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Objective: The study aimed to evaluate whether high-flow oxygen therapy (HFOT) during training was more effective than oxygen in improving exercise capacity in hypoxemic chronic obstructive pulmonary disease (COPD)., Methods: A total of 171 patients with COPD and chronic hypoxemia were consecutively recruited in 8 rehabilitation hospitals in a randomized controlled trial. Cycle-ergometer exercise training was used in 20 supervised sessions at iso inspiratory oxygen fraction in both groups. Pre- and post-training endurance time (Tlim), 6-minute walking distance (6MWD), respiratory and limb muscle strength, arterial blood gases, Barthel Index, Barthel Dyspnea Index, COPD Assessment Test, Maugeri Respiratory Failure questionnaire, and patient satisfaction were evaluated., Results: Due to 15.4% and 24.1% dropout rates, 71 and 66 patients were analyzed in HFOT and Venturi mask (V-mask) groups, respectively. Exercise capacity significantly improved after training in both groups with similar patient satisfaction. Between-group difference in post-training improvement in 6MWD (mean: 17.14 m; 95% CI = 0.87 to 33.43 m) but not in Tlim (mean: 141.85 seconds; 95% CI = -18.72 to 302.42 seconds) was significantly higher in HFOT. The minimal clinically important difference of Tlim was reached by 47% of patients in the V-mask group and 56% of patients in the HFOT group, whereas the minimal clinically important difference of 6MWD was reached by 51% of patients in the V-mask group and 69% of patients in the HFOT group, respectively., Conclusion: In patients with hypoxemic COPD, exercise training is effective in improving exercise capacity., Impact Statement: The addition of HFOT during exercise training is not more effective than oxygen through V-mask in improving endurance time, the primary outcome, whereas it is more effective in improving walking distance., (© The Author(s) 2020. Published by Oxford University Press on behalf of American Physical Therapy Association. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Purpose: The interrelations among chest wall kinematics (displacement and configuration), ventilatory profile and dyspnea relief following cycle exercise training (EXT) have not been systematically evaluated in hyperinflated chronic obstructive pulmonary disease (COPD) patients. We hypothesize that a decrease in ventilation affects dyspnea relief, regardless of the changes in chest wall kinematics., Methods: Fourteen patients were studied before and after 24-session exercise training program. We evaluated the volumes of chest wall and its compartments (rib cage, and abdomen) using optoelectronic plethysmography., Results: At iso-time EXT (i) reduced ventilation, respiratory frequency and dyspnea (by Borg scale), mildly improved rib cage configuration, but left operational volumes unchanged; (ii) Borg was much smaller for any comparable inspiratory reserve volume (IRVcw), and a decrease in IRVcw was tolerated much better for any given Borg., Conclusions: Regardless of the changes in chest wall kinematics, a decrease in ventilation attenuates dyspnea following EXT., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Anxiety and depression can increase the intensity of dyspnea out of proportion to the impairment in cardiorespiratory function and may contribute to the degree of disability associated with dyspnea. The effect of anxiety/depression on the sensory and affective components of reported dyspnea in patients with respiratory disorders might be of particular importance in improving the accuracy of the diagnostic process. However, the exact cause-relationship between dyspnea and anxiety/depression are unclear. A multidimensional model of dyspnea subsuming sensory components (i.e. intensity and quality) and affective components has recently been proposed. Affective responses drive patients to seek treatment which can cause them to alter their lifestyle to avoid dyspnea. Brain imaging techniques help identify distinct cortical structures involved in processing the discrete components of dyspnea., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

We hypothesized that arm training might affect unsupported arm exercise-related perception by decreasing motor output to arm/torso muscles in patients with chronic obstructive pulmonary disease (COPD). Eleven patients were studied at 80% of peak incremental arm exercise, before and after unsupported arm training. Training increased endurance time, decreased respiratory effort and much more arm effort (by Borg scale) without affecting chest wall dynamic hyperinflation or configuration. Ventilatory response to carbon dioxide output was the same before and after training so that at isotime the reduction in ventilation correlated strongly with a simultaneous reduction in metabolic output. These changes reflect a reduced ventilatory drive. We conclude that: (i) a reduced level of ventilation, relative to a decrease in central motor output, is the contribution of arm training to symptom alleviation during unsupported arm exercise in COPD patients, and (ii) arm training improved patients' exercise-related perception without affecting chest wall operational volumes or configuration., (Copyright © 2013. Published by Elsevier B.V.)

