Effects of obesity on respiratory function
ABSTRACT Obesity, because it alters the relationship between the lungs, chest wall, and diaphragm, has been expected to alter respiratory function. We studied 43 massively obese but otherwise normal, nonsmoking, young adults with spirometry, lung volume measurement by nitrogen washout, and single-breath diffusing capacity for carbon monoxide (DLCO). Changes in respiratory function were of two types, those that changed in proportion to degree of obesity--expiratory reserve volume (ERV) and DLCO--and those that changed only with extreme obesity--vital capacity, total lung capacity, and maximal voluntary ventilation. When compared with commonly used predicting equations, we found that mean values of subjects grouped by degree of obesity were very close to predicted values, except in those with extreme obesity in whom weight (kg)/height (cm) exceeded 1.0. In 29 subjects who lost a mean of 56 kg, significant increases in vital capacity, ERV, and maximal voluntary ventilation were found, along with a significant decrease in DLCO. Because most subjects fell within the generally accepted 95% confidence limits for the predicted values, we concluded that obesity does not usually preclude use of usual predictors. An abnormal pulmonary function test value should be considered as caused by intrinsic lung disease and not by obesity, except in those with extreme obesity.
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- "RV/TLC may be increased in obesity reflecting air trapping secondary to increased volume-dependent airway closure   , although Jones and Nzekwu found no significant difference in this ratio between BMI groups . Vital capacity (VC) may decline as BMI increases but generally into the lower normal range    . However, the inspiratory capacity (IC) and the IC/TLC ratio increase with increasing the BMI reflecting the relative preservation of TLC in the presence of decreased EELV  . "
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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- "reduced resting arterial PO 2 and increased alveolar-to-arterial PO 2 difference (Fritts et al., 1959; Dempsey et al., 1966a, 1966b; Holley et al., 1967; Barrera et al., 1969, 1973; Ray et al., 1983; Babb et al., 1989, 2002, 2008b; Thomas et al., 1989; Rubinstein et al., 1990; Pelosi et al., 1996, 1997, 1998, 1999; Pankow et al., 1998; Weiner et al., 1998; Kress et al., 1999; Eichenberger et al., 2002; Aaron et al., 2004; Chlif et al., 2005, 2007; DeLorey et al., 2005; Watson and Pride, 2005; Jones and Nzekwu, 2006; Collet et al., 2007; Ofir et al., 2007; Salome et al., 2007; Sutherland et al., 2008; Zavorsky and Hoffman, 2008). "
ABSTRACT: The healthy human respiratory system has impressive ventilatory reserve and can easily meet the demands placed upon it by strenuous exercise. Several acute physiological adaptations during exercise ensure harmonious neuromechanical coupling of the respiratory system, which allow healthy humans to reach high levels of ventilation without perceiving undue respiratory discomfort (breathlessness). However, in certain circumstances, such as pregnancy, obesity and natural aging, ventilatory reserve becomes diminished and exertional breathlessness is present. In this review, we focus on what is known about the mechanisms of increased activity-related breathlessness in these populations. Notwithstanding the obvious physiological differences between the three conditions, they share some common perceptual and ventilatory responses to exercise. Breathlessness intensity ratings (described as an increased "sense of effort") are consistently higher than normal at any given submaximal power output; and central motor drive to the respiratory muscles is consistently increased, reflecting increased ventilatory stimulation. The increased contractile respiratory muscle effort required to support the increased ventilatory requirements of exercise remains the most plausible source of increased activity-related breathlessness in pregnant, obese and elderly humans. In all three conditions, static and dynamic respiratory mechanical/muscular function is, to some extent, altered or impaired. Nevertheless, breathlessness intensity ratings are not significantly increased (compared to normal) at any given exercise ventilation in any of these three conditions. This strongly suggests that respiratory mechanical/muscular factors, per se, may be less important in the genesis of breathlessness. Moreover, in pregnancy and obesity, we present evidence that effective physiological adjustments exist to counterbalance the potentially negative sensory consequences of the altered respiratory mechanical/muscular function peculiar to these conditions.Respiratory Physiology & Neurobiology 06/2009; 167(1):87-100. DOI:10.1016/j.resp.2009.01.011
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- "Patients with OSAS are frequently overweight and may exhibit lung function abnormalities related to their weight. These include a decrease in the functional residual capacity (FRC) due mainly to a decrease in the expiratory reserve volume (ERV) and a decrease in compliance of the respiratory system (Naimark and Cherniack, 1960; Ray et al., 1983). These functional abnormalities cause an increase in the energy cost of breathing. "
ABSTRACT: To investigate whether cardiac dysfunction or abnormal measurements on cardiopulmonary exercise testing (CPET) are present in patients with obstructive sleep apnea syndrome (OSAS) and what factors are responsible for exercise limitation in these patients. We enrolled 20 patients with moderate or severe OSAS in the OSA group and 20 subjects without OSAS in the control group. All subjects underwent a sleep study and cardiac evaluation by radionuclide scanning and CPET. There was no difference in left ventricular ejection fraction (VEF) between the two groups, but the OSA group had a lower right VEF. Patients in the OSA group had a lower VO2(peak), VO2(peak/kg) and workpeak than the control group. The OSA group had a higher breathing reserve and a greater decrease in anaerobic threshold (AT) and oxygen pulse. In conclusion, patients with moderate to severe OSAS had abnormal CPET results. These abnormalities may be due to cardiac disease, pulmonary vascular disease, or possible lack of fitness.Respiratory Physiology & Neurobiology 02/2006; 150(1):27-34. DOI:10.1016/j.resp.2005.01.008