Rationale: Although exertional dyspnea in obesity is an important and prolific clinical concern, the underlying mechanism remains unclear.
Objectives: To investigate whether dyspnea on exertion in otherwise healthy obese women was associated with an increase in the oxygen cost of breathing or cardiovascular deconditioning.
Methods: Obese women with and without dyspnea on exertion participated in two independent experiments (n = 16 and n = 14). All participants underwent pulmonary function testing, hydrostatic weighing, ratings of perceived breathlessness during cycling at 60 W, and determination of the oxygen cost of breathing during eucapnic voluntary hyperpnea at 40 and 60 L/min. Cardiovascular exercise capacity, fat distribution, and respiratory mechanics were determined in 14 women in experiment 2. Data were analyzed between groups by independent t test, and the relationship between the variables was determined by regression analysis.
Measurements and Main Results: In both experiments, breathlessness during 60 W cycling was markedly increased in over 37% of the obese women (P < 0.01). Age, height, weight, lung function, and %body fat were not different between the groups in either experiment. In contrast, the oxygen cost of breathing was significantly (P < 0.01) and markedly (38–70%) greater in the obese women with dyspnea on exertion. The oxygen cost of breathing was significantly (P < 0.001) correlated with the rating of perceived breathlessness obtained during the 60 W exercise in experiment 1 (r2 = 0.57) and experiment 2 (r2 = 0.72). Peak cardiovascular exercise capacity, fat distribution, and respiratory mechanics were not different between groups in experiment 2.
Conclusions: Dyspnea on exertion is prevalent in otherwise healthy obese women, which seems to be strongly associated with an increased oxygen cost of breathing. Exercise capacity is not reduced in obese women with dyspnea on exertion.
Most obese patients with dyspnea on exertion are generally considered to be deconditioned. However, there are preliminary data that challenge this premise.
The results of this study demonstrate that breathlessness during exercise in obese women seems to be strongly associated with an increased oxygen cost of breathing and that peak cardiovascular exercise capacity is not decreased.
The best options for dealing with this epidemic are to prevent the development of obesity or treat it before comorbidity complications develop (2–5). 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 (6, 7). As a result, many do not participate in regular physical activity. Therefore, exertional dyspnea in obese adults is not only an important and prolific clinical concern; it is also an obstacle to the prevention and treatment of obesity and coexisting comorbidities (3).
Most obese patients with dyspnea on exertion are generally considered to be deconditioned. However, in our prior studies in obese volunteers we have not found them to be deconditioned (8, 9), which challenges this conventional wisdom. Therefore, it is unclear if exertional dyspnea in otherwise healthy obese adults is due to obesity-related changes in respiratory function or to cardiovascular deconditioning.
The overall purpose of this study was to investigate whether exertional dyspnea in otherwise healthy obese women was associated with obesity-related respiratory limitations, specifically an increase in the oxygen cost of breathing (i.e., increased work of breathing) or cardiovascular deconditioning.
To address this objective, we performed two closely related experiments. In experiment 1, we investigated the relationships between simple measures of body composition, pulmonary function, dyspnea on exertion during cycling, and the oxygen cost of breathing (n = 16). In experiment 2, we investigated the measurements in experiment 1 plus new measures of gas exchange, cardiovascular exercise capacity, fat distribution, and respiratory mechanics in a new group of subjects (n = 14). These experiments represent a two-step approach to address our overall question, and the results of each experiment are supportive of each other.
The purpose of the first experiment was as follows: (1) to investigate the prevalence and range of breathlessness in otherwise healthy, obese women during constant load exercise, and (2) to measure the oxygen cost of breathing in obese women during eucapnic voluntary hyperpnea (10). We thought it necessary to address these basic questions before initiating more detailed and invasive procedures in experiment 2. We hypothesized that (1) the intensity of breathlessness during exercise would be increased in a large proportion of otherwise healthy obese women, (2) the oxygen cost of breathing would be increased in the obese women with exertional dyspnea as compared with obese women without exertional dyspnea, and (3) the rating of perceived breathlessness (RPB) during 60 W of constant load cycling exercise would be correlated with the increase in the oxygen cost of breathing in obese women.