Purpose: Whether dyspnea, chest wall dynamic hyperinflation, and abnormalities of rib cage motion are interrelated phenomena has not been systematically evaluated in patients with chronic obstructive pulmonary disease (COPD). Our hypothesis that they are not interrelated was based on the following observations: (i) externally imposed expiratory flow limitation is associated with no rib cage distortion during strenuous incremental exercise, with indexes of hyperinflation not being correlated with dyspnea, and (ii) end-expiratory chest wall volume may either increase or decrease during exercise in patients with COPD, with those who hyperinflate being as breathless as those who do not., Methods: Sixteen patients breathed either room air or 50% supplemental O2 at 75% of peak exercise in randomized order. We evaluated the volume of chest wall (V(cw)) and its compartments: the upper rib cage (V(rcp)), lower rib cage (V(rca)), and abdomen (V(ab)) using optoelectronic plethysmography; rib cage distortion was assessed by measuring the phase angle shift between V(rcp) and V(rca)., Results: Ten patients increased end-expiratory V(cw) (V(cw,ee)) on air. In seven hyperinflators and three non-hyperinflators, the lower rib cage paradoxed inward during inspiration with a phase angle of 63.4° ± 30.7° compared with a normal phase angle of 16.1° ± 2.3° recorded in patients without rib cage distortion. Dyspnea (by Borg scale) averaged 8.2 and 9 at the end of exercise on air in patients with and without rib cage distortion, respectively. At iso-time during exercise with oxygen, decreased dyspnea was associated with a decrease in ventilation regardless of whether patients distorted the rib cage, dynamically hyperinflated, or deflated the chest wall., Conclusions: Dyspnea, chest wall dynamic hyperinflation, and rib cage distortion are not interrelated phenomena.

Background: It has yet to be determined whether the language of dyspnea responds to pulmonary rehabilitation programs (PRP)., Objective: We tested the hypothesis that PRP affect both the intensity and quality of exercise-induced dyspnea in patients with chronic obstructive pulmonary disease (COPD)., Methods: We studied 49 patients equipped with a portable telemetric spiroergometry device during the 6-min walking test before and 4 weeks after PRP. In a first screening visit, appropriate verbal descriptors of dyspnea were chosen that patients were familiar with during daily living activities. Tidal volume, respiratory frequency, inspiratory capacity, inspiratory reserve volume (IRV) and dyspnea intensity were evaluated by a modified Borg scale every minute during the test., Results: Qualitative descriptors of dyspnea were defined by three different sets of cluster descriptors (a-c) at the end of the exercise test, before and after PRP: a - work/effort (W/E); b - inspiratory difficulty (ID) and chest tightness (CT), and c - W/E, ID and/or CT. The three language subgroups exhibited similar lung function at baseline, and similar rating of dyspnea and ventilatory changes during exercise. The rehabilitation program shifted the Borg-IRV relationship (less Borg at any given IRV) towards the right without modifying the set of descriptors in most patients., Conclusions: Rehabilitation programs allowed patients to tolerate a greater amount of restrictive dynamic ventilatory defect by modifying the intensity, but not necessarily the quality of dyspnea., (Copyright © 2010 S. Karger AG, Basel.)

Background: For patients with limited physical activities who use oral communication for most social activities, the assessment of dyspnea during speech activities (DS) may provide relevant measurement criteria. Although speech production is altered by lung disease it has not been included in current dyspnea assessment tools., Objectives: We evaluated DS in patients with chronic obstructive pulmonary disease (COPD) with the aim of assessing: (i) the responsiveness to treatment of this newly developed evaluative dyspnea tool and (ii) whether DS is an independent measurement of other traditional outcomes., Methods: We assessed lung function, the 6-min walking test (6'WT), chronic exertional dyspnea (MRC and BDI/TDI), and DS using the speech section of the University of Cincinnati Dyspnea Questionnaire (UCDQ) before and after a pulmonary rehabilitation program in 31 patients with COPD., Results: The following items of the speech section of the UCDQ caused dyspnea: conversation, raising the voice, phoning, speaking to a group, talking in a noisy place, and singing. The mean overall DS score was 60 ± 23% of a maximal potential DS score. Pulmonary rehabilitation reduced each item of DS independently of change in lung function, chronic exertional dyspnea, and 6'WT., Conclusions: We concluded that DS is responsive to a respiratory rehabilitation program in patients with COPD. Evidence of independent objective measures supports the validity of a routine multivariable assessment including DS. We recommend assessment of DS particularly for patients who rely extensively on speech for communication., (Copyright © 2010 S. Karger AG, Basel.)

