Altered Resting and Exercise Respiratory Physiology in Obesity

doi:10.1016/j.ccm.2009.05.003

Clinics in Chest Medicine

Volume 30, Issue 3, September 2009, Pages 445-454

https://doi.org/10.1016/j.ccm.2009.05.003 Get rights and content

Obesity, particularly severe obesity, affects resting and exercise-related respiratory physiology. Severe obesity classically produces a restrictive ventilatory abnormality characterized by reduced expiratory reserve volume. Obstructive ventilatory abnormality may also be associated with abdominal obesity. Decreased peak work rates are usually seen among obese subjects in a setting of normal or decreased ventilatory reserve and normal cardiovascular response to exercise. Weight loss may reverse many adverse physiologic consequences of severe obesity on the respiratory system.

Section snippets

Altered resting respiratory physiology in obesity

Obesity affects various resting respiratory physiologic parameters, such as compliance, neuromuscular strength, work of breathing, lung volumes, spirometric measures, respiratory resistance, diffusing capacity, gas exchange, and airway responsiveness to methacholine (Table 1).

Airway responsiveness to methacholine

The association between obesity and asthma has been covered elsewhere in great detail (see the article by Beuther in this issue). It is, however, worth mentioning that the mechanical effects of obesity on the lungs may alter airway smooth muscle contractility and increase airway responsiveness.⁵⁷ Breathing voluntarily at low lung volumes may increase airway responsiveness to methacholine in lean nonasthmatic subjects.⁵⁸ In obese subjects breathing at low lung volumes, the airways remain at a

Oxygen Consumption

Obesity is associated with increased rates of basal metabolism and ${\dot{V}}_{O_{2}}$ at rest (Table 2).⁶⁵ Because adipose tissue has a lower metabolic rate than other tissues, however, if ${\dot{V}}_{O_{2}}$ is standardized by expressing it per kilogram of actual body weight, lower than normal values are obtained in obese individuals.⁶⁵ Similarly, an active, otherwise healthy, obese subject has a reduced peak ${\dot{V}}_{O_{2}}$ if it is correlated to actual body weight but a normal or high peak ${\dot{V}}_{O_{2}}$ if it is correlated to height,⁶⁶

Summary

Obesity, particularly severe obesity, affects resting and exercise-related respiratory physiology. Obesity markedly reduces the ERV and respiratory system compliance, classically producing a restrictive ventilatory abnormality. Less often, a reduced FEV₁/VC ratio (associated with abdominal obesity) and reduced maximum expiratory flow rates at low lung volumes may produce an obstructive ventilatory abnormality as well. Arterial hypoxemia resulting from ventilation-perfusion mismatch usually

Acknowledgments

The author thanks Mark Schuyler, MD, University of New Mexico, and Cheryl Salome, PhD, Woolcock Institute of Research, University of Sydney, for their careful critique of this article.

References (73)

National Center for Health Statistics
Chartbook on trends in the health of Americans, Health, United States, 2006
(2006)
C.S. Ray et al.
Effects of obesity on respiratory function
Am Rev Respir Dis
(1983)
A. Naimark et al.
Compliance of the respiratory system and its components in health and obesity
J Appl Phys
(1960)
D.F. Rochester et al.
Current concepts in the pathogenesis of the obesity-hypoventilation syndrome. Mechanical and circulatory factors
Am J Med
(1974)
S.M. Koenig
Pulmonary complications of obesity
Am J Med Sci
(2001)
M. Chlif et al.
Inspiratory muscle activity during incremental exercise in obese men
Int J Obes (Lond)
(2007)
M. Chlif et al.
Noninvasive assessment of the tension-time index of inspiratory muscles at rest in obese male subjects
Int J Obes (Lond)
(2005)
P. Weiner et al.
Influence of excessive weight loss after gastroplasty for morbid obesity on respiratory muscle performance
Thorax
(1998)
J.T. Sharp et al.
Diaphragmatic responses to body position changes in obese patients with obstructive sleep apnea
Am Rev Respir Dis
(1986)
M. Krotkiewski et al.
Increased muscle dynamic endurance associated with weight reduction on a very-low-calorie diet
Am J Clin Nutr
(1990)