The purpose of the second experiment was as follows: (1) to confirm the results of the first study in a second sample of otherwise healthy obese women; (2) to investigate ventilatory response, gas exchange, and breathing mechanics during constant load exercise at 60 W; (3) to investigate peak cardiovascular exercise capacity; (4) to investigate breathing mechanics at rest and during eucapnic voluntary hyperpnea; and (5) to investigate the relationships between the oxygen cost of breathing and body composition, especially the distribution of chest wall fat in otherwise healthy obese women with and without dyspnea on exertion. We hypothesized that, in otherwise healthy obese women with exertional dyspnea as compared with obese women without exertional dyspnea, (1) cardiovascular exercise capacity would not be decreased; (2) ventilation, gas exchange, and breathing mechanics during constant load exercise would be similar; (3) breathing mechanics during eucapnic voluntary hyperpnea would be similar; and (4) although overall body composition would be similar, fat distribution would be different.
In accordance with the University of Texas Southwestern Medical Center review board, all details of the experiments were discussed with the volunteers, and informed consent was obtained before participation. Obese women were recruited through local advertisements. Volunteers were screened based on BMI, and obesity was confirmed by underwater weighing (30 ⩽ %body fat ⩽ 52). No subject had a history of smoking, asthma, cardiovascular disease, or musculoskeletal abnormalities that would preclude maximal exercise or had participated in regular vigorous exercise for the last 6 months. Subjects not meeting these guidelines and individuals with respiratory symptoms were excluded.
After the initial screening, the participants returned to the laboratory on two separate occasions: once for constant load exercise testing and once for measuring the oxygen cost of breathing.
The obese women were assigned to one of two groups according to their RPB (0–10 Borg scale) during minute 6 of constant load exercise at 60 W. Those with a rating of 4 or higher were designated as obese women with breathlessness, and those with a rating of 3 or less were designated as obese women without breathlessness. This grouping was based on our previous finding that lean and obese women have an average RPB of 2 ± 1 at ventilatory threshold during incremental exercise (9). Of the 16 obese volunteers screened, eight women had an RPB of 3 or less, and eight had an RPB of 4 or higher.
Standard measures of height and weight were made upon initial screening of the subjects. Body size (height and weight) and circumference measurements (chest, waist, and hip) were made to characterize differences (if any) in overall body size and general fat distribution (weight-to-height ratio and waist-to-hip ratio) among the subjects. Hydrostatic weighing, with the measurement of residual volume during weighing, was performed to determine percent body fat, lean body mass, and total body fat mass.
All subjects had standard spirometry, lung volume, and diffusing capacity determinations (model 6200 or V62W body plethysmograph; SensorMedics, Yorba Linda, CA). Pulmonary function testing was performed according to the guidelines of the American Thoracic Society (13). Predicted values for spirometry, lung volumes, and diffusing capacity were based on the norms of Knudson and colleagues (14, 15), Goldman and Becklake (16), and Burrows and colleagues (17), respectively.
All qualified participants were familiarized to exercise on the cycle ergometer, given detailed written instructions regarding rating the intensity of breathlessness during exercise, and instructed to avoid exercise, food, and caffeine for at least 2 hours before exercise testing.
Testing began with the subjects seated on the cycle ergometer while baseline measurements were made. After 3 minutes of baseline measurements, the subjects performed a 6-minute constant load exercise cycling test at 60 W on an electronically braked cycle ergometer to assess the intensity of breathlessness (i.e., RPB) experienced by the subjects during exertion. An exercise work rate of 60 W was chosen based on the results of a prior study on obese women who obtained ventilatory threshold at approximately 60 W (9). RPB was measured every 2 minutes of the test, and the last value recorded was used for analysis. Briefly, the intensity of breathlessness was rated using a modified Borg 0–10 scale with verbal expressions of severity anchored to specific numbers (18). Consistent and specific instructions for rating breathlessness were provided to the subjects in written script form before testing. Borg RPB results have been demonstrated to be reliable and valid (18).
