Work of breathing and respiratory drive in obesity

Abstract

Obesity, particularly severe central obesity, affects respiratory physiology both at rest and during exercise. Reductions in expiratory reserve volume, functional residual capacity, respiratory system compliance and impaired respiratory system mechanics produce a restrictive ventilatory defect. Low functional residual capacity and reductions in expiratory reserve volume increase the risk of expiratory flow limitation and airway closure during quiet breathing. Consequently, obesity may cause expiratory flow limitation and the development of intrinsic positive end expiratory pressure, especially in the supine position. This increases the work of breathing by imposing a threshold load on the respiratory muscles leading to dyspnoea. Marked reductions in expiratory reserve volume may lead to ventilation distribution abnormalities, with closure of airways in the dependent zones of the lungs, inducing ventilation perfusion mismatch and gas exchange abnormalities. Obesity may also impair upper airway mechanical function and neuromuscular strength, and increase oxygen consumption, which in turn, increase the work of breathing and impair ventilatory drive. The combination of ventilatory impairment, excess CO2 production and reduced ventilatory drive predisposes obese individuals to obesity hypoventilation syndrome.

Acute respiratory muscle unloading by normoxic helium–O2 breathing reduces the O2 cost of cycling and perceived exertion in obese adolescents

“…The effects of He-O 2 on the O 2 cost of breathing (and, as a consequence, on the O 2 cost of cycling) could be mediated, for example, by a decrease in the operating lung volumes, which would decrease respiratory muscle work and the amplitude of the slow component (Cross et al 2010b). One of the main effects of obesity on respiratory function is represented by the reduced functional residual capacity and expiratory reserve volume, which could determine tidal expiratory flow limitation and dynamic pulmonary hyperinflation (Lin and Lin 2012); these effects would increase the O 2 cost of breathing (Cross et al 2010a). In obese patients, He-O 2 breathing could attenuate these effects.…”

“…In obese patients, the presence of adipose tissue around the rib cage, abdomen and in the visceral cavity loads the chest wall and reduces the functional residual capacity, the expiratory reserve volume and the respiratory system compliance (Babb 1999;Lin and Lin 2012). The tendency to breathe at low lung volumes exposes the obese patients to an increased risk of expiratory flow limitation during exercise (Babb 1999;Lin and Lin 2012).…”

“…The tendency to breathe at low lung volumes exposes the obese patients to an increased risk of expiratory flow limitation during exercise (Babb 1999;Lin and Lin 2012). Overall, the restrictive and obstructive alterations mentioned above increase respiratory pressures, the work of breathing (Babb 1999;Lin and Lin 2012), the O 2 cost of breathing (Babb et al 2008;Bernhardt et al 2013;Ofir et al 2007), and may lead to inspiratory muscle fatigue (Chlif et al 2007) and ultimately to exertional dyspnea.…”

“…Overall, the restrictive and obstructive alterations mentioned above increase respiratory pressures, the work of breathing (Babb 1999;Lin and Lin 2012), the O 2 cost of breathing (Babb et al 2008;Bernhardt et al 2013;Ofir et al 2007), and may lead to inspiratory muscle fatigue (Chlif et al 2007) and ultimately to exertional dyspnea. The increased cost of breathing contributes to the increase in the O 2 cost of exercise (Wasserman and Whipp 1975;Salvadego et al 2010;Mendelson et al 2012) and to the reduced exercise tolerance (Salvadego et al 2010;Lin and Lin 2012;Mendelson et al 2012), which represents one of the hallmarks of obesity. The substitution of helium (He) for nitrogen in normoxic gas breathing (21 % O 2 -79 % helium, He-O 2 ) obtains a gas mixture with a density which is 0.34 times that of air, and a viscosity which is 1.1 times that of air (Hess et al 2006).…”

Correlation of Self-Reported Breathlessness with Post Exercise Dyspnea in Obesity

“…Paradoxically, increase in weight has little effect on airway caliber [6]. Cardiopulmonary exercise test in the obese population also showed increased oxygen consumption, increased CO 2 production, and impaired ventilatory mechanics [5] [7]. Overall, obese patients end up having multiple tests to determine the pulmonary and cardiovascular component of their breathlessness.…”