P. Damsbo et al.

Reduced glycogen synthase activity in skeletal muscle from obese patients with and without type 2 (non-insulin-dependent) diabetes mellitus

Diabetologia

(1991)

C. Lennmarken et al.

Skeletal muscle function and metabolism in obese women

JPEN J Parenter Enteral Nutr

(1986)

D.J. Newham et al.

The strength, contractile properties and radiological density of skeletal muscle before and 1 year after gastroplasty

Clin Sci (Lond)

(1988)

E.J. Fadell et al.

Fatty infiltration of respiratory muscles in the Pickwickian syndrome

N Engl J Med

(1962)

D. Rochester

Obesity and pulmonary function

C. Perrin et al.

Pulmonary complications of chronic neuromuscular diseases and their management

Muscle Nerve

(2004)

J.P. Kress et al.

The impact of morbid obesity on oxygen cost of breathing (VO(2RESP)) at rest

Am J Respir Crit Care Med

(1999)

G.N. Bedell et al.

Pulmonary function in obese persons

J Clin Invest

(1958)

T.J. Sutherland et al.

The effect of adiposity measured by dual-energy X-ray absorptiometry on lung function

Eur Respir J

(2008)

S.C. Jenkins et al.

The effects of mild obesity on lung function

Respir Med

(1991)

R.L. Jones et al.

The effects of body mass index on lung volumes

Chest

(2006)

G.J. Gibson

Obesity, respiratory function and breathlessness

Thorax

(2000)

I. Rubinstein et al.

Airflow limitation in morbidly obese, nonsmoking men

Ann Intern Med

(1990)

F.G. Douglas et al.

Influence of obesity on peripheral airways patency

J Appl Phys

(1972)

M.S. Biring et al.

Pulmonary physiologic changes of morbid obesity

Am J Med Sci

(1999)

R. Lazarus et al.

Effects of obesity and fat distribution on ventilatory function: the normative aging study

Chest

(1997)

P.S. Thomas et al.

Respiratory function in the morbidly obese before and after weight loss

Thorax

(1989)

H.E. Refsum et al.

Pulmonary function and energy expenditure after marked weight loss in obese women: observations before and one year after gastric banding

Int J Obes

(1990)

H.J. Sugerman

Pulmonary function in morbid obesity

Gastroenterol Clin North Am

(1987)

N. Leone et al.

Lung function impairment and metabolic syndrome: the critical role of abdominal obesity

Am J Respir Crit Care Med

(2009)

P. Enright

Overindulgence → overweight → reduced vital capacity → reduced longevity

Am J Respir Crit Care Med

(2009)

R. Cancello et al.

Adiposity signals, genetic and body weight regulation in humans

Diabete Metab

(2004)

M.W. Steffes et al.

Serum adiponectin in young adults—interactions with central adiposity, circulating levels of glucose, and insulin resistance: the CARDIA study

Ann Epidemiol

(2004)

F.M. Franssen et al.

Obesity and the lung: 5. Obesity and COPD

Thorax

(2008)

A.W. Fogarty et al.