During the exercise test, the following variables were also measured: heart rate (HR), blood pressure, ratings of perceived exertion (RPE) (6–20 Borg scale), end-tidal Pco2 (PetCO2), (Poet TE capnograph; Criticare Systems, Waukesha, WI); and pulse oximetry (SaO2%) as required for participant safety during any standardized exercise test. Blood pressure was monitored with the use of an automated system (model 4240; Suntech, Raleigh, NC).
The oxygen cost of breathing was determined from 6-minute measurements of o2 and e at rest and during voluntary eucapnic hyperpnea at 40 and 60 L/minute. The subjects breathed from a 1,000-L inspiratory reservoir bag containing 4 or 5% CO2 (21% O2 and balance N2), respectively, to maintain eucapnia (19). Breathing frequency at each level was set with a metronome at 30 or 35 bpm, respectively. The e was called out for the subject, who was aware of the ventilation goal (i.e., 40 or 60 L/min). If their ventilation was too high or too low, then the subject was requested to take a smaller or larger breath. The oxygen cost of breathing was assessed by calculating the slope of the o2 (ml/min) versus e (L/min) relationship at rest and voluntary eucapnic hyperpnea at 40 and 60 L/minute (Figure 1). The intensity of breathlessness during voluntary hyperpnea was determined by RPB during the last minute of each segment of the test. HR, blood pressure, PetCO2, end-tidal Po2, and pulse oximetry (SaO2%) were monitored during the test for participant safety.
Differences between groups were determined by an independent t test. Relationships among variables were determined with Pearson correlation coefficients. A P value less than 0.05 was considered significant.
After initial screening, the participants returned to the laboratory on three separate occasions: once for exercise testing, once for the measurement of the oxygen cost of breathing, and once for the measurement of fat distribution, which was determined by magnetic resonance imaging (MRI) at the Rogers Center at UT Southwestern (see details below).
As in experiment 1, obese women were assigned to one of two groups based on their RPB (0–10 Borg scale) during Minute 6 of exercise at 60 W. Those with an RPB of 4 or higher were designated obese women with breathlessness. To better delineate differences between the two groups, women with a rating of 3 were excluded from further study in experiment 2, and those with an RPB of 2 or less were designated as obese women without breathlessness. Of the 19 volunteers screened, seven obese women had an RPB of 2 or lower, and seven (37%) had an RPB of 4 or higher.
Body composition and pulmonary function tests were performed as described in experiment 1.
The intensity of RPB was taken during the last minute of constant load exercise, which was performed as described in experiment 1. Unlike in experiment 1, in experiment 2, gas exchange and simple breathing mechanics were measured to characterize differences among the subjects (if any) in ventilation, breathing pattern, tidal flow–volume patterns, and lung volume at rest and during exercise. End-expiratory lung volume (EELV) was estimated from measurement of inspiratory capacity (IC) and TLC measured in the body plethysmograph (EELV = TLC − IC) and reported as a percentage of TLC ([EELV/TLC] × 100) (20).
After the submaximal exercise test, cardiovascular exercise capacity was determined by graded cycle ergometry to exhaustion and evidenced by peak HR, peak work rate, and peak o2. During both of the exercise tests, we monitored ECG (model CS 100; Schiller, Baar, Switzerland) HR, blood pressure, RPB, RPE, pulmonary gas exchange (e, o2, and co2), PetCO2, and pulse oximetry (SaO2%) as is required for participant safety with any standardized cardiopulmonary exercise test.
The oxygen cost of breathing was measured as described in experiment 1. In addition, respiratory mechanics measurements were made that included breathing pattern, lung volumes, tidal flow–volume patterns, and respiratory pressures. Breathing mechanics were measured to characterize differences among the subjects (if any) at rest and during eucapnic voluntary hyperpnea. Expiratory and inspiratory flow was measured at rest and continuously as described previously (21). IC was measured at rest and during exercise to determine placement of tidal flow–volume loops within the maximal flow–volume loop as previously described (21, 22). IC was measured during the last 20 seconds of each exercise increment and tidal flow–volume loops were measured continuously. EELV was estimated from measurement of IC and reported as a percentage of TLC. End-inspiratory lung volume was calculated (EILV = EELV + Vt) and expressed as a percentage of TLC. This assumes that TLC does not change significantly with body position (20) or exercise (23–25). Respiratory pressures (pleural, transpulmonary, and gastric) were used for estimating the mechanical work of breathing and the magnitude of breathing effort with inspiration and expiration. These measurements required the subjects to swallow esophageal and gastric balloons (9, 26–28).