Aim: To test the hypothesis that obese individuals may either hyperinflate or deflate the lung when exercising. In both cases breathlessness is an inescapable consequence., Methods: Ventilatory variables, end-expiratory lung volume and end-inspiratory lung volume, and dyspnoea score (Borg scale) were studied in 20 class II-III obese subjects and 14 healthy controls during incremental symptom-limited cycle exercise., Results: Ventilation increased with increasing work rate, in obese and in control subjects; most obese subjects had to increase end-expiratory lung volume to escape from flow limitation; in contrast, like controls, a few subjects deflated the lung on heavy-to-peak exercise. Dyspnoea was equal in degree at anaerobic threshold and peak exercise in obese as in control subjects, and in obese who hyperinflated as in those who deflated the lung. In particular, end-expiratory lung volume at baseline (r = -0.84, P = 0.04) was negatively correlated with changes in Borg score in obese who did not hyperinflate: the lower the former the higher the latter. On the other hand, tidal volume (r = 0.54, P = 0.045) and decrease in inspiratory reserve volume (r = 0.59, P = 0.028) were positively correlated with the Borg score in obese subjects who hyperinflated. No other independent variable correlated with the Borg score., Conclusions: We conclude that not all obese subjects had to increase end-expiratory lung volume on heavy-to-peak exercise. Changes in dyspnoea for unit changes in ventilation were similar in obese who did hyperinflate as well as in those who did not, suggesting that the increase in respiratory neural drive, associated with an increase in ventilation, is an important source of dyspnoea in obese as well as in control subjects.

Aim: We hypothesize that different patterns of chest wall (CW) kinematics and respiratory muscle coordination contribute to sensation of dyspnoea during unsupported arm exercise (UAE) and leg exercise (LE)., Methods: In six volunteer healthy subjects, we evaluated the volumes of chest wall (V(cw)) and its compartments, the pulmonary apposed rib cage (V(rc,p)), the diaphragm-abdomen apposed rib cage (V(rc,a)) and the abdomen (V(ab)), by optoelectronic plethysmography. Oesophageal, gastric and trans-diaphragmatic pressures were simultaneously measured. Chest wall relaxation line allowed the measure of peak rib cage inspiratory muscle, expiratory muscle and abdominal muscle pressures. The loop V(rc,p)/V(rc,a) allowed the calculation of rib cage distortion. Dyspnoea was assessed by a modified Borg scale., Results: There were some differences and similarities between UAE and LE. Unlike LE with UAE: (i) V(cw) and V(rc,p) at end inspiration did not increase, whereas a decrease in V(rc,p) contributed to decreasing CW end expiratory volume; (ii) pressure production of inspiratory rib cage muscles did not significantly increase from quiet breathing. Not unlike LE, the diaphragm limited its inspiratory contribution to ventilation with UAE with no consistent difference in rib cage distortion between UAE and LE. Finally, changes in abdominal muscle pressure, and inspiratory rib cage muscle pressure predicted 62% and 41.4% of the variability in Borg score with UAE and LE, respectively (P < 0.01)., Conclusion: Leg exercise and UAE are associated with different patterns of CW kinematics, respiratory muscle coordination, and production of dyspnoea.