Systemic inflammation and decline in lung function in a general population: a prospective study

Thorax

(2007)

B. Thyagarajan et al.

Plasma fibrinogen and lung function: the CARDIA Study

Int J Epidemiol

(2006)

Cited by (60)

Correlation between levels of adipokines and inflammatory mediators with spirometric parameters in individuals with obesity and symptoms of asthma: Cross-sectional study
2022, Pulmonology
Citation Excerpt :
Bronchial hyperresponsiveness to an inhaled antigen can lead to an inflammatory cascade of airways and degranulation of mast cells, activation of T cells and alveolar macrophages, cytokine production, and recruitment and activation of eosinophils in the airway, resulting in epithelial scaling.28 In view of this, all mechanical and inflammatory changes in the lungs of morbidly obese individuals may lead to changes in the permeability of the smaller airways, reflecting FEV1, PEF and FEF25–75%.13 Thus, the treatment of these patients should involve therapy for weight loss and symptomatic respiratory improvement.
The adipose tissue secretes adipokines and influences the release of inflammatory mediators contributing to a state of low-grade systemic inflammation that may change lung function.
To correlate levels of adipokines and inflammatory mediators with lung function in individuals with obesity and bronchial asthma symptoms.
A cross-sectional study, including women with obesity (grade II and III) with symptoms and clinical diagnosis of asthma. Anthropometric measurements (weight, height, BMI), pulmonary function test (spirometry), asthma control test questionnaire, collection of systemic inflammatory markers (blood collection) and pulmonary markers (sputum collection) were collected and were analyzed: IL-6, IL-8, TNF-α, adiponectin, resistin, leptin and C-reactive protein (CRP). The patients were stratified into two groups according to asthma control.
80 women were analyzed and 40% had an ACT score greater than or equal to 18 and were classified as “controlled asthma”. More than half of the patients of ACT < 18 score obtaining measures of FEV1, PEF and FEF25–75% below and 80% of predicted. There was a significant and negative correlation between IL-6 in the sputum with FVC and FEF25–75% in the group ACT < 18 and with FVC and FEV1 in the group ACT ≥ 18.
Therefore, we concluded that the increase of interleukin-6 in the sputum is related to worse pulmonary function even in patients with controlled asthma, especially in the translate airway permeability measures.
Air pollution concentration and period of the day modulates inhalation of PM<inf>2.5</inf> during moderate- and high-intensity interval exercise
2021, Environmental Research
Citation Excerpt :
In this scenario, even the benefits of exercise have been put in check, once the performance of exercise in a polluted environment results in superior inhalation of air pollutants. The elevation of minute ventilation (VE) in response to higher oxygen uptake (VO2) and carbon dioxide production (VCO2), together with alterations in breathing pattern during exercise explain the increased inhalation of air pollutants on active conditions compared to rest (Chlif et al., 2007; Sood 2009). Furthermore, some exercise characteristics as volume and intensity have an important role in VE increasing and, consequently, on the inhaled dose of air pollutants.
The increase in minute ventilation during exercise led to higher inhalation of air pollution and, consequently, to exacerbation of health issues. Therefore, the intensity of exercise and the air pollution concentration of the environment could be determinant variables to poor outcomes. This study aimed to investigate the inhaled dose of particulate matter 2.5 (PM_2.5) during a moderate- and high-intensity interval exercise session performed in the morning and evening at different locations of Porto Alegre City. Eighteen individuals performed a cardiopulmonary exercise test, a moderate-intensity interval exercise (MIIE), and a high-intensity interval exercise (HIIE). Heart rate was monitored to estimate minute ventilation and total ventilation of the session. The concentration of PM_2.5 was measured during the morning (6–8a.m.) and evening (6–8p.m.) by fixed-site monitors placed at five points of Porto Alegre City. The PM_2.5 inhalation during MIIE and HIIE performed in the morning and evening in the monitoring points was estimated. HIIE showed higher minute ventilation (VE) (p = 0.0048) and total ventilation did not differ between groups (p = 0.4648). PM_2.5 concentrations were higher during the mornings (p < 0.001). Monitored point 1 had higher levels of PM_2.5 in the morning and evening (p < 0.001). The inhalation of PM_2.5 in the morning showed no difference in MIIE (p = 0.8172) and HIIE (p = 0.7306) groups among the points. In the evening, the inhalation of PM_2.5 was higher in point 1 in MIIE and HIIE group (p < 0.001). MIIE and HIIE had higher inhalation of PM_2.5 in the morning than in the evening (p < 0.001). Total ventilation of exercise is a crucial factor that contributes to the inhalation dose of air pollution.