Multiple MRI scans through the chest and abdomen were used to estimate subcutaneous chest fat (i.e., rib cage), abdominal fat (which was divided into anterior subcutaneous abdominal fat and visceral fat), posterior subcutaneous fat, and peripheral fat (total body fat minus chest, posterior, and abdominal fat).
MRI data were obtained using a whole body magnet. A supine position with arms above the head was maintained throughout the examination. For assessment of fat in the upper torso (chest), three axial images were obtained through the upper rib cage (one through the sternal notch, one through the xiphoid process, and one halfway between these two). For assessment of fat in the abdominal region of the torso, nine axial views were obtained through the abdomen and pelvis (one through the T12 vertebra, one at each lumbar level, and one through the S1 vertebra). The images were manually analyzed with Osiris (version 4.18; University Hospital of Geneva, Geneva, Switzerland) where adipose tissue was easily identified (29, 30). These procedures have been described previously (31–34), and the data were similar to those produced by comparable MRI techniques (29, 35, 36).
Subject characteristics, including body composition and pulmonary function measures, were not significantly different between the obese women with or without exertional dyspnea (Tables 1 and 2). Based on NHLBI clinical guidelines for BMI, the obese subjects in this experiment were classified as mild (class I, n = 4), moderate (class II, n = 10), or extreme (class III, n = 2). All subjects had normal spirometry based on predicted values. However, DlCO was reduced in all subjects (Table 2).
Fat Wt (kg)
|Obese (n = 8)||31 ± 8||164 ± 7||97 ± 14||36 ± 5||42 ± 5||41 ± 11||55 ± 5||112 ± 15||125 ± 12||0.89 ± 0.05||0.59 ± 0.08|
|Obese DOE (n = 8)||36 ± 5||162 ± 5||98 ± 15||37 ± 4||41 ± 7||41 ± 13||57 ± 6||107 ± 11||127 ± 10||0.84 ± 0.07||0.61 ± 0.08|
|Obese (n = 8)||106 ± 15||98 ± 9||80 ± 4||114 ± 12||101 ± 13||74 ± 14||131 ± 31||96 ± 12||39 ± 6||69 ± 12||22 ± 3|
|Obese DOE (n = 8)||94 ± 10||88 ± 11||80 ± 4||107 ± 22||97 ± 20||66 ± 11||134 ± 10||88 ± 11||40 ± 10||74 ± 21||27 ± 6|
During constant load cycling exercise at 60 W, 50% of the obese volunteers had an RPB of 4 or greater, and their mean value was significantly (P < 0.01) higher than in the women without exertional dyspnea (Figure 2).
The oxygen cost of breathing (ml/L) was markedly (38%) and significantly (P < 0.01) increased in the obese women with dyspnea on exertion (Figure 3). There was also a significant (P < 0.001) relationship between the oxygen cost of breathing and the RPB during exercise at 60 W (r2 = 0.57). Measurements during the eucapnic voluntary hyperpnea bouts of 40 and 60 L/minute are presented in Table 3.
