J Appl Physiol 2011 Ora Japplphysiol.01131

8/4/2019 J Appl Physiol 2011 Ora Japplphysiol.01131

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Effect of Obesity on Respiratory Mechanics during Rest and Exercise in1

COPD23

4

Authors:5

Josuel Ora, Pierantonio Laveneziana, Karin Wadell, Megan Preston, Katherine A. Webb, Denis6

E. ODonnell.7

8

Affiliation:9

Respiratory Investigation Unit, Department of Medicine, Queens University and Kingston10

General Hospital, Kingston, Ontario, Canada.11

12

Correspondence to: Denis E. ODonnell, MD, FRCP(I), FRCP(C)13

102 Stuart Street, Kingston, Ontario, Canada K7L 2V614

E-mail: [email protected]

16

Running head: Obesity effects on exercise in COPD17

18

19

Articles in PresS. J Appl Physiol (February 24, 2011). doi:10.1152/japplphysiol.01131.2010


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ABSTRACT20

21

The presence of obesity in COPD appears not to be a disadvantage with respect to22

dyspnea and weight-supported cycle exercise performance. We hypothesized that one23

explanation for this might be that the volume-reducing effects of obesity convey mechanical and24

respiratory muscle function advantages. Twelve obese COPD (OB) (FEV1=60%predicted; body25

mass index (BMI)=321 kg/m2; meanSD) and 12 age-matched, normal-weight COPD (NW)26

(FEV1=59%predicted; BMI=232 kg/m2) subjects were compared at rest and during symptom-27

limited constant-work-rate exercise at 75% of their maximum. Measurements included28

pulmonary function tests, operating lung volumes, esophageal pressure and gastric pressure. OB29

vs. NW had a reduced total lung capacity (109 vs. 124 %predicted; p


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INTRODUCTION45

46

Obesity is increasingly recognized as an important comorbidity in patients with COPD (11,43).47

The coexistence of these two common conditions has potentially important physiological (34),48

clinical and even prognostic implications that are currently poorly understood (13).49

In patients without airway disease, obesity is associated with a restrictive ventilatory50

deficit due to reduced respiratory system compliance (4,27,36). The lower static lung volumes in51

obesity predispose to increased airway resistance and expiratory flow limitation (33,35). The52

lower resting end-expiratory lung volume (EELV) [and expiratory reserve volume (ERV)] in53

obese individuals is associated with an increased resting inspiratory capacity (IC) compared with54

lean individuals (18,33). We have suggested that this, in conjunction with dynamic increases in55

EELV during exercise towards the predicted natural relaxation volume of the respiratory system,56

may counterbalance some of the negative mechanical effects of obesity (3,33).57

The evaluation of the combined mechanical effects of mild obesity and COPD is highly58

relevant given the evidence that EELV diminishes exponentially with increasing BMI and that59

significant volume effects are seen even in the overweight range (29,18). We have recently60

reported that resting IC, symptom-limited peak oxygen uptake (VO2) and exertional dyspnea61

intensity ratings were not negatively impacted by obesity in patients with COPD (34). A recent62

retrospective analysis of a larger COPD cohort again confirmed that increased BMI was not a63

disadvantage with respect to resting IC, constant work rate cycle endurance time or dyspnea64

intensity (20). The main objective of the current study was to better understand this surprising65


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factors. Potential negative influences include increased elastic loading of the respiratory69

muscles, increased metabolic and ventilatory requirements and increased airway dysfunction and70

pulmonary resistance at the lower absolute lung volumes. Potential positive counterbalancing71

effects include improved operating length of the diaphragm at a lower EELV and increased72

driving pressure for expiratory flow due to increased static lung recoil. The current study73

extends our previous work by measuring these complex interactions in some detail. Specifically,74

our objective was to determine the effect of obesity on ventilatory mechanics and respiratory75

muscle function during rest and exercise in patients with COPD. Our hypothesis was that76

obesity in COPD would be associated with increased static lung recoil pressure, a reduced77

EELV, a preserved or enhanced IC, increased intra-abdominal pressure and improved78

diaphragmatic function during exercise. These obesity-related physiological differences would79

ensure that neuromechanical uncoupling of the respiratory system and the associated exertional80

dyspnea are not further amplified when compared with normal weight COPD patients. To test81

this hypothesis, we compared dyspnea ratings, operating lung volumes, breathing pattern,82

respiratory pressure-derived measurements at rest and during symptom-limited constant work83

rate cycle exercise in obese and normal weight patients with moderate to severe COPD.84

