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.
Highlights
Diabetes is associated with increased premature cardiovascular morbidity and mortality[1]
As outcome we modeled the different continuous variables, and included conditions, breathing patterns and participant groups as categorical covariates
Oxygen and slow breathing produce similar favorable autonomic modifications, their effects are the opposite with respect to blood pressure and arterial function: oxygen impaired and slow breathing improved them
Summary
Diabetes is associated with increased premature cardiovascular morbidity and mortality[1]. A functional – potentially reversible- component of autonomic and vascular abnormalities have been identified by our group, and others[4, 5] Following these concepts, we observed that the parasympathetic cardiac arm of the baroreflex could be transiently ameliorated by two simple physiological interventions, namely slow breathing[5] and oxygen administration[6]. Slow breathing did not increase or it even reduced the blood pressure[8] These findings lead to the question of whether these two interventions, which at first sight produce similar autonomic effects, might have entirely different mechanisms of action, based on the responses in blood pressure and arterial function, and its possible consequences in stimulating the parasympathetic nervous system. We reasoned that if oxygen and slow breathing act through independent mechanisms their combination should produce some additive or even multiplicative effects, whereas if they act through the same mechanism in opposite directions, their combination should cancel their individual effects
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