In patients with a number of cardio-respiratory disorders, breathlessness is the most common symptom limiting exercise capacity. Increased respiratory effort is frequently the chosen descriptor cluster both in normal subjects and in patients with chronic obstructive pulmonary disease (COPD) during exercise. The body of evidence indicates that dyspnea may be due to a central perception of an overall increase in central respiratory motor output directed preferentially to the rib cage muscles. On the other hand, the disparity between respiratory motor output and mechanical response of the system is also thought to play an important role in the increased perception of exercise in patients. The expiratory muscles also contribute to exercise dyspnea: a decrease in Borg scores is related to a decrease in end-expiratory lung volume and to a decrease in end-expiratory gastric pressure at isowork after lung volume reduction surgery. Changes in respiratory mechanics and intrathoracic pressure surrounding the heart can reduce cardiac output by affecting the return of blood to the heart from the periphery, or by interfering with the ability of the heart to eject blood into the peripheral circulation. Change in arterial blood gas content may affect breathlessness via direct or indirect effects. Old and more recent data have demonstrated that hypercapnia makes an independent contribution to breathlessness. In hypercapnic COPD patients an increase in PaCO2 seems to be the most important stimulus overriding all other inputs for dyspnea. Hypoxia may act indirectly by increasing ventilation (VE), and directly, independent of change in VE. Finally, chemical (metabolic) ventilatory stimuli do not have a specific effect on breathlessness other than via their stimulation of VE. We conclude that exercise provides a stimulus contributing to dyspnea, which can be applied to many diseases.

To our knowledge no data have been reported on the contribution to acute increase in dyspnea by the respiratory muscles in obese nonsmoking subjects. To better focus on this topic, we studied seven obese subjects and an age-matched normal control group, assessing baseline pulmonary function, breathing pattern, esophageal pressure (Pes), and gastric (Pga) and transdiaphragmatic (Pdi) pressures. Pes was also recorded during a sniff maneuver (Pessn). During a hypercapnic rebreathing test we recorded inspiratory swing in Pes (Pessw), expiratory changes in Pga, and inspiratory swings in Pdi (Pdisw). Change in inspiratory capacity was considered the mirror image of end-expiratory lung volume (EELV). Dyspnea was assessed by a modified Borg scale. Under control conditions, patients exhibited a reduced expiratory reserve volume and intrinsic positive end-expiratory pressure (PEEPi). At the end of hypercapnic stimulation, compared with controls our obese subjects exhibited greater respiratory frequency (Rf), shorter expiratory time, greater Pessw, and lower Pdisw. Increases in EELV and PEEPi were found in the obese subjects but not in controls. Changes in Borg correlated with changes in PETCO2, VE, Pessw (%Pessn), and Pdisw to a greater extent in patients than in controls. Stepwise regression analysis indicated the amount of variability in Borg that was predicted by both Pdisw (r2 = 0.31, p < 0.0004), and Pessw (%Pessn) (r2 = 0.09, p < 0.005) in controls, and by Pessw (%Pessn) (r2 = 0.40, p < 0.00001) in obese subjects. We conclude that the rib cage muscles contributed to dyspnea to a greater extent in this subset of obese subjects.

Background: Unlike studies on leg exercise, reports on the regulation of dynamic hyperinflation during arm exercise are scanty. We ascertained the following in patients with COPD: (1) whether and to what extent upper-limb exercise results in dynamic hyperinflation, and (2) the mechanism whereby an arm-training program (ATP) reduces arm effort and dyspnea., Patients: Twelve patients with moderate-to-severe COPD were tested during incremental, symptom-limited arm exercise after a non-intervention control period (pre-ATP) and after ATP., Methods: Exercise testing (1-min increments of 5 W) was performed using an arm ergometer. Oxygen uptake (V(O2)), carbon dioxide output, minute ventilation (Ve), tidal volume, and respiratory rate (RR) were measured continuously during the tests. Inspiratory capacity (IC), exercise dyspnea, and arm effort using a Borg scale were assessed at each step of exercise., Results: Arm exercise resulted in a significant decrease in IC and significant positive relationships of IC with an increase in V(O2) and exercise dyspnea and arm effort. The results of ATP were as follows: (1) a significant increase in exercise capacity (p < 0.001); (2) no change in the relationships of exercise dyspnea and arm effort with Ve and IC, and of IC with V(O2); (3) at a standardized work rate, Ve, exercise dyspnea, and arm effort significantly decreased, while the decrease in IC was significantly less (p < 0.01) than before the ATP; the decrease in Ve was accomplished primarily by a decrease in RR; and (4) at standardized Ve, exercise dyspnea and arm effort decreased significantly., Conclusions: Arm exercise results in the association of dynamic hyperinflation, exercise dyspnea, and arm effort in COPD patients. An ATP increases arm endurance, modulates dynamic hyperinflation, and reduces symptoms.