85


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METHODS86

87

Subjects88

We studied 12 subjects with mild obesity (OB) (BMI 30.0-34.9 kg/m2) and 12 age-matched89

normal-weight subjects (NW) (BMI 18.5-24.9 kg/m2). Subjects were clinically stable men or90

women, 55-85 years of age, with a clear diagnosis of COPD (FEV1/FVC


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DL; SensorMedics, Yorba Linda, CA) according to recommended standards (1,21,24,46). Static111

lung compliance (CLst) and static lung recoil pressure (PLst) were also measured (Vmax229d;112

SensorMedics) (15). Measurements were expressed as percentages of predicted normal values113

(5,7,8,9,16,19,26); predicted inspiratory capacity (IC) was calculated as predicted TLC minus114

predicted FRC.115

Symptom-limited exercise tests were conducted on an electrically braked cycle ergometer116

(Ergometrics 800S; SensorMedics) with a cardiopulmonary exercise testing system (Vmax229d;117

SensorMedics) as previously described (30). Incremental tests consisted of a 1-min warm-up of118

loadless pedaling followed by 1-min increments of 10 W each. CWR tests consisted of a 1-min119

warm-up followed by an increase in work rate to 75% of the maximal incremental work rate;120

endurance time was defined as the duration of loaded pedaling. Measurements included: breath-121

by-breath cardiopulmonary and metabolic parameters; intensity of dyspnea (breathing122

discomfort) and leg discomfort rated using the 10-point Borg scale (6); operating lung volumes123

derived from IC maneuvers (31); esophageal pressure (Pes)- and gastric pressure (Pga)-derived124

respiratory mechanical measurements collected continuously with an integrated data-acquisition125

setup (30). Exercise parameters were compared with the predicted normal values of Jones (17).126

Peak VO2 was standardized as a percentage of the predicted normal value corrected for ideal127

body weight (47). Ventilation (VE) was compared with the maximal ventilatory capacity128

(MVC) estimated by multiplying the measured FEV1 by 35 (14).129

130


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Sniff and cough maneuvers were performed pre-exercise at rest and immediately at end-exercise134

to obtain maximum values for Pes (Pes,sniff), Pdi (Pdi,sniff) and Pga (Pga,cough) (1).135

The tidal swing (Pes,tidal) and the inspiratory swing (Pes,insp) were defined as the136

amplitude of the Pes waveform during tidal breathing and during inspiration, respectively.137

Accepted formulae were used to calculate: total lung resistance (RL); dynamic lung compliance138

(CLdyn); the pressure-time product of the respiratory (PTPes), diaphragm (PTPdi) and expiratory139

muscles (PTPga); and the tension-time index of the diaphragm (TTIdi) and the inspiratory140

muscles (TTIes) (1,45). Activation of the expiratory muscles was evaluated by measurement of141

the expiratory gastric rise (Pga,rise) and the peak expiratory Pga (Pga,exp) during tidal breathing142

(48). End-expiration (EE) was the beginning of the inspiratory effort from the Pes waveform.143

Dynamic intrinsic positive end-expiratory pressure (PEEPi) was measured as the negative144

deflection in Pes from EE to the onset of inspiratory flow (46) and corrected (PEEPi,corr) by145

subtracting Pga,rise (28). The ventilatory muscle recruitment (VMR) index was determined as146

the slope of the line between points of zero flow at end-expiration (EE 0flow) and end-147

inspiration (EI0flow) for the Pga-Pes plots (Pga/Pes): negative slopes represent increased148

contribution by the diaphragm, more positive slopes represent increased contribution by149

inspiratory muscles of the ribcage and the expiratory muscles (23).150

151

Statistical Analysis152

Results are expressed as meansSD unless otherwise specified. A p


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(i.e., rest, a standardized exercise time of 2-min, peak exercise) meant that an uncorrected p157

value of


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RESULTS163

164

Twelve COPD patients with mild obesity (OB) and 12 age-, gender- and FEV1-matched normal-165

weight (NW) COPD patients were studied (Table 1). Chronic activity-related dyspnea was of166

moderate degree (i.e., shortness of breath while walking or climbing stairs) and largely similar167

across groups. Measurements of work rate, VO2 and VE at the peak of incremental cycle168

exercise were also similar across groups. The presence of the following comorbidities was169

balanced between groups: controlled hypertension (n= 6 OB, 5 NW), hypercholesterolemia (6170

