Deep breathing acutely improves arterial dysfunction in obese children: evidence of functional impairment?

BACKGROUND AND AIMS: Similarly to diabetes type 2, patients with obesity show insulin resistance and autonomic and vascular abnormalities associated with increased morbidity and mortality. We tested whether arterial dysfunction in obese children may have a functional nature, reversible with appropriate interventions (e.g., by reduction of sympathetic activity), or else results from anatomic arterial modifications (likely irreversible). For this purpose, we tested whether deep breathing (an intervention known to transiently reduce sympathetic activity) could acutely improve arterial function, hence showing a functional abnormality. METHODS AND RESULTS: A total of 130 obese children and 67 age-matched healthy normal-weight control children were recruited. Arterial function was measured by augmentation index (AIx), by direct analysis of blood pressure contour, and by pulse wave velocity (PWV), during spontaneous and controlled breathing. The markers of metabolic syndrome were evaluated at baseline. AIx showed increased values in obese male participants as compared with the control group. Slow breathing acutely reduced Aix in obese children, to a greater extent than in normal-weight control children. Similarly, the blood pressure contour showed higher values in obese children that were significantly attenuated by slow breathing. Baseline PWV was not altered in obese participants. The markers of metabolic syndrome correlated with AIx and PWV. CONCLUSIONS: Obese subjects showed impaired arterial function. The acute improvement in vascular abnormalities with reduction in sympathetic activity indicates that this alteration was largely functional, likely related to initial autonomic dysfunction and to metabolic abnormalities. As a consequence, this study provides a rationale for strategies aiming at preventing arterial function deterioration in the early ages.

Deep breathing improves blunted baroreflex sensitivity even after 30 years of type 1 diabetes.

AIMS/HYPOTHESES: Cardiovascular autonomic neuropathy is associated with increased morbidity in patients with type 1 diabetes. Although it is conventionally considered to be an organic, irreversible disorder, we previously demonstrated in patients with short-duration type 1 diabetes that reduced baroreflex sensitivity (BRS) could be corrected by slow, deep breathing, indicating a functional component to the disorder. We have now tested whether autonomic abnormalities in long-term diabetes progress to a stage that cannot be modified by functional manoeuvres, indicating a switch towards predominantly organic dysfunction. METHODS: We studied 117 patients with a short duration (8.9 ± 0.1 years) and 37 patients with a long duration (33.7 ± 0.5 years) of type 1 diabetes, 73 healthy controls and 12 heart-transplanted participants (surgical heart denervation). An autonomic score was calculated from autonomic function tests. Spectral analysis of heart rate and blood pressure variability, and BRS, were obtained from recordings during normal (15 breaths per min) and slow, deep (six breaths per min) controlled breathing. RESULTS: BRS was reduced in all patients, but more in patients with a long duration of diabetes or with increasing autonomic involvement, although the effect of duration disappeared after adjustment for age. Slow breathing increased the BRS to the level of the control participants at a normal rate of breathing (15 per min) in all patients except those with an abnormal autonomic score. CONCLUSIONS/INTERPRETATION: Patients with type 1 diabetes have a blunted BRS that in the majority of patients can be restored by slow breathing, irrespective of disease duration. Even after a long duration of diabetes, the abnormal BRS is at least in part of functional origin.