Determinants of Cardiorespiratory Fitness After Bariatric Surgery: Insights From a Randomised Controlled Trial of a Supervised Training Program
2021, Canadian Journal of Cardiology
Severely obese patients have decreased cardiorespiratory fitness (CRF) and poor functional capacity. Bariatric surgery–induced weight loss improves CRF, but the determinants of this improvement are not well known. We aimed to assess the determinants of CRF before and after bariatric surgery and the impact of an exercise training program on CRF after bariatric surgery.
Fifty-eight severely obese patients (46.1 ± 6.1 kg/m², 78% women) were randomly assigned to either an exercise group (n = 39) or usual care (n = 19). Exercise training was conducted from the 3rd to the 6th months after surgery. Anthropometric measurements, abdominal and mid-thigh computed tomographic scans, resting echocardiography, and maximal cardiopulmonary exercise testing was performed before bariatric surgery and 3 and 6 months after surgery.
Weight, fat mass, and fat-free mass were reduced significantly at 3 and 6 months, without any additive impact of exercise training in the exercise group. From 3 to 6 months, peak aerobic power (V̇O_2peak) increased significantly (P < 0.0001) in both groups but more importantly in the exercise group (exercise group: from 18.6 ± 4.2 to 23.2 ± 5.7 mL/kg/min; control group: from 17.4 ± 2.3 to 19.7 ± 2.4 mL/kg/min; P value, group × time = 0.01). In the exercise group, determinants of absolute V̇O_2peak (L/min) were peak exercise ventilation, oxygen pulse, and heart rate reserve (r² = 0.92; P < 0.0001), whereas determinants of V̇O_2peak indexed to body mass (mL/kg/min) were peak exercise ventilation and early-to-late filling velocity ratio (r² = 0.70; P < 0.0001).
A 12-week supervised training program has an additive benefit on cardiorespiratory fitness for patients who undergo bariatric surgery.
Les patients atteints d’obésité sévère présentent une capacité cardiorespiratoire (CCR) abaissée et une faible capacité fonctionnelle. La perte de poids induite par une chirurgie bariatrique améliore la CCR, mais les déterminants de cette amélioration ne sont pas bien connus. Nous avions pour objectif d’évaluer d’une part les déterminants de la CCR avant et après une chirurgie bariatrique et, d’autre part, l’impact d’un programme d’entraînement physique sur la CCR après une chirurgie bariatrique.
Cinquante-huit patients atteints d’obésité sévère (46,1 ± 6,1 kg/m², 78 % de sexe féminin) ont été répartis au hasard dans deux groupes pour suivre un programme d’entraînement physique (n = 39) ou recevoir le traitement habituel (n = 19). Le programme d’entraînement s’est déroulé du 3^e au 6^e mois de la période postopératoire. Des mesures anthropométriques, l’acquisition par tomodensitométrie d’images de l’abdomen et du milieu de la cuisse, une échocardiographie au repos et une épreuve d’effort cardiorespiratoire maximal ont été effectuées avant la chirurgie bariatrique ainsi que 3 et 6 mois après celle-ci.
Le poids, la masse grasse et la masse maigre avaient diminué de façon significative 3 et 6 mois après la chirurgie bariatrique; le programme d’entraînement physique n’a pas eu d’effet additif sur ces valeurs au sein du groupe qui l’a suivi. Du 3^e au 6^e mois, la puissance aérobie maximale (V̇O_2max) a augmenté significativement (p < 0,0001) dans les deux groupes, mais de façon plus marquée au sein du groupe qui a suivi le programme d’entraînement physique (de 18,6 ± 4,2 à 23,2 ± 5,7 ml/kg/min dans le groupe qui a suivi le programme d’entraînement physique; de 17,4 ± 2,3 à 19,7 ± 2,4 ml/kg/min dans le groupe témoin; valeur p, groupe × temps = 0,01). Dans le groupe qui a suivi le programme d’entraînement physique, les déterminants de la valeur absolue du V̇O_2max (l/min) étaient la ventilation à l’effort maximal, le pouls d’oxygène et la fréquence cardiaque de réserve (r² = 0,92; p < 0,0001), tandis que les déterminants du V̇O_2max rapporté à la masse corporelle (ml/kg/min) étaient la ventilation à l’effort maximal et le rapport remplissage rapide-remplissage lent (r² = 0,70; p < 0,0001).