OB, 4 NW), diabetes mellitus type 2 (2 OB, 2 NW), and stable ischemic heart disease (2 OB, 2171

NW). Chest CT scans done clinically were available for evaluation of emphysema in 6 NW and172

10 OB subjects: emphysema was present in all 6 (4 mild, 2 moderate) of these NW subjects and173

in 8 (3 mild, 5 moderate-severe) out of the 10 OB subjects.174

175

Pulmonary Function and Static Respiratory Mechanical Measurements176

Resting pulmonary function and respiratory mechanical measurements are summarized in Table177

2. Compared with NW, OB had a significantly (p


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between 10-40 W. Within each group, the peak VO2 and VE were similar for the incremental188

(Table 1) and CWR (Table 3) cycle tests.189

Cardiopulmonary responses to the CWR exercise test are summarized in Table 3 and190

shown in Figure 1. The CWR work rate (5316 and 5429 watts) and exercise endurance time191

(6.02.1 and 5.73.5 min) were similar in OB and NW, respectively. At the end of the CWR192

test, both groups stopped when they reached a critical ventilatory reserve: VE/MVC >85% and193

a reduced IRV


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Respiratory muscle/mechanical measurements are provided in Table 4. Pressure-derived211

measurements were largely similar in the OB and NW groups at rest, except expiratory and end-212

expiratory Pes and Pga were significantly (p


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(partial r=0.711), IRV%prTLC (partial r=0.707), VT/IC (partial r=0.710) and tidal Pes/Pes,sniff234

(partial r=0.678). PTPes/min (partial r=0.873), tidal Pes/Pes,sniff (partial r=0.665) and VT/IC235

(partial r=0.841) increased in direct proportion (p


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DISCUSSION239

240

The main findings of this study are as follows: 1) at rest, static lung volumes were lower, while241

PLst and Pga were higher in the OB compared with the NW groups; 2) exercise performance was242

not diminished in the obese; 3) despite lower absolute operating lung volumes, pulmonary243

resistance during exercise was not increased in OB; 4) ventilatory muscle recruitment patterns244

were broadly similar in the two groups apart from minor delays early in exercise in the increase245

in the VMR index determined from Pga/Pes plots (i.e., diaphragmatic de-recruitment) in the246

obese; and 5) resting IC, effort-displacement ratios and dyspnea/VE plots during exercise were247

not significantly affected by the presence of mild obesity.248

Patients in the two COPD groups were well matched for smoking history, severity of249

airway obstruction (FEV1), distribution of comorbidities and sex representation. They showed250

comparable reduction in exercise capacity (mean peak VO2 was reduced by ~30% compared251

with predicted normal values) with severe exertional dyspnea due to limiting respiratory252

mechanical constraints. Thus, at the limits of tolerance, breathing reserve (as reflected by high253

VE/MVC and VT/IC ratios) was critically reduced in both groups. Peak symptom-limited VO2254

was similar during the incremental and CWR cycle tests in both groups. This confirms that the255

CWR cycle endurance test was indeed a maximal effort test: physiological limits were reached256

and patients expended maximal motivational effort and reported severe dyspnea.257

258

Differences in Resting Respiratory Mechanics259


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reflects the decreased chest wall and lung compliance known to be associated with obesity263

(27,36,37,40). Despite the lower lung volumes in OB, plethysmographically-determined airway264

resistance and other measures of airway obstruction were not significantly increased.265

The elastic properties of the lung were different in OB and NW. Thus, the static lung266

elastic recoil as measured by PLst and the coefficient of retraction was greater, and closer to267

values predicted for health, in OB. We believe that differences in lung elastance reflect268

independent effects of obesity in patients with the heterogeneous pathophysiology of COPD269

rather than the fortuitous selection of different clinical phenotypes of COPD in the obese and270

lean groups (i.e., airways disease versus emphysema predominant, respectively): 1) we excluded271

underweight patients with clinically overt advanced emphysema; 2) DLCO was moderately272

reduced and not significantly different across the two groups; 3) although patients in the OB273

COPD group had comparatively lower lung volumes they still had had significant lung274

hyperinflation (FRC = 130% predicted) and; 4) qualitative radiological assessments of available275