PetCO2 (mm Hg)
|Obese (n = 8)||9 ± 1||0.54 ± 0.17||16 ± 4||0.23 ± 0.03||42 ± 2||—|
|Obese DOE (n = 8)||9 ± 2||0.64 ± 0.18||14 ± 4||0.24 ± 0.03||40 ± 4||—|
|40 L/min EVH|
|Obese (n = 8)||42 ± 2||1.25 ± 0.16||33 ± 5||0.30 ± 0.04||39 ± 1||2 ± 1|
|Obese DOE (n = 8)||43 ± 2||1.39 ± 0.06||30 ± 1||0.33 ± 0.05||38 ± 1*||2 ± 2|
|60 L/min EVH|
|Obese (n = 8)||64 ± 3||1.40 ± 0.36||46 ± 14||0.36 ± 0.05||43 ± 1||3 ± 2|
|Obese DOE (n = 8)||62 ± 2*||1.55 ± 0.19*||39 ± 5*||0.39 ± 0.04*||43 ± 1†||3 ± 2|
| P value||NS||NS||NS||NS||<0.05||NS|
With the exception of BMI, subject characteristics including body composition and pulmonary function measures were not significantly different between the obese women with or without dyspnea on exertion (Tables 4 and 5). Based on NHLBI clinical guidelines for BMI, the obese subjects in this experiment were classified as mild (Class I, n = 6), moderate (class II, n = 4), or extreme (class III, n = 4). Overall, the subjects in experiment 2 were very similar to the subjects in experiment 1. Fat distribution, as determined from MRI scans, was similar between the women with and without dyspnea on exertion (Table 6). All subjects had normal spirometry based on predicted values.
Fat Wt (kg)
|Obese (n = 7)||29 ± 7||164 ± 6||92 ± 16||34 ± 4||41 ± 4||38 ± 10||54 ± 8||107 ± 18||121 ± 12||0.88 ± 0.10||0.56 ± 0.08|
|Obese DOE (n = 7)||34 ± 7||160 ± 10||100 ± 11||39 ± 4||44 ± 5||44 ± 8||55 ± 7||111 ± 8||128 ± 8||0.87 ± 0.07||0.62 ± 0.06|
|Obese (n = 7)||107 ± 12||100 ± 9||80 ± 4||115 ± 9||102 ± 8||76 ± 9||107 ± 14||96 ± 9||38 ± 4||68 ± 16||22 ± 6|
|Obese DOE (n = 7)||95 ± 11||92 ± 10||83 ± 5||109 ± 11||96 ± 18||72 ± 6||122 ± 19||89 ± 11||38 ± 10||65 ± 12||22 ± 3|
Ant Sub Q (kg)
Post Sub Q (kg)
|Obese (n = 7)||5.5 ± 1.8||6.3 ± 2.8||2.7 ± 1.0||8.3 ± 2.3||15.7 ± 3.4|
|Obese DOE (n = 7)||6.5 ± 1.0||6.3 ± 1.1||2.4 ± 0.5||10.0 ± 2.1||19.0 ± 4.4|
Seven (37%) of the 19 obese volunteers had an RPB of 4 or greater (5 ± 1; P < 0.0001) during constant load cycling exercise at 60 W as compared with seven (26%) obese women with an RPB of 2 or less (1 ± 0.7). These findings for RPB during exercise at 60 W were very similar to those observed in experiment 1 for the obese women with and without exertional dyspnea.
Cardiorespiratory measures during constant load exercise at 60 W including EELV (%TLC) were not significantly different between the women with and without exertional dyspnea (Table 7). Based on HR (% peak HR) or e (e/MVV [maximal voluntary ventilation] ratio), the intensity of exercise was not different between the two groups. However, based on the relative oxygen uptake (% peak o2), exercise intensity was significantly greater (P < 0.05) in the obese women with exertional dyspnea as compared with the obese women without dyspnea. The o2 during exercise at 60 W was larger, although not significantly, in the obese women with exertional dyspnea, probably due to the increased oxygen cost of breathing. RPE during constant load exercise was 9 ± 1 for the obese women without dyspnea and 13 ± 1 for the obese women with dyspnea (P < 0.0001).
