This study analyzed the relationships between dyspnea in daily living, lung function, and body composition assessed by DXA in obese patients and demonstrates that disabling dyspnea in daily living was associated with lower lung volumes and 6MWT distance, and a higher BMI and fat mass, especially in the central regions of the body.
In large cohorts, 80% of obese adults experience dyspnea after climbing two flights of stairs (30) and approximately one-third of obese adults report dyspnea when walking up a hill (1). Obese adults are also twice as likely as adults with normal BMI to have dyspnea mMRC score ≥ 2 (3). The prevalence of dyspnea in our cohort was similar to previous studies with about three-quarters of the patients experiencing dyspnea in daily living (mMRC ≥ 1) and more than a third describing disabling dyspnea in daily living (mMRC score ≥ 2, i.e. walk slower than people of the same age on level ground) and severe dyspnea on exertion (Borg ≥ 5 after 6MWT) (5,6). Interestingly, there was no difference in dyspnea severity between men and women in this study.
Dyspnea encompasses an array of unpleasant respiratory sensations that vary according to the underlying cause and patient characteristics. Psychological state (especially comorbid anxiety and depression) could modify the perception of dyspnea (31). In this study, demographic characteristics, medical comorbidities except for hypertension, QD2A depression score, and smoking status were similar between patients with and without disabling dyspnea in daily living according to the mMRC dyspnea scale.
As expected, patients with disabling dyspnea in daily living (mMRC ≥ 2), who had also higher BMI and fat mass than patients with mMRC <2, covered a lower distance during the 6MWT than patients with mMRC < 2 (5).
It is well known that obesity causes substantial changes to the mechanics of the lungs and chest wall that affect lung function. The most frequent abnormality associated with obesity is a decrease in ERV, which is exponentially correlated with increased BMI (9). While obesity significantly reduces ERV and consequently FRC (FRC = ERV + RV), it has very little effect on VC and TLC (9). RV is typically within the normal range in the presence of obesity. Other dynamic measures of lung function such as FEV1 and FVC are slightly reduced in people with obesity (32), but FEV1/FVC ratio is usually unaffected. We found similar results concerning lung function in this cohort of obese patients, showing that patients with disabling dyspnea in daily living (mMRC ≥2), who had also higher BMI, had a significant reduction in measures of lung function affected by obesity (VC, FVC, FEV1, ERV, FRC, TLC).
Effects of obesity on inspiratory and expiratory muscle strength are variable and inconsistent (10,11,33). Respiratory muscle function might be impaired by a myopathy or by the load imposed on the diaphragm by obesity itself. Contrary to Collet et al (4), we did not find a significant association between disabling dyspnea and inspiratory muscle strength. A possible explanation is that respiratory muscle strength is assessed by volitional methods and the patient’s motivation and effort can affect the results.
Despite the absence of consensus on the definition of sarcopenic obesity, it is commonly accepted as the combination of obesity and muscle impairment, either defined by low muscle mass and/or poor muscle strength/function. In a large cohort from the National Health and Nutrition Surveys, the prevalence of sarcopenic obesity is 17% in obese patients aged 60 to 70 years (34). In our study, patients were younger with no patient exhibiting a low appendicular lean mass and very few patients with low handgrip strength. Furthermore, there was no association between these variables assessing muscle impairment and the presence of disabling dyspnea.
Disabling dyspnea according to mMRC was associated with an increase in weight, BMI, and fat mass in absolute value for all body segments. Interestingly, patients with disabling dyspnea also presented an increase in the percentage of fat mass for the central regions of the body: trunk and android region. Sutherland et al. also showed that both thoracic and abdominal body fat had an impact on lung volumes (15). In our study, patients with disabling dyspnea had also lower lung volumes. Taken together, these data support the hypothesis that dyspnea may be mediated by the deposition of adipose tissue around the thorax restricting expansion, and/or by abdominal adiposity impeding diaphragmatic excursion.
Our results have several clinical implications. First, it provides clinicians with a glimpse of the dyspnea endured by obese patients especially in patients with high and very high BMI (Figure 1). Second, there is a significant effect of adiposity on dyspnea and this relationship is robust regardless of the adiposity measurement (BMI, weight, fat mass in all analyzed body segments). Thus, assessing the effect of adiposity on dyspnea may be adequately undertaken using a simple measurement, such as BMI, in clinical practice.
One of the strengths of our study is the assessment of the relationships between dyspnea according to the mMRC scale, a very complete respiratory assessment (6MWT, arterial blood gases, PFTs, inspiratory and expiratory muscle strength), laboratory parameters, depression scale, and body composition assessed by DXA. Our results highlight a significant association between the presence of disabling dyspnea, reduction in lung volumes, and increase in BMI and fat mass, especially in the central region of the body which is known to be associated with lung volume reduction. Nevertheless, the body composition and the fat mass repartition are probably not the only predictors of dyspnea in patients with obesity. Several other factors such as anxiety (35,36) may be involved in dyspnea perception in patients with obesity and were not analyzed in this study. This study has several other limitations. First, it was conducted in a single center, which may limit the generalizability of the results. Second, the study cohort included only candidates for bariatric surgery (predominantly women, relatively young) and consequently does not reflect the whole population of obese individuals. Moreover, our study does not provide information regarding the effects of interventions like bariatric surgery. It has been shown that bariatric surgery improves dyspnea in about two-thirds of patients (6). As body composition significantly changes after bariatric surgery with reduced whole-body and regional fat mass and especially decreased percentage of android fat mass (37), it would be interesting to study the relationships between body composition modification and dyspnea improvement after bariatric surgery.