CT scans in 10/12 obese COPD patients indicated the presence of structural emphysema ranging276

from mild to moderate severity in the majority.277

Intra-abdominal pressure measured by gastric balloon (in the sitting position) in a278

subgroup of patients was consistently elevated in OB by close to 10 cmH2O compared with NW.279

This likely reflects the mass loading effects of adipose tissue on the chest wall and abdomen280

(39,41). Measures of static respiratory muscle strength (including the diaphragm) were not281

significantly higher in the obese group despite the significantly lower EELV. Lack of inter-282


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Differences in Dynamic Respiratory Mechanics and Muscle Function during Exercise286

Peak symptom-limited VO2 (expressed as a percentage of predicted based on ideal body287

weight), exercise endurance times and dyspnea intensity ratings were similar in both groups. In288

contrast to our previous study using incremental cycle exercise, the rise in VO2 and VE was not289

significantly increased in the OB versus the NW group during CWR exercise. This reflects the290

balance between the modestly increased metabolic load in OB and improved ventilatory291

efficiency in this group: ventilatory equivalent for CO2 was lower at rest and during exercise in292

OB (Figure 1). A better ventilatory efficiency is consistent with the notion that ventilation-293

perfusion relations were less disrupted in the OB patients during exercise (49). The finding of a294

lack of group differences in ventilatory responses to exercise was fortuitous with respect to the295

comparison of dynamic mechanics and respiratory muscle performance that we undertook.296

Despite the relatively lower lung volumes in OB, the ability to generate maximal tidal297

expiratory flow rates and to increase alveolar ventilation in pace with metabolic demand was not298

compromised to a greater extent in OB than in NW. Thus, the changes in PETCO2 and SpO2 from299

rest to exercise termination were similar in both groups. It is possible that in the OB group, the300

better preserved PLst (and the attendant increased driving pressure for expiratory flow)301

compensated for the possible disadvantage with respect to airway function of breathing at lung302

volumes closer to residual volume. It is interesting to speculate that better preservation of the303

elastic properties of the lungs and in operating lung volumes seen in the obese group may lead to304

improved airway and respiratory muscle function. We could find no evidence of greater305


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is noteworthy that measured pulmonary resistance was not increased in OB despite the lower309

EELV (Figure 3). In fact, in contrast to NW, pulmonary resistance transiently but consistently310

fell slightly at the onset of exercise as EELV dynamically increased. This suggests the presence311

of a greater lung volume-dependent component in the increased resistance in OB compared with312

control.313

The static strength of the inspiratory and expiratory muscles (measured at rest) was not314

diminished at the limits of tolerance in either group. Intra-abdominal pressures were significantly315

elevated at rest and to a similar degree throughout exercise. However, the pattern of expiratory316

muscle activation (measured by Pga,rise) was similar in both groups. The pressure-time product317

and the tension-time index of the inspiratory and expiratory muscles during exercise were also318

similar.319

We were particularly interested in comparing diaphragmatic function in obese and lean320

COPD as the lower absolute lung volumes (by almost 1.0 L) and increased intra-abdominal321

pressures in OB patients could theoretically optimize the configuration (i.e., cephaloid shift) and322

length-tension relations of this muscle. However, we were unable to show any such advantages323

in the OB group other than a minor delay in the time course of de-recruitment of the diaphragm324

(and recruitment of accessory muscles) during early exercise in the OB compared with NW325

patients as indicated by analysis of the tidal Pes and Pga plots (Figure 4) (23,25). The pressure-326

time product and pattern of rise in Pdi during exercise were not different in the two groups. The327

lack of a significant between-group difference in Pga is probably related to inadequate power as328


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However, measures of CLdyn and PEEPi during exercise were not significantly different between332

groups. This contention that the elastic load is increased in obesity is supported by the finding333

that the pressure requirements to generate IC of similar magnitude at rest and serially throughout334

exercise were consistently higher in the obese patients (Figure 2B). It is noteworthy that during335

spontaneous breathing throughout exercise, tidal pressure swings (for a similar VT) relative to336

maximum were not different between the groups suggesting that the net load-capacity ratio of the337

respiratory muscles was essentially similar.338

339

Lack of Increase in Exertional Dyspnea Intensity in Obesity340

341

In contrast to our previous study (34), dyspnea/VE slopes in OB were not lower but similar to342

