Dyspnea and emotional states in health and disease.

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.

Tidal volume inflection and its sensory consequences during exercise in patients with stable asthma.

Sixteen patients with stable asthma performed a symptom-limited constant work-rate CWR cycle exercise during which breathing pattern, operating lung volumes, dyspnea intensity and its qualitative descriptors were measured. An inflection in the relation between tidal volume (V(T)) and ventilation (V˙(E)) was observed in each subject. The sense of "work/effort" was the dominant dyspnea descriptor selected up to the V(T)/V˙(E) inflection, whereas after it dyspnea intensity and the selection frequency of "unsatisfied inspiration" rose steeply in 37.5% of subjects in whom inspiratory reserve volume (IRV) had decreased to a critical level of 0.6L at the V(T) inflection point. In contrast, dyspnea increased linearly with exercise time and V˙(E), and "work/effort" was the dominant descriptor selected throughout exercise in 62.5% of subjects in whom the V(T)/V˙(E) inflection occurred at a preserved IRV. The V(T) inflection during exercise in patients with stable asthma marked a mechanical event with important sensory consequences only when it occurred at a critical reduced IRV.

Chest wall kinematics and breathlessness during unsupported arm exercise in COPD patients.

We hypothesised that chest wall displacement inappropriate to increased ventilation contributes to dyspnoea more than dynamic hyperinflation or dyssynchronous breathing during unsupported arm exercise (UAE) in COPD patients. We used optoelectronic plethysmography to evaluate operational volumes of chest wall compartments, the upper rib cage, lower rib cage and abdomen, at 80% of peak incremental exercise in 13 patients. The phase shift between the volumes of upper and lower rib cage (RC) was taken as an index of RC distortion. With UAE, no chest wall dynamic hyperinflation was found; sometimes the lower RC paradoxed inward while in other patients it was the upper RC. Phase shift did not correlate with dyspnoea (by Borg scale) at any time, and chest wall displacement was in proportion to increased ventilation. In conclusions neither chest wall dynamic hyperinflation nor dyssynchronous breathing per se were major contributors to dyspnoea. Unlike our prediction, chest wall expansion and ventilation were adequately coupled with each other.

Dyspnea during speech in chronic obstructive pulmonary disease patients: effects of pulmonary rehabilitation.

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.

Impact of a rehabilitation program on dyspnea intensity and quality in patients with chronic obstructive pulmonary disease.

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.

Do obstructive and restrictive lung diseases share common underlying mechanisms of breathlessness?

This review tries to answer two main questions: (i) What are the neurophysiological underpinnings of the most commonly selected cluster descriptors which define the qualitative dimension of dyspnea in patients? (ii) How do mechanical constraints affect dyspnea? (iii) Do obstructive and restrictive lung diseases share some common underlying mechanisms? Qualitative dimensions of dyspnea, which allude to increased respiratory work/effort breathing, reflect a harmonious coupling between increased respiratory motor output and lung volume displacement in healthy subjects. Descriptors that allude to unsatisfied inspiration are the dominant qualitative descriptors in patients with a variety of respiratory diseases. It is possible that sensory feedback from a multitude of mechanoreceptors throughout the respiratory system (in the muscle, chest wall, airways and lung parenchyma) collectively convey information to the consciousness that volume/flow or chest wall displacement is inadequate for the prevailing respiratory drive. The data would lend support to the idea that: (i) an altered afferent proprioceptive peripheral feedback signals that ventilatory response is inadequate to the prevailing motor drive, reflecting neuromechanical uncoupling (NMU), (ii) mechanical constraints on volume expansion (dynamic restriction) play a pivotal role in dyspnea causation in patients with a variety of either obstructive or restrictive respiratory disorders, and (iii) all of the physiological adaptations that optimize neuromechanical coupling in obstructive and restrictive disorders are seriously disrupted so that an NMU underpins cluster descriptors of dyspnea which are similar in obstructed and in restricted patients.

The respiratory muscles in eucapnic obesity: their role in dyspnea.

