Expiratory flow limitation and breathing strategies in overweight adolescents during submaximal exercise

Gibson, Noula; Johnston, Kylie; Bear, Natasha; Stick, Stephen M.; Logie, Karla; Hall, Graham L.

doi:10.1038/ijo.2013.137

Cited by 24 publications

(41 citation statements)

References 27 publications

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“…Our findings of lower FEV 1 /FVC ratio (38, 39), FRC, and RV among obese minority adolescents corroborate with those reported among predominantly white obese adolescents (6)(7)(8). Higher IC in conjunction with low FEV 1 /FVC ratio, ERV, FRC, and RV have also been reported among obese adults with (40,41) and without asthma (42,43), where they correlated with the duration of obesity (44).…”

Section: Original Researchsupporting

confidence: 80%

“…It is known that obese adolescents with a clinical diagnosis of asthma have a lower FEV 1 /FVC ratio (31, 39) but do not display a higher degree of bronchial hyperreactivity than normal-weight adolescents with asthma (46,47). Although few studies have measured lung volumes (6,8,47), ERV is the one pulmonary function index that is consistently reduced among obese subjects with pulmonary symptoms (5,6,48). Airway resistance in obese adults has been associated with lower ERV and FRC, rather than with an inherent decrease in FEV 1 or FEV 1 /FVC ratio, because reduced ERV and FRC are associated with closure of dependent airways, decreased expiratory flows, increased airway resistance, and decreased lung compliance (48).…”

Section: Original Researchmentioning

confidence: 99%

“…BMI was calculated as weight (in kilograms)/ height squared (in meters) and was used to calculate BMI z-score to adjust for sex and age differences (22). The participants also underwent a fasting blood draw from which serum was separated and stored at 280 8 …”

Section: Study Measuresmentioning

confidence: 99%

“…Obese children have more lower airway obstruction as measured by lower FEV 1 /FVC ratio and have lower lung volumes, including residual volume (RV), expiratory reserve volume (ERV), and FRC (6)(7)(8). However, the underlying pathogenesis for pulmonary function deficits observed among obese children and adolescents remains poorly understood.…”

mentioning

confidence: 99%

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Association of Pulmonary Function with Adiposity and Metabolic Abnormalities in Urban Minority Adolescents

Rastogi

Bhalani²,

Hall³

et al. 2014

Annals ATS

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Rationale: Childhood obesity is a known risk factor for pulmonary diseases, likely due to obesity-mediated alteration of pulmonary function. Inflammation and mechanical fat load are two proposed causative mechanisms for altered pulmonary function among obese children; however, the association of metabolic abnormalities with pulmonary function among children is poorly understood.Objectives: We investigated the independent association of truncal and general adiposity and metabolic abnormalities with pulmonary function in a sample of urban minority adolescents.Methods: Spirometry and lung volume indices were compared between adolescents with general (body mass index [BMI] . 95th percentile) or truncal adiposity (waist circumference . 90th percentile) and normal-weight (BMI , 85th percentile or waist circumference < 90th percentile) and between those with metabolic abnormalities (homeostatic model assessment of insulin resistance [HOMA-IR] in the top quartile or high-density lipoprotein [HDL] , 40 mg/dl) and those with a normal metabolic profile.Measurements and Main Results: Obese adolescents had lower lung volumes, including residual volume (RV), RV/TLC ratio, expiratory reserve volume (ERV), and FRC, and higher inspiratory capacity (IC) than normal-weight adolescents, but did not differ in measures of lower airway obstruction, FEV 1 /FVC ratio, and mid-expiratory flow rate. Adolescents with high HOMA-IR had lower FEV 1 /FVC ratio, RV, RV/TLC ratio, ERV, and FRC and higher IC, whereas those with low HDL had lower FEV 1 /FVC and RV/TLC ratios. After adjusting for adiposity, HOMA-IR remained a predictor of ERV (b = 21.4; P = 0.02) and FEV 1 /FVC ratio (b = 20.5; P = 0.03), and HDL remained a predictor of FEV 1 /FVC ratio (b = 0.1; P = 0.01). General adiposity was a predictor of FRC (b = 20.5; P , 0.001), IC (b = 0.3; P , 0.001), RV (b = 20.8; P , 0.0001), and RV/TLC ratio (b = 20.2; P , 0.0001), and truncal adiposity was a predictor of RV (b = 220.3; P = 0.03) and FRC (b = 213.8; P = 0.004). Thus, adiposity and metabolic abnormalities were independent predictors of ERV, but only metabolic abnormalities independently predicted FEV 1 /FVC ratio. Although general adiposity predicted RV and RV/TLC ratio, truncal adiposity was predictive of RV and FRC, conferring additional risk above general adiposity. Conclusions:These results suggest that metabolic abnormalities and adiposity are independently associated with pulmonary function deficits among urban adolescents. Metabolic assessment of obese adolescents may identify those at risk of developing obesity-associated pulmonary morbidity.