that of NW during exercise. This finding confirms the results reported by Laviolette et al.(20) in343

a large group of men with COPD and lung hyperinflation using a similar CWR protocol. There344

are several possible reasons for the apparent disparity between results of our two studies. 1) This345

study, unlike the previous study (n=18 per group)(34), may not have been sufficiently powered346

to detect significant differences in dyspnea between the groups. 2) The current study includes347

patients with only mild obesity (BMI 30-35 kg/m2) and more moderate airway obstruction, while348

our previous study included subjects with a greater BMI range and more severe COPD. We have349

recently reported that the volume-reducing effects of increased BMI are most pronounced in350

those with severe COPD (29). We postulate, therefore, that the effects of obesity on operating351

lung volumes would be greater and more consistent in a sample of patients with higher BMI and352


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in this study (CWR) was different from that used in our previous study (incremental). 4)356

Relatively small sample sizes in both studies can potentially result in greater variability in357

physiological responses within and between studies (low power).358

The relationship between dyspnea intensity and VE during exercise in COPD reflects the359

extent of the underlying mechanical abnormalities and respiratory muscle function. Thus,360

manipulations of the mechanical load by bronchodilators in COPD patients have been shown to361

consistently affect this relationship; dyspnea is diminished at a given VE (38). The finding that362

dyspnea/VE plots were similar in obese and lean COPD groups bolsters the argument that the363

net balance between intrinsic mechanical loading of the respiratory muscles and their maximal364

force-generating capacity was similar. We have previously argued that the IC is an important365

predictor of dyspnea intensity in COPD (31). The smaller the IC, the more VT encroaches during366

exercise on the upper reaches of the respiratory systems sigmoidal pressure-volume curve where367

there is widening disparity between central neural drive and the mechanical response of the368

respiratory system, i.e., neuromechanical uncoupling. Despite the difference in absolute lung369

volumes, the dynamic IC and IRV were similar throughout exercise in both groups so it is not370

surprising that the relationship between contractile respiratory muscle effort and VT displacement371

(i.e., effort-displacement ratio) and corresponding dyspnea intensity ratings were also similar.372

Moreover, by correlative analysis, previously established contributory factors to dyspnea373

intensity which included indices of mechanical constraints on tidal volume expansion (VT/IC,374

IRV) and increased respiratory effort (pressure-time product, Pes/Pes,sniff) were similar across375


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Limitations379

Our patients had mild to moderate increases in BMI and the results may not be applicable to380

patients with morbid obesity. Accurate measurements of body composition and adipose tissue381

distribution were not available to confirm and quantify the extent of obesity. However, recent382

reports suggest that mechanical derangements of obesity are more closely correlated with383

increasing BMI than with fat distribution patternsper se (2,44). We believe that the changes in384

static lung volumes and resting respiratory mechanics in higher BMI group are consistent with385

the presence of significant obesity. We may have underestimated the mechanical consequences386

in the OB group as measures of chest wall compliance were not available. Estimates of fat-free387

mass were higher in subsets of OB than in NW which raises the possibility that increased skeletal388

muscle strength played a role in maintaining exercise performance in the former. Our studies389

were conducted using cycle ergometry, thus, our results may have been different had we used390

treadmill where the metabolic load is known to be greater.391

392

In conclusion, increased BMI was shown to have consistent effects on static lung recoil393

pressure and on operating lung volumes and ventilatory efficiency during exercise, all of which394

were potentially advantageous. There were small but consistent improvements in pulmonary395

resistance and diaphragmatic function early in exercise in OB that were not seen in NW. In396

obesity, the lower EELV did not compromise airway function likely because of the preservation397

of static lung recoil pressure driving expiratory flow. Furthermore, the increased elastic loading398


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lack of greater respiratory discomfort or exercise curtailment in obese COPD patients402

fundamentally reflects the fact that, regardless of differences in absolute lung volumes, the403

resting IC was similar to the lean group. Thus, breathing pattern, the dynamic performance of the404

respiratory muscles and effort-displacement ratios were remarkably similar throughout exercise405

in lean and obese COPD patients.406

407

ACKNOWLEDGEMENTS: The authors wish to acknowledge Yuk-Miu Lam, PhD408

(Department of Community Health & Epidemiology, Queens University) for providing his409

statistical expertise.410

GRANTS: Canadian/OntarioThoracic Society Grant-in Aid411412

DISCLOSURES: The authors have no conflicts of interest related to this manuscript to report.413