Regular exercise appears to be one of the best predictors of successful weight maintenance. Although physical activity and exercise are important components in the prevention and treatment of obesity, many obese adults without coexisting disorders are unable to exercise due to dyspnea on exertion. As a result they may not participate in regular physical activity. Therefore exertional dyspnea in obese adults is also an obstacle to the prevention and treatment of obesity and coexisting comorbidities. The available data suggest that increased respiratory muscle force generation, and the concomitant increase in respiratory neural drive associated with increased ventilation are an important source of sensation of respiratory effort in obese subjects. Whether activity-related breathlessness is due to either abnormal respiratory mechanical factors (flow limitation and/or chest elastic loading) or the increased metabolic demand of locomotion in obesity, or both of these together, the available data indicate that intensity of dyspnea at any given ventilation and oxygen uptake does not increase in obese subjects as compared with normal weight control subjects. Does this mean that respiratory mechanical factors are unlikely to be contributory? Nonetheless, the component of metabolic cost of breathing may not be accounted for in the measured mechanical work of breathing because of the number of included complex variables. That a decrease in efficiency of the respiratory muscles during exercise contributes to dyspnea in hyperinflating obese subjects should not be disregarded.

Optoelectronic Plethysmography has Improved our Knowledge of Respiratory Physiology and Pathophysiology.

It is well known that the methods actually used to track thoraco-abdominal volume displacement have several limitations. This review evaluates the clinical usefulness of measuring chest wall kinematics by optoelectronic plethysmography [OEP]. OEP provides direct measurements (both absolute and its variations) of the volume of the chest wall and its compartments, according to the model of Ward and Macklem, without requiring calibration or subject cooperation. The system is non invasive and does not require a mouthpiece or nose-clip which may modify the pattern of breathing, making the subject aware of his breathing. Also, the precise assessment of compartmental changes in chest wall volumes, combined with pressure measurements, provides a detailed description of the action and control of the different respiratory muscle groups and assessment of chest wall dynamics in a number of physiological and clinical experimental conditions.

Chest wall kinematics and Hoover's sign.

BACKGROUND: No attempt has been made to quantify the observed rib cage distortion (Hoover's sign) in terms of volume displacement. We hypothesized that Hoover's sign and hyperinflation are independent quantities. METHODS: Twenty obstructed stable patients were divided into two groups according to whether or not they exhibited Hoover's sign during clinical examination while breathing quietly. We evaluated the volumes of chest wall and its compartments: the upper rib cage, the lower rib cage and the abdomen, using optoelectronic plethysmography. RESULTS: The volumes of upper rib cage, lower rib cage and abdomen as a percentage of absolute volume of the chest wall were similar in patients with and without Hoover's sign. In contrast, the tidal volume of the chest wall, upper rib cage, lower rib cage, their ratio and abdomen quantified Hoover's sign, but did not correlate with level of hyperinflation. CONCLUSIONS: Rib cage distortion and hyperinflation appear to define independently the functional condition of these patients.

Inhaled furosemide does not alleviate respiratory effort during flow-limited exercise in healthy subjects.

Expiratory muscle loading results in increased perception of respiratory effort; this response is mediated by non-vagal reflexes originating in the chest wall. Furosemide, due to its vagal effect, might not affect the perception of respiratory effort during expiratory flow-limited incremental exercise. In this study, we compared in nine healthy subjects the following determinants of exercise performance such as respiratory effort (Borg), workload (W'), ventilation (V'E), tidal volume (VT), respiratory frequency (f), and mean inspiratory flow (VT/TI), an index of central respiratory drive, during either standard incremental cycling exercise, or expiratory flow-limited incremental exercise. In addition we examined the effect of inhaled placebo, furosemide (40 or 80 mg) on the perception of respiratory effort following standard incremental cycling exercise and expiratory flow-limited incremental exercise. Compared with standard incremental cycling exercise, expiratory flow-limited incremental exercise increased the Borg score and VT/Ti, and decreased W',V'E ,VT, and f in all subjects at iso-workload. Neither placebo nor furosemide modified peak ventilatory variables, slopes, or intercepts of the relationships of the Borg score with W', V'E, VT/TI and VT during expiratory flow-limited incremental exercise. We conclude that (a) compared with standard incremental exercise, expiratory flow limited exercise increases central respiratory drive and perception of respiratory effort, and (b) furosemide does not affect the sensation of respiratory effort under the present conditions of increased drive to the respiratory muscles.

