Abstract
To evaluate the effects of inspiratory loading on blood flow of resting and exercising limbs in patients with diabetic autonomic neuropathy. Ten diabetic patients without cardiovascular autonomic neuropathy (DM), 10 patients with cardiovascular autonomic neuropathy (DM-CAN) and 10 healthy controls (C) were randomly assigned to inspiratory muscle load of 60% or 2% of maximal inspiratory pressure (PImax) for approximately 5 min, while resting calf blood flow (CBF) and exercising forearm blood flow (FBF) were measured. Reactive hyperemia was also evaluated. From the 20 diabetic patients initially allocated, 6 wore a continuous glucose monitoring system to evaluate the glucose levels during these two sessions (2%, placebo or 60%, inspiratory muscle metaboreflex). Mean age was 58 ± 8 years, and mean HbA1c, 7.8% (62 mmol/mol) (DM and DM-CAN). A PImax of 60% caused reduction of CBF in DM-CAN and DM (P<0.001), but not in C, whereas calf vascular resistance (CVR) increased in DM-CAN and DM (P<0.001), but not in C. The increase in FBF during forearm exercise was blunted during 60% of PImax in DM-CAN and DM, and augmented in C (P<0.001). Glucose levels decreased by 40 ± 18.8% (P<0.001) at 60%, but not at 2%, of PImax. A negative correlation was observed between reactive hyperemia and changes in CVR (Beta coefficient = -0.44, P = 0.034). Inspiratory muscle loading caused an exacerbation of the inspiratory muscle metaboreflex in patients with diabetes, regardless of the presence of neuropathy, but influenced by endothelial dysfunction. High-intensity exercise that recruits the diaphragm can abruptly reduce glucose levels.
Highlights
Cardiovascular autonomic neuropathy causes increased morbidity and mortality to diabetic patients [1]
The reactive hyperemia in the study groups was decreased in both diabetes without autonomic neuropathy (DM) and DM-CAN subjects as compared with the C group
Lower maximal voluntary ventilation (MVV), PImax, endurance time, Rpeak and VO2peak were observed in DM and DM-CAN as compared to C
Summary
Cardiovascular autonomic neuropathy causes increased morbidity and mortality to diabetic patients [1]. Respiratory muscle weakness in diabetic patients may be associated with peripheral [7] and autonomic neuropathy [4,5] Another possible explanation may be the activation of the inspiratory muscle metaboreflex, which occurs when fatiguing contractions of the inspiratory muscles during exercise cause accumulation of metabolic products. These products stimulate skeletal muscle neural afferents, resulting in increased sympathetic vasoconstrictor activity [8], thereby decreasing the locomotor muscle perfusion. Blunting of the inspiratory muscle metaboreflex with improvement in limb blood flow and endurance capacity can be obtained by endurance training in healthy individuals [11] and by respiratory muscle training in patients with heart failure [12,13]. It is not yet known if this kind of training activates or blunt the inspiratory muscle metaboreflex in patients with diabetes
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