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Section: Original Researchsupporting

confidence: 80%

Section: Original Researchmentioning

confidence: 99%

Section: Study Measuresmentioning

confidence: 99%

mentioning

confidence: 99%

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Association of Pulmonary Function with Adiposity and Metabolic Abnormalities in Urban Minority Adolescents

Rastogi

Bhalani²,

Hall³

et al. 2014

Annals ATS

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show abstract

“…In children with PWS, alterations in pulmonary function may be more greatly affected by respiratory muscle weakness as well as additional pulmonary issues linked to obesity, such as asthma [36,37]. Obesity in children has also been shown to produce expiratory flow limitation during exercise, suggesting that obesity further perturbs ventilatory function in obese children when the cardiorespiratory system is under increased stress and demand [38]. …”

Section: Pulmonary Mechanicsmentioning

confidence: 99%

Disorders of Sleep and Ventilatory Control in Prader-Willi Syndrome

Gillett

Perez

2016

Diseases

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Prader-Willi syndrome (PWS) is an imprinted genetic disorder conferred by loss of paternal gene expression from chromosome 15q11.2-q13. Individuals with PWS have impairments in ventilatory control and are predisposed toward sleep disordered breathing due to a combination of characteristic craniofacial features, obesity, hypotonia, and hypothalamic dysfunction. Children with PWS progress from failure to thrive during infancy to hyperphagia and morbid obesity during later childhood and onward. Similarly, the phenotype of sleep disordered breathing in PWS patients also evolves over time from predominantly central sleep apnea in infants to obstructive sleep apnea (OSA) in older children. Behavioral difficulties are common and may make establishing effective therapy with continuous positive airway pressure (CPAP) more challenging when OSA persists after adenotonsillectomy. Excessive daytime sleepiness (EDS) is also common in patients with PWS and may continue after OSA is effectively treated. We describe here the characteristic ventilatory control deficits, sleep disordered breathing, and excessive daytime sleepiness seen in individuals with PWS. We review respiratory issues that may contribute to sudden death events in PWS patients during sleep and wakefulness. We also discuss therapeutic options for treating sleep disordered breathing including adenotonsillectomy, weight loss, and CPAP. Lastly, we discuss the benefits and safety considerations related to growth hormone therapy.

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Pediatric obesity‐related asthma: A prototype of pediatric severe non‐T2 asthma

Rastogi

2020

Pediatric Pulmonology

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Childhood obesity contributes to many diseases, including asthma. There is literature to suggest that asthma developing as a consequence of obesity has a nonallergic or non‐T2 phenotype. In this review, obesity‐related asthma is utilized as a prototype of non‐T2 asthma in children to discuss several nonallergic mechanisms that underlie childhood asthma. Obesity‐related asthma is associated with systemic T helper (Th)1 polarization occurring with monocyte activation. These immune responses are mediated by insulin resistance and dyslipidemia, metabolic abnormalities associated with obesity, that are themselves associated with pulmonary function deficits in obese asthmatics. As in other multifactorial diseases, there is both a genetic and an environmental contribution to pediatric obesity‐related asthma. In addition to genetic susceptibility, differential DNA methylation is associated with non‐T2 immune responses in pediatric obesity‐related asthma. Initial investigations into the biology of non‐T2 immune responses have identified the upregulation of genes in the CDC42 pathway. CDC42 is a RhoGTPase that plays a key role in Th cell physiology, including preferential naïve Th cell differentiation to Th1 cells, and cytokine production and exocytosis. Although these novel pathways are promising findings to direct targeted therapy development for obesity‐related asthma to address the disease burden, there is evidence to suggest that dietary interventions, including diet modification, rather than caloric restriction alone, decrease disease burden. Adoption of a diet rich in micronutrients, including carotenoids and 25‐OH cholecalciferol, a vitamin D metabolite, may be beneficial since these are positively correlated with pulmonary function indices, while being protective against metabolic abnormalities associated with the obese asthma phenotype.

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Expiratory flow limitation and breathing strategies in overweight adolescents during submaximal exercise

Cited by 24 publications

References 27 publications

Association of Pulmonary Function with Adiposity and Metabolic Abnormalities in Urban Minority Adolescents

Association of Pulmonary Function with Adiposity and Metabolic Abnormalities in Urban Minority Adolescents

Disorders of Sleep and Ventilatory Control in Prader-Willi Syndrome

Pediatric obesity‐related asthma: A prototype of pediatric severe non‐T2 asthma

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