Patterns of chest wall kinematics during volitional pursed-lip breathing in COPD at rest.

BACKGROUND: Analysis of chest wall kinematics can contribute to identifying the reasons why some patients benefit from pursed-lip breathing (PLB). MATERIAL AND METHODS: We evaluated the displacement of the chest wall and its compartments, the rib cage and abdomen, by optoelectronic plethysmography (OEP), during supervised PLB maneuver in 30 patients with mild to severe chronic obstructive pulmonary disease (COPD). RESULTS: OEP showed two different patterns. A first pattern characterized the 19 most severely obstructed and hyperinflated patients in whom PLB decreased end-expiratory volumes of the chest wall and abdomen, and increased end-inspiratory volumes of the chest wall and rib cage. Deflation of the abdomen and inflation of the rib cage contributed to increasing tidal volume of the chest wall. The second pattern characterized 11 patients in whom, compared to the former group, PLB resulted in the following: (i) increased end-expiratory volume of the rib cage and chest wall, (ii) greater increase in end-inspiratory volume of the rib cage and abdomen, and (iii) lower tidal volume of the chest wall. In the patients as a whole changes in end-expiratory chest wall volume were related to change in Borg score (r(2)=0.5, p<0.00002). CONCLUSIONS: OEP helps identifying the reason why patients with COPD may benefit from PLB at rest.

Exercise dyspnea in patients with COPD.

Dyspnea, a symptom limiting exercise capacity in patients with COPD, is associated with central perception of an overall increase in central respiratory motor output directed preferentially to the rib cage muscles. On the other hand, disparity between respiratory motor output, mechanical and ventilatory response of the system is also thought to play an important role on the increased perception of exercise in these patients. Both inspiratory and expiratory muscles and operational lung volumes are important contributors to exercise dyspnea. However, the potential link between dyspnea, abnormal mechanics of breathing and impaired exercise performance via the circulation rather than a malfunctioning ventilatory pump per se should not be disregarded. Change in arterial blood gas content may affect dyspnea via direct or indirect effects. An increase in carbon dioxide arterial tension seems to be the most important stimulus overriding all other inputs from dyspnea in hypercapnic COPD patients. Hypoxia may act indirectly by increasing ventilation and indirectly independent of changes in ventilation. A greater treatment effect is often achieved after the addition of pulmonary rehabilitation with pharmacological treatment.

Is there a link between the qualitative descriptors and the quantitative perception of dyspnea in asthma?

BACKGROUND: There is no obvious link between qualitative descriptors and overall intensity of dyspnea during bronchoconstriction in patients with asthma. AIMS: To determine whether qualitative and quantitative perception of methacholine-induced bronchoconstriction independently contribute to characterizing clinically stable asthma. MATERIAL AND METHODS: We assessed changes in inspiratory capacity, and quantitative (by Borg scale) and qualitative (by a panel of eight dyspnea descriptors) sensations of dyspnea at 20 to 30% fall in FEV(1) during methacholine inhalation in 49 asthmatics. Furthermore, we calculated the level of perception of bronchoconstriction at 20% fall in FEV(1) (PB(20)). RESULTS: Descriptors selected by patients during methacholine inhalation allowed us to define three language subgroups: (1) chest tightness (subgroup A, n = 21); (2) work/effort (subgroup B, n = 7); and (3) both descriptors (subgroup C, n = 13). Eight of the 49 patients (subgroup D) were not able to make a clear-cut distinction among descriptors. The subgroups exhibited similar function at baseline and during methacholine inhalation. Most importantly, patients selected chest tightness to a greater extent (42.85%), and work/effort (14.3%) and both descriptors (26.5%) to a lesser extent at the lowest level of bronchoconstriction (FEV(1) fall < 10%) as at 20% fall in FEV(1). Thirty-two patients were normoperceivers (PB(20) > or = 1.4 to < 5 arbitrary units [au]), 7 patients were hyperperceivers (PB(20) > or = 5 au), and 10 patients were hypoperceivers (PB(20) < 1.4 au). Language subgroups were equally distributed across the perceiver subgroups. CONCLUSIONS: In patients with clinically stable asthma, PB(20) and language of dyspnea independently contribute to defining the condition of the disease. However, the possibility that this independence may be due to a beta-error should be taken into account.