Un programme d’entraînement physique supervisé de 12 semaines a un effet bénéfique additif sur la CCR des patients qui ont subi une chirurgie bariatrique.
Respiratory Muscle Performance Screening for Infectious Disease Management Following COVID-19: A Highly Pressurized Situation
2020, American Journal of Medicine
The 2019-2020 coronavirus pandemic elucidated how a single highly infectious virus can overburden health care systems of even highly economically developed nations. A leading contributor to these concerning outcomes is a lack of available intensive care unit (ICU) beds and mechanical ventilation support. Poorer health is associated with a higher risk for severe respiratory complications from the coronavirus. We hypothesize that impaired respiratory muscle performance is an underappreciated factor contributing to poor outcomes unfolding during the coronavirus pandemic. Although impaired respiratory muscle performance is considered to be rare, it is more frequently encountered in patients with poorer health, in particular obesity. However, measures of respiratory muscle performance are not routinely performed in clinical practice, including those with symptoms such as dyspnea. The purpose of this article is to discuss the potential role of respiratory muscle performance from the perspective of the coronavirus pandemic. We also provide a theoretical patient management model to screen for impaired respiratory muscle performance and intervention, if identified, with the goal of unburdening health care systems during future pandemic crises.
Effect of obesity on the respiratory system
2020, Obesity Hypoventilation Syndrome: From Physiologic Principles to Clinical Practice
Obesity has many effects on the respiratory system. Obese patients have higher respiratory rates and lower tidal volumes. Their total respiratory system compliance is reduced. Their lung volumes tend to be smaller, the expiratory lung volume being the most consistently affected. Spirometry, gas exchange, and airway resistance are relatively preserved when they are adjusted for lung volumes. Obese patients may be mildly hypoxemic, likely from ventilation perfusion mismatch in the bases of the lungs where obesity causes microatelectasis. Obese patients have a higher metabolic rate, lower exercise capacity, and more dyspnea. Weight loss reverses these changes.
Overweight, Obesity, and Lung Function in Children and Adults—A Meta-analysis
2018, Journal of Allergy and Clinical Immunology: In Practice
There is conflicting evidence on the effect of obesity on lung function in adults and children with and without asthma. We aimed to evaluate the relation between overweight or obesity and lung function, and whether such relationship varies by age, sex, or asthma status.
We searched PubMed, Scopus, CINAHL, Cochrane, and EMBASE for all studies (in English) reporting on obesity status (by body mass index) and lung function, from 2005 to 2017. Main outcomes were forced expiratory volume in 1 second (FEV₁), forced vital capacity (FVC), FEV₁/FVC, forced expiratory flow between 25th and 75th percentile of the forced vital capacity (FEF_25-75), total lung capacity (TLC), residual volume (RV), and functional residual capacity (FRC). Random-effects models were used to calculate the pooled risk estimates; each study was weighed by the inverse effect size variance. For each outcome, we compared overweight or obese (“obese”) subjects with those of normal weight.
All measures of lung function were decreased among obese subjects. Obese adults showed a pattern (lower FEV₁, FVC, TLC, and RV) different from obese children (more pronounced FEV₁/FVC deficit with unchanged FEV₁ or FVC). There were also seemingly different patterns by asthma status, in that subjects without asthma had more marked decreases in FEV₁, TLC, RV, and FRC than subjects with asthma. Subjects who were obese (as compared with overweight) had even further decreased FEV₁, FVC, TLC, RV, and FRC.
Obesity is detrimental to lung function, but specific patterns differ between children and adults. Physicians should be aware of adverse effects of obesity on lung function, and weight control should be considered in the management of airway disease among the obese.

