pdi and SMdi, respectively. During closed-airways maneuvers, mean Pdi correlated to mean SMdi in all participants [ r ranged from 0.77 to 0.96, all P < 0.01; R = 0.82, 95% confidence intervals (0.76, 0.86), P < 0.01]. During ventilation against inspiratory threshold loading, Pdi swing correlated to maximal SMdi in all participants [ r ranged from 0.40 to 0.90, all P < 0.01; R = 0.70, 95% confidence intervals (0.66, 0.73), P < 0.001]. Changes in diaphragm stiffness as assessed by SWE reflect changes in transdiaphragmatic pressure. SWE provides a new opportunity for direct and noninvasive assessment of diaphragm function. NEW & NOTEWORTHY Accurate and specific estimation of diaphragm effort is critical for evaluating and monitoring diaphragm dysfunction. The measurement of transdiaphragmatic pressure requires the use of invasive gastric and esophageal probes. In the present work, we demonstrate that changes in diaphragm stiffness assessed with ultrasound shear wave elastography reflect changes in transdiaphragmatic pressure, therefore offering a new noninvasive method for gauging diaphragm effort.
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Wetter, Thomas J., Craig A. Harms, William B. Nelson, David F. Pegelow, and Jerome A. Dempsey. "Influence of respiratory muscle work onV˙o 2 and leg blood flow during submaximal exercise." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 643–51. http://dx.doi.org/10.1152/jappl.1999.87.2.643.
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The work of breathing (Wb) normally incurred during maximal exercise not only requires substantial cardiac output and O2 consumption (V˙o 2) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q˙leg). We wondered whether the Wbnormally incurred during submaximal exercise would also reduceQ˙leg. Therefore, we investigated the effects of changing the Wb onQ˙leg via thermodilution in 10 healthy trained male cyclists [maximalV˙o 2(V˙o 2 max) = 59 ± 9 ml ⋅ kg−1 ⋅ min−1] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% ofV˙o 2 max. Inspiratory muscle work was 1) reduced 40 ± 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 ± 8% by addition of inspiratory resistive loads. Increasing the Wb during submaximal exercise caused V˙o 2 to increase; decreasing the Wb was associated with lowerV˙o 2(ΔV˙o 2 = 0.12 and 0.21 l/min at 50 and 75% ofV˙o 2 max, respectively, for ∼100% change in Wb). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, orQ˙leg when Wb was reduced or increased. Why are LVR, norepinephrine spillover, andQ˙leg influenced by the Wb at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal Wbrequired makes insufficient demands forV˙o 2 and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50–70% increase in Wb during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR orQ˙leg.
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Amann, Markus, David F. Pegelow, Anthony J. Jacques, and Jerome A. Dempsey. "Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 5 (November 2007): R2036—R2045. http://dx.doi.org/10.1152/ajpregu.00442.2007.
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Our aim was to isolate the independent effects of 1) inspiratory muscle work (Wb) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O2 fraction (FiO2) = 0.15, arterial hemoglobin saturation (SaO2) = 81 ± 1%; 8.6 ± 0.5 min, 273 ± 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (SaO2 = 95 ± 1%; Normoxia-Ctrl). These trials were repeated, but with a 35–80% reduction in Wb achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of Wb in hypoxia on quadriceps fatigue, independent of reductions in SaO2, were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of SaO2 ( P = 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Qtw,pot) decreased by 30 ± 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 ± 4%; P = 0.0007). This effect of Wb on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing Wb had no significant effect on fatigue. The isolated effects of reduced SaO2 on quadriceps fatigue, independent of changes in Wb, were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of Wb. Qtw,pot decreased by 15 ± 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (−22 ± 3%; P = 0.034). We conclude that both arterial hypoxemia and Wb contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work rates during which, in normoxia, Wb has no effect on peripheral fatigue.
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Loring, Stephen H., Mauricio Garcia-Jacques, and Atul Malhotra. "Pulmonary characteristics in COPD and mechanisms of increased work of breathing." Journal of Applied Physiology 107, no. 1 (July 2009): 309–14. http://dx.doi.org/10.1152/japplphysiol.00008.2009.
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Mechanical characteristics and gas exchange inefficiencies of the lungs contribute to increased work of ventilation in chronic obstructive pulmonary disease (COPD) at rest and exercise, and the energy cost of ventilation is increased in COPD at any external work level. Assuming typical ventilatory variables and respiratory characteristics, we estimated the relative contributions of inspiratory and expiratory resistance, dynamic elastance, intrinsic positive end-expiratory pressure, and gas exchange inefficiency to the work of breathing, finding that the last of these is likely to be of major importance. Dynamic hyperinflation can be seen as both an impediment to inspiratory muscle function and an essential component of adaptation to severe obstruction. Extrinsic restriction, in which the chest wall fails to achieve and maintain abnormally high lung volumes in COPD, can limit ventilatory function and contribute to disability.