Respiratory muscle energetics during exercise in healthy subjects and patients with COPD.

The energy expenditure required by the respiratory muscles during exercise is a function of their work rate, cost of breathing, and efficiency. During exercise, ventilatory requirements increase further exacerbating the potential imbalance between inspiratory muscle load and capacity. High level of exercise intensity in conjunction with contracting respiratory muscles is the reason for respiratory muscle fatigue in healthy subjects. Available evidence would suggest that fatigue of the diaphragm and other respiratory muscles is an important mechanism involved in redistribution of blood flow. Reflex mechanisms of sympathoexcitation are triggered in fatigued diaphragm during heavy exercise when cardiac output is not sufficient to adequately meet the high metabolic requirements of both respiratory and limb musculature. It is very likely that local changes in locomotor muscle blood flow may occur during exhaustive endurance exercise and that changes may have important effect on O2 transport to the working locomotor muscles and, therefore, on their fatigability. In a condition when the respiratory muscles receive their share of blood flow at the expense of limb locomotor muscles, minimizing mechanical work of breathing and therefore its metabolic cost allows a greater amount of cardiac output to be available to be delivered to working limb muscles. Malfunction in any of the multiple components responsible for circulatory flow and O2 delivery will limit the blood supply therefore inhibiting the supply of O2 and the energy substrate to the contracting muscles. Studies are needed to overcome these limitations.

Dyspnea and asthma.

PURPOSE OF REVIEW: Dyspnea--the perception of respiratory discomfort--is a primary symptom of asthma. This review examines possible ways to link mechanisms, measurement and treatment that will increase our understanding of this condition. RECENT FINDINGS: Functional neuroimaging methods have proven to be powerful tools that serve as advanced models of sensor motor brain function. Studies examining functional neuroimaging methods have revealed activation of distinct brain areas associated with increased dyspnea. Pulmonary hyperinflation has been proposed to influence the perception of dyspnea. The association of hyperinflation with minor levels of bronchoconstriction reflects the partition of the sensory effect of airway narrowing per se from that of the attendant elastic loading of the inspiratory muscles. There is evidence to suggest, however, that hyperinflation does not play an important role in the pathogenesis of exercise dyspnea as it does during induced bronchoconstriction. Decreased levels of perception of airway obstruction may be a risk factor associated with life-threatening asthma. A poor perceiver may be vulnerable to further hypoxia-induced suppression of respiratory sensation. Monitoring the response to bronchodilator therapy with formoterol and salbutamol in patients with acute or chronic asthma has resulted in significantly faster improvement in dyspnea, within 2 min. SUMMARY: Regardless of the factors involved, much variability in dyspnea scores remains unexplained. Quantitative and qualitative assessment of the perception of dyspnea, symptom measurement and quality of life complement physiological measurements and contribute to our understanding of dyspnea in asthma.

Perception of airway obstruction and airway inflammation in asthma: a review.

Dyspnea has a multifactorial nature and the exact mechanism that causes breathlessness in asthma is not fully understood. There is compelling evidence that factors other than merely mechanical ones take part in the pathophysiology of breathlessness. Some recent reports attribute airway inflammation, which may contribute to the unexplained variability in the perception of dyspnea associated with bronchoconstriction. Eosinophil airway inflammation has been proposed as a determinant of breathlessness via mechanisms affecting either the mechanical pathways that control breathlessness or the afferent nerves involved in perception of dyspnea. In this review, data on the interrelation between inflammation and dyspnea sensation and the impact of treatment on dyspnea sensation are discussed. We conclude that regardless of whether mechanical or chemical inflammatory factors are involved, much variability in dyspnea scores remains unexplained.

Pathophysiology of exercise dyspnea in healthy subjects and in patients with chronic obstructive pulmonary disease (COPD).

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.

Arm exercise and hyperinflation in patients with COPD: effect of arm training.

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 during exercise.

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.

Respiratory muscles and dyspnea in obese nonsmoking subjects.

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.