414

415


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Johnson D, MacIntyre N, McKay R, Miller MR, Navajas D, Pellegrino R, Viegi G;534

ATS/ERS Task Force. Standardisation of the measurement of lung volumes.Eur Respir J535

26: 511-522, 2005.536

47. Wasserman K, Hansen JE, Sue DY, Casaburi R, Whipp BJ. Principles of Exercise537Testing and Interpretation. Baltimore: Lippincott Williams & Wilkins, 1999.538

48. Yan S, Sinderby C, Bielen P, Beck J, Comtois N, Sliwinski P. Expiratory muscle539pressure and breathing mechanics in chronic obstructive pulmonary disease. Eur Respir J540

16: 684-690, 2000.541

49. Zavorsky GS, Hoffman SL. Pulmonary gas exchange in the morbidly obese. Obes Rev 9:542326-339, 2008.543

544

545


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TABLE 1. Subject characteristics546

NW (n=12) OB (n=12)

Male, n (%) 6 (50) 6 (50)

Age, yrs 68 8 68 4

Height, cm 169 13 167 9

Weight, kg 67.3 12.0 90.3 12.1 *

Weight, % of ideal 95 8 131 5 *

Body mass index, kg/m2

23.4 1.8 32.2 1.2 *

Smoking history, pack-yrs 61 35 68 54

COPD duration, yrs 8 6 10 10

Baseline Dyspnea Index,focal score 0-12:

Magnitude of Effort 0-4

Magnitude of Task 0-4

Functional Impairment 0-4

6.7 1.2

2.4 0.5

1.9 0.3

2.3 0.8

6.2 0.8

1.8 0.4 *

1.8 0.5

2.6 0.7

Medical Research Council

dyspnea scale, 1-5 2.4 0.7 2.7 0.8

Peak incremental work rate,

watts (% predicted maximum)

71 36

(56 20)

70 19

(59 21)

Peak incremental VO2, L/min

(% predicted maximum)

1.14 0.58

(73 19)

1.18 0.31

(71 18)

Peak incremental VE, L/min (%

estimated MVC)

43.7 24.1

(95 15)

39.2 8.6

(92 18)

Values are means SD.547

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TABLE 2. Pulmonary function and static respiratory mechanical measurements556

NW OB

FEV1, L (%predicted) 1.33 0.64 (59 17) 1.26 0.21 (60 13)

FVC, L (%predicted) 3.10 1.18 (95 16) 2.80 0.60 (92 20)

FEV1/FVC,% 42 8 47 12

PEFR, L/s (%predicted) 4.4 1.4 (68 16) 4.4 0.7 (73 16)

FEF50, L/s (%predicted) 0.5 0.4 (12 8) 0.5 0.2 (14 6)

TLC, L (%predicted) 7.44 1.97 (124 15) 6.35 1.66 (109 30 *)IC, L (%predicted) 2.24 0.86 (81 18) 2.18 0.35 (84 15)

FRC, L (%predicted) 5.20 1.37 (158 27) 4.18 1.51 (130 38 *)

RV, L (%predicted) 3.83 1.04 (170 43) 3.42 1.29 (154 53)

RV/TLC, % 52 11 52 9

ERV, L (%predicted) 1.37 0.69 (134 50) 0.76 0.42 * (80 38 *)

sRaw, cmH2Os (%predicted) 22.5 9.3 (544 218) 21.5 11.8 (512 270)

DLCO, mL/min/mmHg (%predicted) 13.9 6.5 (75 26) 14.6 5.0 (67 20)

DLCO/VA, mL/min/mmHg/L

(%predicted)2.86 0.69 (77 16) 3.45 0.88 (93 23)

MIP, cmH2O (%predicted) -67 22 (89 30) -76 16 (108 38)

MEP, cmH2O (%predicted) 121 28 (75 17) 125 46 (77 24)CLst, L/cmH2O 0.37 0.13 0.29 0.12

PLst, cmH2O (%predicted) 21.3 5.9 (77 37) 27.4 8.1 * (97 25)

Coefficient of retraction, cmH2O/L 3.1 1.4 4.5 1.5 *

Sniff Pes, cmH2O -64 18 -65 11

Sniff Pdi, cmH2O 114 27 127 25

Cough Pga, cmH2O 137 66 177 69

Values are means SD with percentage of the predicted normal value in parentheses.557