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Shee, C. D., Y. Ploy-Song-Sang, and J. Milic-Emili. "Decay of inspiratory muscle pressure during expiration in conscious humans." Journal of Applied Physiology 58, no. 6 (June 1, 1985): 1859–65. http://dx.doi.org/10.1152/jappl.1985.58.6.1859.
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In eight conscious spontaneously breathing adults we studied the decay of pressure developed by the inspiratory muscles during expiration (PmusI). PmusI was obtained according to the following equation: PmusI(t) = Ers X V(t) - Rrs X V(t), where V is volume and V is flow at any instant t during spontaneous expiration, and Ers and Rrs are, respectively, the passive elastance and resistance of the total respiratory system. Ers was determined with the relaxation method, and resistance with the interrupter method. All subjects showed marked braking of expiratory flow by PmusI. The mean time for PmusI to reduce to 50 and 0% amounted, respectively, to 23 and 79% of expiratory time. During expiration, 24–55% of the elastic energy stored during inspiration was used as resistive work and the remainder (45–76%) as negative work.
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Belman, M. J., and R. Shadmehr. "Targeted resistive ventilatory muscle training in chronic obstructive pulmonary disease." Journal of Applied Physiology 65, no. 6 (December 1, 1988): 2726–35. http://dx.doi.org/10.1152/jappl.1988.65.6.2726.
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To overcome the problem of altered breathing strategy during resistive ventilatory muscle training (VMT), we used a single-orifice inspiratory resistance together with a target feedback device (TFD) in patients with chronic obstructive pulmonary disease (COPD). In a preliminary study (study A), we showed that the resistance plus TFD was effective in controlling breathing strategy. We subsequently used the resistor plus TFD in a 5-wk study (study B) of VMT in 17 COPD patients who were randomized into high-intensity (HI) and low-intensity (LI) training groups. Compared with the LI group, the HI group showed significant increases in static maximal inspiratory pressure (21.3 vs. 5.0 cmH2O), maximal sustained ventilatory capacity (MSVC, 3.2 vs -0.1 l/min, sustained maximal mouth pressure (12.1 vs. 0.6 cmH2O), mean mouth pressure (6.9 vs. 3.9 cmH2O), peak inspiratory flow rate (12.3 vs. 4.0 l/min), and maximal sustained work rate (12.2 vs. 4.2 cmH2O.l-1.min-1). We conclude that targeted VMT with control of breathing strategy improves both ventilatory muscle strength and endurance.
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Hanel, Birgitte, and Niels H. Secher. "Maximal oxygen uptake and work capacity after inspiratory muscle training: A controlled study." Journal of Sports Sciences 9, no. 1 (March 1991): 43–52. http://dx.doi.org/10.1080/02640419108729854.
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Guslits, B. G., S. E. Gaston, M. H. Bryan, S. J. England, and A. C. Bryan. "Diaphragmatic work of breathing in premature human infants." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1410–15. http://dx.doi.org/10.1152/jappl.1987.62.4.1410.
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Present methods of assessing the work of breathing in human infants do not account for the added load when intercostal muscle activity is lost and rib cage distortion occurs. We have developed a technique for assessing diaphragmatic work in this circumstance utilizing measurements of transdiaphragmatic pressure and abdominal volume displacement. Eleven preterm infants without evidence of lung disease were studied. During periods of minimal rib cage distortion, inspiratory diaphragmatic work averaged 5.9 g X cm X ml-1, increasing to an average of 12.4 g X cm X ml-1 with periods of paradoxical rib cage motion (P less than 0.01). Inspiratory work was strongly correlated with the electrical activity of the diaphragm as measured from its moving time average (P less than 0.05). Assuming a mechanical efficiency of 4% in these infants, the caloric cost of diaphragmatic work may reach 10% of their basal metabolic rate in periods with rib cage distortion. When lung disease is superimposed, the increased metabolic demands of the diaphragm may predispose preterm infants to fatigue and may contribute to a failure to grow.
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Dodd, D. S., J. Yarom, S. H. Loring, and L. A. Engel. "O2 cost of inspiratory and expiratory resistive breathing in humans." Journal of Applied Physiology 65, no. 6 (December 1, 1988): 2518–23. http://dx.doi.org/10.1152/jappl.1988.65.6.2518.
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In six normal male subjects we compared the O2 cost of resistive breathing (VO2 resp) between equivalent external inspiratory (IRL) and expiratory loads (ERL) studied separately. Each subject performed four pairs of runs matched for tidal volume, breathing frequency, flow rates, lung volume, pressure-time product, and work rate. Basal O2 uptake, measured before and after pairs of loaded runs, was subtracted from that measured during resistive breathing to obtain VO2 resp. For an equivalent load, the VO2 resp during ERL (184 +/- 17 ml O2/min) was nearly twice that obtained during IRL (97 +/- 9 ml O2/min). This twofold difference in efficiency between inspiratory and expiratory resistive breathing may reflect the relatively lower mechanical advantage of the expiratory muscles in overcoming respiratory loads. Variable recruitment of expiratory muscles may explain the large variation of results obtained in studies of respiratory muscle efficiency in normal subjects.