PetCO2 (mm Hg)
HR (% peak)
|Obese (n = 7)||1.07 ± 0.09||61 ± 5||1.08 ± 0.15||36 ± 8||1.6 ± 0.4||25 ± 8||33 ± 5||41 ± 5||31 ± 8||40 ± 4||76 ± 9|
|Obese DOE (n = 7)||1.15 ± 0.08||69 ± 8||1.20 ± 0.10||38 ± 3||1.3 ± 0.1||30 ± 5||32 ± 4||44 ± 5||36 ± 9||42 ± 4||78 ± 7|
Exercise capacity was not different between the women with and without dyspnea on exertion based on peak work rate, peak o2, and peak HR (Figure 4). None of the cardiorespiratory measures at peak exercise was different (Table 8). Aerobic fitness was also similar between the obese women without and with exertional dyspnea (o2 = 19 ± 3 and 17 ± 2 ml/kg/min, respectively).
Exercise Time (min)
PetCO2 (mm Hg)
|Obese (n = 7)||7.57 ± 0.79||1.76 ± 0.18||1.24 ± 0.06||82 ± 11||1.8 ± 0.3||46 ± 10||37 ± 5||34 ± 4||70 ± 10||18 ± 2||7 ± 3|
|Obese DOE (n = 7)||7.14 ± 0.69||1.68 ± 0.17||1.25 ± 0.09||71 ± 7||1.6 ± 0.4||46 ± 8||34 ± 2||38 ± 4||67 ± 7||18 ± 3||8 ± 3|
The oxygen cost of breathing (ml/L) was markedly (70%) and significantly (P < 0.05) increased in the obese women with exertional dyspnea as compared with the obese women without exertional dyspnea (3.04 ± 1.08 vs. 1.79 ± 0.39), which confirmed the finding in experiment 1. There was also a significant (P < 0.001) relationship between the oxygen cost of breathing and the RPB during constant load exercise at 60 W (r2 = 0.72; P < 0.0001), which was even stronger than that observed in experiment 1 (Figure 5). Based on this association, approximately 72% of the RPB during exertion could be explained by the increase in the oxygen cost of breathing.
In contrast to the finding in experiment 1, RPB was greater in the obese women with exertional dyspnea during the 40 (4 ± 2 vs. 2 ± 1) and 60 L/minute (5 ± 2 vs. 2 ± 1) bouts of the eucapnic voluntary hyperpnea test (P ⩽ 0.05). This was despite a slightly lower e and Vt during the 60-L/minute bout in the obese women with dyspnea on exertion (Table 9; P > 0.05). Respiratory pressures were successfully obtained in four of the obese women with exertional dyspnea and three of the obese women without dyspnea (i.e., some subjects were unable to tolerate the placement of balloon catheters for the lengthy testing procedure, and in one woman balloon volume leaked during the test). The only difference in breathing mechanics between the two groups was in EILV, which was larger (P < 0.05) during voluntary hyperpnea at 40 L/minute in the obese women with dyspnea (Table 9). Thus, the mechanical work of breathing was not different between the two groups, despite the finding that the oxygen cost of breathing was greater in the obese women with exertional dyspnea.
PetCO2 (mm Hg)
Peak Insp. Ptp (cm H2O)
P(tpinsp−tpexp) (cm H2O)
P(plinsp−plexp) (cm H2O)
P(gainsp−gaexp) (cm H2O)
|Obese (n = 7)||8 ± 1||0.6 ± 0.1||13 ± 3||0.23 ± 0.03||39 ± 3||43 ± 7||57 ± 9||3.5 ± 0.9*||−3.5 ± 2*||7.7 ± 2*||8.5 ± 2*||9.5 ± 2†|
|Obese DOE (n = 7)||8 ± 1||0.6 ± 0.1||15 ± 2||0.22 ± 0.03||40 ± 3||41 ± 7||56 ± 9||3.6 ± 1.0‡||−3.9 ± 3‡||7.7 ± 2‡||8.5 ± 2‡||7.3 ± 3‡|
|40 L/min EVH|
|Obese (n = 7)||40 ± 1||1.4 ± 0.0||30 ± 0||0.29 ± 0.02||37 ± 1||42 ± 3||69 ± 4||38 ± 4*||−9.5 ± 2*||14.5 ± 3*||18.1 ± 3*||11.3 ± 2†|
|Obese DOE (n = 7)||40 ± 1||1.3 ± 0.0||30 ± 1||0.30 ± 0.03||38 ± 1||45 ± 5||76 ± 6||40 ± 12‡||−11.6 ± 3‡||15.8 ± 5‡||19 ± 5‡||12.5 ± 2‡|
|60 L/min EVH|
|Obese (n = 7)||62 ± 3||1.7 ± 0.1||36 ± 0||0.32 ± 0.04||41 ± 1||43 ± 5||79 ± 6||86 ± 13*||−11.9 ± 2*||19.0 ± 2*||25.8 ± 3*||11.5 ± 1†|
|Obese DOE (n = 7)||58 ± 3||1.6 ± 0.1||36 ± 1||0.37 ± 0.05||43 ± 2||49 ± 5§||86 ± 7§||81 ± 37‡||−15.1 ± 6‡||22.1 ± 9‡||30.7 ± 11‡||11.3 ± 6‡|
| P value||<0.05||<0.05||NS||NS||<0.05||NS||NS||NS||NS||NS||NS||NS|