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: This work was supported in part by University of New Mexico Clinical Translational Science Center grant NIH NCRR M01-RR-00997. The author has no financial relation to a commercial company that has an interest in the subject matter or materials discussed in this article.

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Altered Resting and Exercise Respiratory Physiology in Obesity

Section snippets

Altered resting respiratory physiology in obesity

Airway responsiveness to methacholine

Oxygen Consumption

Summary

Acknowledgments

Chartbook on trends in the health of Americans, Health, United States, 2006

Effects of obesity on respiratory function

Am Rev Respir Dis

Compliance of the respiratory system and its components in health and obesity

J Appl Phys

Current concepts in the pathogenesis of the obesity-hypoventilation syndrome. Mechanical and circulatory factors

Am J Med

Pulmonary complications of obesity

Am J Med Sci

Inspiratory muscle activity during incremental exercise in obese men

Int J Obes (Lond)

Noninvasive assessment of the tension-time index of inspiratory muscles at rest in obese male subjects

Int J Obes (Lond)

Influence of excessive weight loss after gastroplasty for morbid obesity on respiratory muscle performance

Thorax

Diaphragmatic responses to body position changes in obese patients with obstructive sleep apnea

Am Rev Respir Dis

Increased muscle dynamic endurance associated with weight reduction on a very-low-calorie diet

Am J Clin Nutr

Reduced glycogen synthase activity in skeletal muscle from obese patients with and without type 2 (non-insulin-dependent) diabetes mellitus

Diabetologia

Skeletal muscle function and metabolism in obese women

JPEN J Parenter Enteral Nutr

The strength, contractile properties and radiological density of skeletal muscle before and 1 year after gastroplasty

Clin Sci (Lond)

Fatty infiltration of respiratory muscles in the Pickwickian syndrome

N Engl J Med

Obesity and pulmonary function

Pulmonary complications of chronic neuromuscular diseases and their management

Muscle Nerve

The impact of morbid obesity on oxygen cost of breathing (VO(2RESP)) at rest

Am J Respir Crit Care Med

Pulmonary function in obese persons

J Clin Invest

The effect of adiposity measured by dual-energy X-ray absorptiometry on lung function

Eur Respir J

The effects of mild obesity on lung function

Respir Med

The effects of body mass index on lung volumes

Chest

Obesity, respiratory function and breathlessness

Thorax

Airflow limitation in morbidly obese, nonsmoking men

Ann Intern Med

Influence of obesity on peripheral airways patency

J Appl Phys

Pulmonary physiologic changes of morbid obesity

Am J Med Sci

Effects of obesity and fat distribution on ventilatory function: the normative aging study

Chest

Respiratory function in the morbidly obese before and after weight loss

Thorax

Pulmonary function and energy expenditure after marked weight loss in obese women: observations before and one year after gastric banding

Int J Obes

Pulmonary function in morbid obesity

Gastroenterol Clin North Am

Lung function impairment and metabolic syndrome: the critical role of abdominal obesity

Am J Respir Crit Care Med

Overindulgence → overweight → reduced vital capacity → reduced longevity

Am J Respir Crit Care Med

Adiposity signals, genetic and body weight regulation in humans

Diabete Metab

Serum adiponectin in young adults—interactions with central adiposity, circulating levels of glucose, and insulin resistance: the CARDIA study

Ann Epidemiol

Obesity and the lung: 5. Obesity and COPD

Thorax

Systemic inflammation and decline in lung function in a general population: a prospective study

Thorax

Plasma fibrinogen and lung function: the CARDIA Study

Int J Epidemiol