Observations on the physiological interactions between obesity and asthma
ABSTRACT To explore whether asthma and obesity share overlapping pathogenic features, we examined the impact of each alone, and in combination, on multiple aspects of lung function. We reasoned that if they influenced the lungs through similar mechanisms, the individual physiological manifestations in the comorbid state should interact in a complex fashion. If not, then the abnormalities should simply add. We measured specific conductance, spirometry, lung volumes, and airway responsiveness to adrenergic and cholinergic agonists in 52 normal, 53 asthmatic, 52 obese, and 53 asthmatic and obese patients using standard techniques. Six-minute walks were performed in subsets from each group. Asthma significantly lowered specific conductance and the spirometric variables while increasing airway reactivity and residual volume. Obesity also reduced the spirometric variables as well as total lung capacity and functional residual capacity. Residual volume, specific conductance, and airway responsivity were unaltered. With comorbidity, the disease-specific derangements added algebraically. Features that existed in isolation appeared unchanged in the combination, whereas shared ones either added or subtracted depending on the individual directional changes. Synergistic interactions were not observed. Body mass index weakly correlated with spirometry and lung volumes in asthma, but not with specific conductance or bronchial reactivity. Exercise performance did not aid in differentiation. Our findings indicate asthma and obesity appear to influence the respiratory system through different processes.
- SourceAvailable from: Jordan A. Guenette
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- "The reduced EELV in obesity also means that the airways resistance is proportionately increased , in absolute terms , reflecting the reduced airway diameter compared with normal weight individuals. It is noteworthy that when the volume differences in health and obesity are accounted for as with measurements of specific airway resistance or specific conductance, this difference in airway resistance disappears   . In obesity, closing volume may occur at volumes above the lower EELV [37, 44–46]; thus, significant airway closure and gas trapping may occur in basal lung segments during the quiet tidal breathing cycle. "
ABSTRACT: In many parts of the world, the prevalence of obesity is increasing at an alarming rate. The association between obesity, multiple comorbidities, and increased mortality is now firmly established in many epidemiological studies. However, the link between obesity and exercise intolerance is less well studied and is the focus of this paper. Although exercise limitation is likely to be multifactorial in obesity, it is widely believed that the respiratory mechanical constraints and the attendant dyspnea are important contributors. In this paper, we examined the evidence that critical ventilatory constraint is a proximate source of exercise limitation in individuals with mild-to-moderate obesity. We first reviewed existing information on exercise performance, including ventilatory and perceptual response patterns, in obese individuals who are otherwise healthy. We then considered the impact of obesity in patients with preexisting respiratory mechanical abnormalities due to chronic obstructive pulmonary disease (COPD), with particular reference to the effect on dyspnea and exercise performance. Our main conclusion, based on the existing and rather sparse literature on the subject, is that abnormalities of dynamic respiratory mechanics are not likely to be the dominant source of dyspnea and exercise intolerance in otherwise healthy individuals or in patients with COPD with mild-to-moderate obesity.10/2012; 2012:818925. DOI:10.1155/2012/818925
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ABSTRACT: We investigated whether obesity is associated with airway hyperresponsiveness in otherwise healthy humans and, if so, whether this correlates with a restrictive lung function pattern or a decreased number of sighs at rest and/or during walking. Lung function was studied before and after inhaling methacholine (MCh) in 41 healthy subjects with body mass index ranging from 20 to 56. Breathing pattern was assessed during a 60-min rest period and a 30-min walk. The dose of MCh that produced a 50% decrease in the maximum expiratory flow measured in a body plethysmograph (PD50MCh) was inversely correlated with body mass index (r2=0.32, P<0.001) and waist circumference (r2=0.25, P<0.001). Significant correlations with body mass index were also found with the maximum changes in respiratory resistance (r2=0.19, P<0.001) and reactance (r2=0.40, P<0.001) measured at 5 Hz. PD50MCh was also positively correlated with functional residual capacity (r2=0.56, P<0.001) and total lung capacity (r2=0.59, P<0.001) in men, but not in women. Neither PD50MCh nor body mass index correlated with number of sighs, average tidal volume, ventilation, or breathing frequency. In this study, airway hyperresponsiveness was significantly associated with obesity in otherwise healthy subjects. In obese men, but not in women, airway hyperresponsiveness was associated with the decreases in lung volumes.Journal of Applied Physiology 06/2009; 107(2):408-16. DOI:10.1152/japplphysiol.00083.2009 · 3.43 Impact Factor
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ABSTRACT: Obesity and asthma prevalence have been increasing over the past decade. Epidemiological evidence demonstrates that obesity results in an increased risk of developing incident asthma. Even modest levels of increased weight increase asthma risk. Recently published data suggest that obese asthma patients may represent a distinct phenotype of asthma. Obese asthma patients demonstrate increased asthma severity, as indicated by increased exacerbations and decreased asthma control; however, they do not appear to have increased airway cellular inflammation. It seems likely that obesity does not contribute to asthma through conventional Th type 2-mediated inflammatory pathways but, rather, through separate mechanisms that are specific to the obese state. This may explain the variable responses of obese asthma patients to conventional asthma therapies, specifically, relative corticosteroid resistance. Small studies suggest improvements in the disease with weight loss in obese asthma patients, and other interventions to target asthma in obese individuals need to be investigated. Several postulated mechanisms for the occurrence of this distinct phenotype have been postulated: 1) the presence of comorbidities, such as gastroesophageal reflux disease and sleep disordered breathing, 2) systemic inflammation associated with obesity (with elevated levels of circulating cytokines, such as IL-6 and TNF-alpha), 3) increased oxidative stress, and 4) hormones of obesity, such as adiponectin, leptin, and resistin. Although the mechanisms underlying obesity in asthma require further investigation, obesity plays a major role in the asthma epidemic and likely results in a distinct phenotype of the disease.Journal of Applied Physiology 10/2009; 108(3):729-34. DOI:10.1152/japplphysiol.00845.2009 · 3.43 Impact Factor