Dyspnea and leg effort are the major symptoms limiting exercise in healthy subjects and in patients with a variety of respiratory disorders. Quantitative measurement of both symptoms may be obtained by category scales such as VAS and Borg, with the latter being widely used. Furthermore, descriptor clusters of dyspnea help to assess some of the reasons for stopping exercise. The intensity of dyspnea and leg effort are similar in different disease states; this symmetry suggests that the limiting discomfort is a function of the intensity of increased motor drive to peripheral and respiratory muscles. An alternative explanation for the factors which limit exercise is that the subjects stop exercise volitionally when the discomfort associated with continuing exercise exceeds that which they are willing to tolerate. Muscle strength contributes to the intensity of dyspnea and leg effort at a given power output: the greater the muscle force, the lower the symptom. Symptoms also correlate with intensity and duration of a task by a power function in such a way that when minimizing the intensity of a given muscular task by prolonging the duration of activity, the symptom is drastically reduced. Skeletal muscle fatigue may be a factor limiting exercise tolerance both in healthy subjects and in patients with cardiorespiratory disorders. In conclusion, symptom measurement complements physiological measurements, both being essential to a comprehensive understanding of exercise tolerance.

Background: Pursed-lip breathing (PLB) is a strategy often spontaneously employed by patients with COPD during distress situations. Whether and to what extent PLB affects operational lung volume is not known. Also, conflicting reports deal with PLB capability of decreasing breathlessness., Participants and Measurements: Twenty-two patients with mild-to-severe COPD were studied. Volumes of chest wall (CW) compartments (rib cage [RC] and abdomen) were assessed using an optoelectronic plethysmograph. Dyspnea was assessed by a modified Borg scale., Results: Compared to spontaneous breathing, patients with PLB exhibited a significant reduction (mean +/- SD) in end-expiratory volume of the CW (VCW) [VCWee; - 0.33 +/- 0.24 L, p < 0.000004], and a significant increase in end-inspiratory VCW (VCWei; + 0.32 +/- 0.43 L, p < 0.003). The decrease in VCWee, mostly due to the decrease in end-expiratory volume of the abdomen (VAbee) [- 0.25 +/- 0.21 L, p < 0.00002], related to baseline FEV(1) (p < 0.02) and to the increase in expiratory time (TE) [r(2) = 0.49, p < 0.0003] and total time of the respiratory cycle (TTOT) [r(2) = 0.35, p < 0.004], but not to baseline functional residual capacity (FRC). Increase in tidal volume (VT) of the chest wall (+ 0.65 +/- 0.48 L, p < 0.000004) was shared between VT of the abdomen (0.31 +/- 0.23 L, p < 0.000004) and VT of the rib cage (+ 0.33 +/- 0.29 L, p < 0.00003). Borg score decreased with PLB (p < 0.04). In a stepwise multiple regression analysis, decrease in VCWee accounted for 27% of the variability in Borg score at 99% confidence level (p < 0.008)., Conclusions: Changes in VCWee related to baseline airway obstruction but not to hyperinflation (FRC). By lengthening of TE and TTOT, PLB decreases VCWee and reduces breathlessness.

Background: Studies suggest that the increased volume of both abdominal and rib cage compartments of the chest wall contribute to dyspnea during methacholine-induced airway narrowing., Material: Eight male patients with asthma aged 34 +/- 13 years (mean +/- SD) before and during methacholine challenge., Methods: The volume of the chest wall (Vcw), volume of the abdomen (Vab), and volume of the rib cage (Vrc) were measured by using a three-dimensional optoelectronic plethysmography., Results: During methacholine challenge, the increase in end-expiratory Vcw (Vcw,ee) [0.55 +/- 0.23 L, p < 0.001] was due to increased Vrc (0.37 +/- 0.20 L, p < 0.01) and, to a lesser extent, Vab (0.18 +/- 0.10 L, p < 0.005). Linear univariate regression analysis showed that changes in dyspnea (Borg scale) with the highest methacholine dose correlated with both DeltaFEV(1) and DeltaVcw,ee. Multiple regression analysis with the Borg score as dependent variable and all other ventilatory indexes as independent variables showed that DeltaVcw,ee and DeltaFEV(1) were the only significant contributors to the Borg score. Taken together Vcw,ee and FEV(1) explained 56% of variance in the Borg score (r(2) = 0.56), although Vcw,ee explained 48% of it., Conclusions: During methacholine challenge in patients with asthma, the overall increase in Vcw,ee is a better predictor of dyspnea that the reduction in FEV(1).