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TABLE 3. Measurements during CWR exercise at 75% of incremental peak work rate566

567

Rest 2 min PeakNW OB NW OB NW OB

Dyspnea, Borg 0.2 0.4 0.3 0.6 2.7 2.3 2.8 1.8 6.6 2.8 6.8 2.2

Leg discomfort, Borg 0.2 0.6 0.3 0.6 2.8 2.0 2.9 1.1 6.1 3.2 6.6 2.4

Work rate, watts 0 0 54 29 53 16 54 29 53 16

VO2, L/min 0.22 0.10 0.290.10 0.82 0.30 0.93 0.20 1.10 0.47 1.19 0.30

VCO2, L/min 0.18 0.08 0.240.08 0.69 0.27 0.77 0.18 1.04 0.44 1.16 0.33Heart rate, beats/min 77 9 85 13 106 18 113 21 127 19 120 15

SpO2, % 95.5 1.4 95.1 1.8 94.3 2.3 92.3 2.8 93.6 3.4 93.8 3.6

VE, L/min 11.1 3.4 12.1 3.2 27.9 8.3 27.5 3.9 41.7 16.7 40.2 9.3

PETCO2, mmHg 35 4 36 5 39 5 41 6 39 7 41 7

VT, L 0.61 0.12 0.66 0.18 1.14 0.37 1.03 0.16 1.22 0.36 1.15 0.23

TI/TTOT 0.38 0.06 0.36 0.05 0 .4 0 0.06 0.39 0.03 0.41 0.06 0.38 0.03

Peak tidal expiratory

flow, L/s0.60 0.21 0.72 0.16 1.29 0.36 1.57 0.34 1.98 0.69 2.20 0.63

IC, L 2.37 0.77 2.20 0.37 1.84 0.76 1.79 0.38 1.63 0.57 1.66 0.36

IC from rest, L 0 0 -0.53 0.26 -0.46 0.32 -0.74 0.40 -0.59 0.29

IRV, L 1.76 0.69 1.54 0.37 0.71 0.53 0.76 0.30 0.41 0.28 0.510.22

EELV, L 5.33 1.29 4.15 1.50 * 5.60 1.52 4.56 1.67 5.81 1.65 4.69 1.59

EELV, % pred TLC 86 14 70 20 * 93 17 78 23 97 17 80 22 *

EILV/TLC, % 77 6 75 7 91 7 87 5 94 5 92 4

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TABLE 4. Respiratory muscle/mechanical measurements571

572

Rest 2 min PeakNW OB NW OB NW OB

Pes-derived measurements (n=12 per group):

Pes,exp, cmH2O 0.2 2.1 3.0 3.0 * 8.8 6.9 11.2 6.8 11.9 4.9 15.5 11.0

Pes,insp, cmH2O -8.9 3.1 -9.1 2.1 -12.6 4.4 -13.5 4.0 -16.4 5.3 -19.3 4.8

PesEE, cmH2O -1.6 2.1 1.0 3.3 * 7.2 6.6 10.0 6.1 10.4 5.0 14.4 11.0

PesEE0flow, cmH2O -3.5 1.8 -1.8 2.8 -1.6 5.5 -0.2 3.9 -0.7 7.2 -0.6 6.7

TTIes,insp 0.0140.011 0.0240.020 0.0410.043 0.0560.048 0.0660.042 0.0640.057

PTPes, cmH2Os/min 72 33 103 30 194 90 203 49 259 56 285 53

Pga- and Pdi-derived measurements (n=8 NW, n=7 OB):

VMR (Pga/Pes) -3.4 0.9 -3.1 2.0 -0.0 0.9 -1.2 1.7 0.7 0.9 0.4 1.5

PEEPi,corr, cmH2O 1.5 2.1 2.2 2.2 6.3 4.7 8.1 8.8 7.2 11.0 10.5 14.7

Pga,rise, cmH2O 0.8 1.0 0.8 1.4 6.8 5.1 6.2 2.9 12.9 6.9 14.7 5.6

PgaEE0flow, cmH2O 6.5 6.7 16.9 4.9 * 14.0 7.5 20.3 7.3 17.7 12.6 22.9 6.1

Pga,exp, cmH2O 12.6 7.3 20.2 4.5 * 19.4 7.7 25.6 7.8 24.3 13.0 32.3. 8.5

PTPga, cmH2Os/min 59 24 70 21 152 94 151 75 243 148 292 153

Pdi,tidal, cmH2O 12.5 4.5 17.4 6.0 20.0 7.1 22.1 9.6 20.6 13.5 20.3 9.7

TTIdi,insp swing 0.0270.015 0.0390.014 0.0250.013 0.0250.010 0.0250.021 0.0170.005

