Mechanical load the inspiratory muscles during exercise hyperpnea in patients with type 1 (insulin-dependent) diabetes mellitus

• Published in: Diabetologia 1992-05, Vol.35 (5), p.425-428
• Main Authors: WANKE, T, FORMANEK, AUINGER, M, MERKLE, M, LAHRMANN, H, ZWICK, H, IRSIGLER, K
• Format: Article
• Language: English
• Subjects: Adult; Analysis of Variance; Biological and medical sciences; Diabetes Mellitus, Type 1 - physiopathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Esophagus - physiology; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Humans; Inhalation - physiology; Lung Volume Measurements; Medical sciences; Physical Exertion; Pressure; Reference Values; Respiratory Muscles - physiology; Respiratory Muscles - physiopathology; Space life sciences
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/BF02342438

The aim of this study was to evaluate the difference between Type 1 (insulin-dependent) diabetic patients and healthy control subjects regarding inspiratory muscle load during exercise hypernea. For this purpose an incremental progressive exercise test on a cycle ergometer was performed by 36 Type 1 diabetic patients and 40 healthy subjects. In order to determine the mechanical load on the inspiratory muscles breath by breath, we selected the following two parameters, which represent the pressure generated by the inspiratory muscles as well as the duration and velocity of their contraction: (1) the oesophageal tension time index, which is the product of the duty cycle (ratio of inspiratory time to total breath cycle duration) and the mean oesophageal pressure expressed as a percentage of the maximal oesophageal pressure and (2) the mean oesophageal pressure change per time unit during the inspiratory phase of each breathing manoeuver, which is expressed as a fraction of the subject's maximal oesophageal pressure. Comparison of the two groups revealed that at similar levels of ventilation the mechanical load on the inspiratory muscles was significantly higher in the Type 1 diabetic patients than in the control subjects. When the loading was stopped the maximal ventilation was lower in the patients. Nevertheless, they reported a degree of respiratory effort sensation comparable to the control group, which seems to have been caused by an increase of the mechanical load on the ventilatory muscles.