Background: To our knowledge, no data have been reported on the effects of exercise training (EXT) on central respiratory motor output or neuromuscular coupling (NMC) of the ventilatory pump, and their potential association with exertional dyspnea. Accurate assessment of these important clinical outcomes is integral to effective management of breathlessness of patients with COPD., Material and Methods: Twenty consecutive patients with stable moderate-to-severe COPD were tested at 6-week intervals at baseline, after a nonintervention control period (pre-EXT), and after EXT. Patients entered an outpatient pulmonary rehabilitation program involving regular exercise on a bicycle. Incremental symptom-limited exercise testing (1-min increments of 10 W) was performed on an electronically braked cycle ergometer. Oxygen uptake (O(2)), carbon dioxide output (CO(2)), minute ventilation (E), time, and volume components of the respiratory cycle and, in six patients, esophageal pressure swings (Pessw), both as actual values and as percentage of maximal (most negative in sign) esophageal pressure during sniff maneuver (Pessn), were measured continuously over the runs. Exertional dyspnea and leg effort were evaluated by administering a Borg scale., Results: Measurements at baseline and pre-EXT were similar. Significant increase in exercise capacity was found in response to EXT: (1) peak work rate (WR), O(2), CO(2), E, tidal volume (VT), and heart rate increased, while peak exertional dyspnea and leg effort did not significantly change; (2) exertional dyspnea/O(2) and exertional dyspnea/CO(2) decreased while E/O(2) and E/CO(2) remained unchanged. The slope of both exertional dyspnea and leg effort relative to E fell significantly after EXT; (3) at standardized WR, E, and CO(2), exertional dyspnea and leg effort decreased while inspiratory capacity (IC) increased. Decrease in E was accomplished primarily by decrease in respiratory rate (RR) and increase in both inspiratory time (TI) and expiratory time; VT slightly increased, while inspiratory drive (VT/TI) and duty cycle (TI/total time of the respiratory cycle) remained unchanged. The decrease in Pessw and the increase in VT were associated with lower exertional dyspnea after EXT; (4) at standardized E, VT, RR, and IC, Pessw and Pessw(%Pessn)/VT remained unchanged while exertional dyspnea and leg effort decreased with EXT., Conclusion: In conclusion, increases in NMC, aerobic capacity, and tolerance to dyspnogenic stimuli and possibly breathing retraining are likely to contribute to the relief of both exertional dyspnea and leg effort after EXT.

Dyspnoea is not a prominent complaint of resting patients with recent hemispheric stroke (RHS). We hypothesized that, in patients with RHS presenting abnormalities in respiratory mechanics, increased respiratory motor output could translate into an increased perception of dyspnoea. We studied eight wheelchair-bound patients with RHS (mean age 62.4 years), previously evaluated by computerized tomography scanning, and a control group of normal subjects, matched for age and sex. We assessed routine spirometry, inspiratory and expiratory muscle pressures, breathing pattern and dyspnoea using a modified Borg scale. In six patients, we also measured oesophageal pressure during the maximal sniff manoeuvre and tidal inspiratory swing, and mechanical characteristics of the lung in terms of dynamic elastance during both quiet breathing and a hypercapnic/hyperoxic rebreathing test. During room air breathing, ventilation and tidal volume were similar in patients and controls, while tidal inspiratory swings of oesophageal pressure, an index of inspiratory motor output, were greater in patients ( P =0.005). Patients also exhibited a greater dynamic elastance ( P =0.013). During rebreathing, dynamic elastance remained higher ( P =0.01) and a greater than normal inspiratory motor output was found ( P =0.03). Responses of ventilation and tidal volume to carbon dioxide tension were normal, and in all patients but one a lower Borg score for the unit change in carbon dioxide tension and ventilation was found. In conclusion, a higher than normal inspiratory motor output was unexpectedly associated with a blunted perception of dyspnoea in this subset of RHS patients. This is likely to be due to the modulation of the integration process of respiratory sensation.

