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Clinical Trial
. 2017 Jul 20;7(1):6001.
doi: 10.1038/s41598-017-04947-4.

Oxygen-induced impairment in arterial function is corrected by slow breathing in patients with type 1 diabetes

Affiliations
Clinical Trial

Oxygen-induced impairment in arterial function is corrected by slow breathing in patients with type 1 diabetes

Luciano Bernardi et al. Sci Rep. .

Abstract

Hyperoxia and slow breathing acutely improve autonomic function in type-1 diabetes. However, their effects on arterial function may reveal different mechanisms, perhaps potentially useful. To test the effects of oxygen and slow breathing we measured arterial function (augmentation index, pulse wave velocity), baroreflex sensitivity (BRS) and oxygen saturation (SAT), during spontaneous and slow breathing (6 breaths/min), in normoxia and hyperoxia (5 L/min oxygen) in 91 type-1 diabetic and 40 age-matched control participants. During normoxic spontaneous breathing diabetic subjects had lower BRS and SAT, and worse arterial function. Hyperoxia and slow breathing increased BRS and SAT. Hyperoxia increased blood pressure and worsened arterial function. Slow breathing improved arterial function and diastolic blood pressure. Combined administration prevented the hyperoxia-induced arterial pressure and function worsening. Control subjects showed a similar pattern, but with lesser or no statistical significance. Oxygen-driven autonomic improvement could depend on transient arterial stiffening and hypertension (well-known irritative effect of free-radicals on endothelium), inducing reflex increase in BRS. Slow breathing-induced improvement in BRS may result from improved SAT, reduced sympathetic activity and improved vascular function, and/or parasympathetic-driven antioxidant effect. Lower oxidative stress could explain blunted effects in controls. Slow breathing could be a simple beneficial intervention in diabetes.

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Conflict of interest statement

L.B. is a recipient of a grant from the Signe and Ane Gyllenberg Foundation, Helsinki, Finland. P.H.G. has received lecture honorariums from AstraZeneca, Boehringer Ingelheim, Eli Lilly, Genzyme, MSD, Novartis, Novo Nordisk, and Sanofi, and he is an advisory board member of AbbVie, AstraZeneca, Boehringer Ingelheim, Cebix, Eli Lilly, Janssen and Novartis. L.B., D.G., A.S., M.R.B., M.B., and C.F. have no potential conflicts of interest relevant to this article.

Figures

Figure 1
Figure 1
Effect of Slow Breathing (SLB) and Oxygen (O2), alone (middle data of each panel) and combined (right data in each panel) on autonomic function: baroreflex sensitivity (panels a) and heart rate variability (standard deviation of RR intervals, SDNN, panels b), and blood gases: oxygen saturation (panels c) and end-tidal carbon dioxide (CO2-et, panels d). Data from Type 1 diabetic (left panels) and control participants (right panels). Baseline: spontaneous breathing in room air. Within each panel, significances written in red refer to baseline, significances in blue refer to SLB vs O2. Note the additive effect of oxygen and slow breathing in all autonomic and respiratory variables.
Figure 2
Figure 2
Effect of Slow Breathing (SLB) and Oxygen (O2), alone (middle data of each panel) and combined (right data in each panel) on blood pressures: systolic (panels a) and diastolic (panels b), and arterial function: heart rate-adjusted augmentation index (AI75, panels c) and Pulse wave velocity (SI-DVP, panels d). Same explanations as in Fig. 1. Note the opposite effects of slow breathing and oxygen on blood pressure and particularly on each index of arterial function, and the blockade of the oxygen-induced worsening by combining slow breathing.

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