PTPdi, cmH2Os/min 136 70 165 56 203 77 231 98 187 117 227 84

Values are means SD.573

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FIGURES577

Figure 1. Oxygen consumption (VO2), ventilation (VE), the ventilatory equivalent for carbon578

dioxide (VE/VCO2), inspiratory capacity (IC), tidal volume (VT) and breathing frequency (Fb)579

are shown in response to symptom-limited constant work rate cycle exercise in obese COPD580

(OB) subjects () and in normal-weight COPD (NW) subjects (). Values are means SE.581

*p


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subjects () and in normal-weight COPD (NW) subjects (). RL remained stable throughout601

exercise in NW, but decreased significantly (*p


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1.4 50 75NW

0.6

0.8

1.0

1.2

(L/min)

30

40

tion(L/min)

*

55

65

/VCO2

0.0

0.2

0.4

0 1 2 3 4 5 6 7 8

VO

0

10

0 1 2 3 4 5 6 7

V

entila

* *2535

0 1 2 3 4 5 6 7

V

Exercise time (min) Exercise time (min) Exercise time (min)

90

100

)

40

45

VC

) 35

40

in)

60

70

80

C(%predicted

20

25

30

35

T(%predicted

15

20

25

Fb

(breaths/m

500 1 2 3 4 5 6 7

I

Exercise time (min)

15

0 1 2 3 4 5 6 7

Exercise time (min)

10

0 1 2 3 4 5 6 7

Exercise time (min)


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(A) NWOB

ControlTLCNW120

130

LC

)

TLCOB

EILV90

100

110

predictedT

TLCControl

**

VT

60

70

80

volumes(%

EELV

40

50

0 20 40 60 80

Lu

ng

Ventilation (L/min)

(B)

*

min Pes (at TLC)-50

-40

inspiratoryreserve

-30

-20H2O

)

Pes,insp

id l

-10

es(c


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NW

OB12 250.5

6

8

10

cmH2

O/L/s)

10

15

20

Pi(cmH2

O)

*

0.2

0.3

0.4

(L/cmH2

O)

2

4

0 1 2 3 4 5 6 7

RL

(

0

5

0 1 2 3 4 5 6 7

PE

0.0

0.1

0 1 2 3 4 5 6 7

CL

dy

50

60

70

,sn

iff)

1.2

1.4

1.6

1.8

VT/prVC

0.20

0.25

0.30

al

10

20

30

40

estidal(%Pe

0.2

0.4

0.6

0.8

1.0

es/Pes,sniff:

0.05

0.10

0.15

TTIestid

0

0 1 2 3 4 5 6 7

Exercise time (min)

0.0

0 1 2 3 4 5 6 7

Exercise time (min)

0.00

0 1 2 3 4 5 6 7

Exercise time (min)


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-10

-H

2O) NW COPD OB COPD

(A)

-6

-4essure(cm

-2

0

ophagealp

= EI 0 flow

2 min

Peak

Rest

2 min

Peak

1 min 1 min

2

6 8 10 12 14 16 18 20 22 24 26

Es

Gastric pressure (cmH2O)

= ow

1

2(B)NW

OB

-2

-1

0

Pga

/Pes)

*

-3

MR(


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8

9

10

8

9

10 NW

OB

4

5

6

pnea

(Borg)

4

5

6

pnea

(Borg)

0

1

2

0 1 2 3 4 5 6 7

Dy

0

1

2

0 10 20 30 40 50

Dy

Exercise time (min) Ventilation (L/min)

9

10

9

10

T

LC

5

6

7

ea

(Borg)

5

6

7

8

nea

(Borg)

1

2

3Dys

pn

1

2

3Dy

sp

50 100 150 200 250 300 350

PTPes (cmH2O x s/min)

05101520253035

IRV (%pred TLC)

Documents

J Appl Physiol 2011 Ora Japplphysiol.01131