Background: The perception of dyspnea is not a prominent complaint of resting patients with neuromuscular disease (NMD). To our knowledge, no study has been addressed at evaluating the interrelationships among lung mechanics, respiratory motor output, and the perception of dyspnea in patients with NMD receiving ventilatory stimulation., Material: Eleven patients with NMD (mean +/- SD age, 44 +/- 11.8 years; 5 men) of different etiology and a group of normal subjects matched for age and sex (control subjects)., Methods: While patients were breathing room air, lung volumes, arterial blood gases, the pattern of breathing (minute ventilation [E], tidal volume [VT], respiratory frequency, inspiratory time), and maximal (less negative) esophageal pressure during a sniff maneuver (Pessn), as an index of inspiratory muscle strength, were measured. Then we evaluated the response to hypercapnic-hyperoxic stimulation (hypercapnic-hyperoxic rebreathing test [RT]) in terms of breathing pattern, inspiratory swing of pleural pressure (Pessw), and inspiratory effort (Pessw[%Pessn]). During the RT, dyspnea was assessed every 30 s using a modified Borg scale (0 to 10)., Results: Pulmonary volumes were reduced in seven patients, and PCO(2) was out of proportion to E in four patients. Group Pessn was 42.8 +/- 23.6 cm H(2)O in patients and 107 +/- 20.4 cm H(2)O in control subjects (p < 0.001). Dynamic elastance (Eldyn) [p = 0.0016] and Pessw(%Pessn) [p < 0.0005] were higher in patients. During the RT, Borg/CO(2), Pessw(%Pessn)/CO(2), and Borg/Pessw(%Pessn) were similar in the two groups, while E/CO(2) and VT/CO(2) were lower in patients (p < 0.0002 for both). As a consequence, for unit change in VT (percentage of predicted vital capacity [%VC]), greater changes in Pessw(%Pessn) were associated with greater Borg scores in patients. Baseline Eldyn related to Pessw(%Pessn)/VT(%VC) during hypercapnia (r(2) = 0.85), an index of neuroventilatory coupling of the ventilatory pump (NVC). NVC predicted a good amount of the variability in Borg/E (r(2) = 0.46, p < 0.02)., Conclusions: In this subset of NMD patients during hypercapnic stimulation, a normal inspiratory motor output per unit change in PCO(2) results in a shallow breathing pattern. The consequent impairment of NVC underlies the higher scoring of dyspnea in these patients.

Whether, and to what extent, beta 2-agonists protect against respiratory muscle overloading and breathlessness during bronchoconstriction remains to be defined in patients with asthma. In a double blind placebo-controlled study, 100 micrograms of fenoterol were administered to six stable asthmatics before a bronchial provocation test, performed by inhaling doubling concentrations of histamine from a Devilbiss 646 nebulizer. We recorded breathing pattern (tidal volume VT, inspiratory time TI, total time of the respiratory cycle TTOT), inspiratory capacity (IC), dynamic pleural pressure swing (Pplsw), total lung resistance (RL) and FEV1. VT was expressed both in actual values and as % of IC. Changes in VT (%IC) during histamine inhalation reflected changes in dynamic end-inspiratory lung volume (EILV). Pplsw was expressed as % of maximal (the most negative in sign) pleural pressure, obtained under control conditions during a sniff manoeuvre (Pplsn). Pplsw (%Pplsn) is an index of inspiratory muscle effort. The test ended when the concentration of histamine which caused a decrease in FEV1 of > or = 40% post-saline was reached. Dyspnoea rating was scored by a modified Borg scale. At the ultimate degree of bronchoconstriction (UDB) with histamine: (i) decrease in FEV1 was similar after placebo and fenoterol, while increase in RL was lower after fenoterol (P < 0.005); (ii) VT(%IC) increased less after fenoterol (P < 0.027); (iii) increases in Pplsw (%Pplsn) was lower after fenoterol (P < 0.001); (iv) delta Borg (from saline) was lower (P < 0.01) after fenoterol; (v) differences in delta Borg, from placebo to fenoterol, related to concurrent changes in VT(%IC) (r2 = 0.67). In conclusion, at UDB 100 micrograms of fenoterol produced a beneficial effect on the degree of inspiratory muscle loading and breathlessness, an effect greater than it would be expected from measuring FEV1 alone.