BackgroundDyspnea is very frequent in obese subjects. However, its assessment is complex in clinical practice. The modified Medical Research Council scale (mMRC scale) is largely used in the assessment of dyspnea in chronic respiratory diseases, but has not been validated in obesity. The objectives of this study were to evaluate the use of the mMRC scale in the assessment of dyspnea in obese subjects and to analyze its relationships with the 6-minute walk test (6MWT), lung function and biological parameters.MethodsForty-five obese subjects (17 M/28 F, BMI: 43 ± 9 kg/m2) were included in this pilot study. Dyspnea in daily living was evaluated by the mMRC scale and exertional dyspnea was evaluated by the Borg scale after 6MWT. Pulmonary function tests included spirometry, plethysmography, diffusing capacity of carbon monoxide and arterial blood gases. Fasting blood glucose, total cholesterol, triglyceride, N-terminal pro brain natriuretic peptide, C-reactive protein and hemoglobin levels were analyzed.ResultsEighty-four percent of patients had a mMRC ≥ 1 and 40% a mMRC ≥ 2. Compared to subjects with no dyspnea (mMRC = 0), a mMRC ≥ 1 was associated with a higher BMI (44 ± 9 vs 36 ± 5 kg/m2, p = 0.01), and a lower expiratory reserve volume (ERV) (50 ± 31 vs 91 ± 32%, p = 0.004), forced expiratory volume in one second (FEV1) (86 ± 17 vs 101 ± 16%, p = 0.04) and distance covered in 6MWT (401 ± 107 vs 524 ± 72 m, p = 0.007). A mMRC ≥ 2 was associated with a higher Borg score after the 6MWT (4.7 ± 2.5 vs 6.5 ± 1.5, p < 0.05).ConclusionThis study confirms that dyspnea is very frequent in obese subjects. The differences between the “dyspneic” and the “non dyspneic” groups assessed by the mMRC scale for BMI, ERV, FEV1 and distance covered in 6MWT suggests that the mMRC scale might be an useful and easy-to-use tool to assess dyspnea in daily living in obese subjects.
A respiratory-related cortical activity could contribute to the increased neural drive to upper airway and to inspiratory muscles that has previously been described in obstructive sleep apnea, and could therefore contribute to the arousal-dependent compensation of upper airway abnormalities. Whether or not such cortical compensatory mechanisms have cognitive consequences remains to be determined.
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