The oxygen cost of breathing was significantly (P < 0.05) correlated with FEV1 as a percent of predicted (r2 = 0.39), MVV as a percent of predicted (r2 = 0.35), DlCO/VA as a percent predicted (r2 = 0.34), RPE during constant load exercise at 60 W (r2 = 0.52), and o2 as a percent of peak o2 (r2 = 0.62). There was no significant association between any measure of fat distribution and the oxygen cost of breathing.
The results of this study demonstrate four important findings. First, more than 37% of otherwise healthy younger obese women have an elevated intensity of breathlessness during moderate-level, constant load exercise. Second, exertional dyspnea in obese women seems to be strongly associated with an increased oxygen cost of breathing. Third, peak cardiovascular exercise capacity was not decreased in obese women who have dyspnea on exertion. Fourth, obesity-related changes in pulmonary function, body composition (including fat distribution), or breathing mechanics (i.e., during exercise or during eucapnic voluntary hyperpnea) did not seem to further elucidate the reason for differences in breathlessness during exercise between the two groups of obese women studied.
Although breathlessness on exertion is a common complaint of obese persons (6, 7, 37–39), the prevalence of breathlessness during exercise has not been prospectively demonstrated, especially in otherwise healthy younger obese women. In a large epidemiologic survey including all levels of obesity, 80% of obese middle-aged subjects reported shortness of breath after climbing two flights of stairs compared with only 16% of similarly aged nonobese control subjects (40). However, based on a large cohort (n = 16,171) of the NHANES III (National Health and Nutrition Examination Survey III) population (7), 36.5% of men and women (i.e., 17 yr or older, 47 ± 17 yr [mean ± SD]) with a BMI greater than 31 (i.e., obese) and 28% of adults with a BMI between 27 and 31 (i.e., overweight) reported dyspnea when walking up a hill. We observed that more than 37% of otherwise healthy obese women have a significantly elevated rating of breathlessness during exertion. Until now, the physiological mechanism responsible for this exertional dyspnea has not been explored in otherwise healthy obese women.
In carefully selected, otherwise healthy obese adults, peak o2 in L/minute, which represents cardiovascular conditioning, is usually normal (8, 9, 26, 41). Nevertheless, deconditioning remains a popular but unproven postulate of obesity-related exertional dyspnea. Our findings support the conclusion that breathlessness during exertion in otherwise healthy obese women is not due to cardiovascular deconditioning.
We proposed that factors other than simple deconditioning contribute to the development of exertional dyspnea in obesity. The oxygen cost of breathing accounts for the total energy required by the respiratory muscles to overcome respiratory mechanical factors, such as airway resistance and lung compliance, chest wall resistance, breathing inertia, antagonistic activity of respiratory muscles, chest wall distortion, gas compressibility, and work on the abdominal viscera (42, 43). Many of these components are affected by increased adipose tissue on the rib cage, the abdomen, and/or in the visceral cavity, especially during exercise (40, 44, 45). In obese adults, even with a slight increase in ventilation from resting levels, the rate of increase in o2 from respiratory work is considerable, but this rate increases precipitously at higher levels of ventilation like those encountered during exercise (45, 46). In lean subjects, the oxygen cost of breathing is roughly 1.2 ml of O2/L of ventilation, but in moderately obese subjects it can be as much as three times higher at a rate of 3.45 ml/L (46).
