Relationship Between Obesity and Diaphragm Muscle Strength in Diabetes Mellitus

Abstract

Background: Worldwide, diabetes remains prevalent, affecting one in ten adults. As a metabolic disease, diabetes affects nearly all organs and organ systems due to its adverse effects on the macrovascular and microvascular circulation. Diabetes also affects the pulmonary system and is associated with specific pulmonary defects such as airway obstruction, pulmonary restriction, and impaired pulmonary gas exchange. Very recently, the diaphragm has been recognized as a potential target organ for diabetes, with nearly one in five adults with diabetes having impaired diaphragm muscle strength. The biological basis of diaphragm muscle weakness remains uncertain. The effect of fat on diaphragm muscle is one possible influencing factor. Obesity, especially central obesity could restrict the vertical movement of the hemidiaphrams as well as result in metabolic inflammation that could adversely impact the functions of the diaphragm. To date, studies on the relationships of different measures of obesity with diaphragm muscle strength in individuals with diabetes remain unreported. General Aim To investigate the relationships of measures of obesity with diaphragm muscle weakness in adults with diabetes. Methods: This cross-sectional study included 500 participants with an established diagnosis of diabetes, who were managed at the Ghana National Diabetes Management and Research Center, Accra. Spirometry was sequentially done in the sitting and supine positions in compliance with the standards of the American Thoracic Society and European Respiratory Society (ERS). Measured spirometric indices included forced expiratory volume in one second (FEV1), and forced vital capacity (FVC). Diaphragm muscle weakness was defined as a decline in FVC by 10% or more from sitting /upright to supine position (∆FVC ≥ 10%). Isolated or disproportionate bilateral diaphragm weakness is defined ∆ FVC ≥ 30%. Measures of obesity included waist circumference (WC), waist-to-hip ratio (WHR), and body mass index (BMI), General obesity was defined as BMI≥30 kg/m2 for both sexes. Central obesity was defined as WHR > 0.85 in females and > 0.9 in males and/or WC ≥ 80 cm in females and ≥ 94 cm in males. Multivariate logistic regression analyses were used to examine the associations between measures of obesity (independent variable) and diaphragm muscle weakness (dependent variable), with adjustment for potential covariates including age, sex, smoking, HbA1c concentration, diabetes duration, and LDL cholesterol concentration., and peripheral neuropathy. RESULTS: Women were the majority of study participants (73.4%). BMI, sysptolic blood pressure, diastolic blood pressure, duration of diabetes, and mean (± standard deviation) age were 76.27 (±10.82) mmHg, 1315.66 (±17.9) mmHg, 29.16 (±5.75) kg/m2, 61.02 (±10.19) years, and 11.56 (±8.03) years, respectively. The mean HbA1c, fasting plasma glucose, total cholesterol, triglycerides, HDL, and LDL cholesterol concentrations were 8.12 (±1.56) %, 8.93 (±3.14) mmol/L, 4.92 (±1.12) mmol/L, 1.92 (±0.98) mmol/L, 1.24 (±0.34) mmol/L and 3.12 (±0.91) mmol/L respectively. The mean (±) FEV1 pp, FVC pp, and FEV1/FVC ratio were 82.6 (±17.4)%, 85.3 (±18.1)%, and 0.82 (±0.07) respectively. Respectively 17.6% and 0.4% of the study participants had diaphragm muscle weakness and isolated or disproportionate bilateral diaphragm weakness. In a multivariable regression model, peripheral neuropathy (OR 4.72, 95% CI [1.30 - 17.06], p = 0.018) but not general obesity (1.09 [0.41 - 2.86], p=0.868) or central obesity (0.91 [0.17 - 4.71], p=0.907) was significantly associated with diaphragm muscle weakness. In the fully adjusted multivariate regression models, No substantial independent relations between general obesity and (1.38 [0.25 - 7.55], p=0.709) or central obesity (1.55 [0.55 - 4.36], 0.410) with diaphragm muscle weakness. CONCLUSIONS: The study shows a relatively high proportion of diaphragm muscle dysfunction in adults with T2D with nearly one in five study participants affected. This is clinically relevant considering the adverse impact of diaphragm muscle weakness on respiratory function including alveolar minute ventilation and pulmonary gas exchange. Based on this study, the positive associations of general obesity and central obesity with diaphragm muscle weakness were not statistically significant. However, the strength of association could be clinically significant considering the magnitude of the observed odds ratio. Future studies could characterize the clinical consequences of impaired diaphragm muscle strength in the setting of T2D.