Our data suggest that the oxygen cost of breathing is increased as much as 70% in the obese women with exertional dyspnea as compared with obese women without exertional dyspnea. Although we propose that the increase in the oxygen cost of breathing reflects an overall change in respiratory impedance due to obesity-related alterations in respiratory mechanics (e.g., low lung volume breathing, expiratory flow limitation, increased pulmonary resistance, decreased chest wall compliance), in our clinical experience and past obesity studies (8, 9, 47, 48) we have not observed any one obesity-related change in respiratory mechanics that can distinguish between obese patients without exertional dyspnea and those incapacitated by exertional dyspnea. Thus, the increase in the oxygen cost of breathing is novel in its potential ability to distinguish obese patients with exertional dyspnea from those who do not have exertional dyspnea. This is in contrast to pulmonary function, body fatness, gas exchange demands during exercise at 60 W, and basic breathing mechanics measurements that were not different between women with and without dyspnea on exertion.
The mechanical work of breathing was not different between the two groups of women despite the finding that the oxygen cost of breathing was greater in the obese women with exertional dyspnea. We believe there are at least two possible explanations: (1) components of the metabolic cost of breathing may not be accounted for in the measured mechanical work of breathing, such as breathing inertia, distortion of the chest wall, chest wall resistance, or antagonistic activity of the respiratory muscles, gas compressibility, and work on the abdominal viscera (42, 43), and (2) the efficiency of the respiratory muscles may be decreased in the obese women with dyspnea on exertion. These findings need further investigation.
A link between the oxygen cost of breathing and breathing discomfort has been well established in respiratory patients and experimental protocols (18, 49). When the oxygen cost of breathing is increased, the level of central respiratory motor output required to obtain a given level of ventilation rises. If the respiratory effort expended in breathing is out of proportion to the resulting level of ventilation, dyspnea can result at rest (18). During exercise, if the oxygen cost of breathing is out of proportion to the exercise intensity, this could also elicit dyspnea (18, 49–51). We found the oxygen cost of breathing to be strongly related to the intensity of breathlessness during low-level constant load exercise in obese women, with the oxygen cost of breathing explaining roughly 60–70% of the RPB during exertion. Recent publications support the existence of a link between respiratory muscle work and exercise tolerance (52, 53).
We proposed that the oxygen cost of breathing may be increased more in relation to where the fat is located (i.e., fat distribution) rather than to overall body fatness (54–57). However, this association was not apparent in our study. The associations between the oxygen cost of breathing and fat distribution were not significant or insightful. Although both groups of women had large amounts of fat on the chest wall, this does not seem to help explain why some obese women experience exertional dyspnea whereas others do not. In prior work, we found that the distribution of fat in obese women is fairly consistent and similar to that in lean women, which could help explain the lack of association (58).
In conclusion, exertional dyspnea is widely prevalent in otherwise healthy younger obese women. Dyspnea during exercise in obese women is strongly associated with an increased oxygen cost of breathing, which does not seem to be specifically or consistently correlated to obesity-related changes in pulmonary function, body composition, fat distribution, or pulmonary mechanics. In contrast to conventional thinking, exertional dyspnea in otherwise healthy younger obese women is not due to cardiovascular deconditioning. These findings could have an important influence on societal misconceptions of obese patients and on treatment strategies for overweight and obese patients who make up roughly 50% of the U.S. population.
The authors thank B. MacDougall, R. McGehee, and M. Klocko for their assistance in various stages of this project. The authors wish to express their appreciation to T. Tillery, R.T.B. Fox, R.T., J. Payne, P.A.-C., and P. T. Weatherall, M.D., of the Rogers Center at UT Southwestern for their assistance with this project. The authors gratefully acknowledge the editorial contributions of Helen E. Wood, Ph.D.
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