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Context: Type 2 diabetes and peripheral neuropathy exhibit microvascular dysfunction at rest. However, data regarding their microvascular perfusion during exercise remain scarce. Objective: This study investigated changes in microvascular perfusion during postexercise recovery in those with type 2 diabetes, with or without peripheral neuropathy, as well as in healthy controls and those with obesity. Methods: Skin blood perfusion was assessed in each group using laser Doppler flowmetry (LDF) and laser speckle contrast imaging before and immediately after a 6-minute walking test. LDF recordings underwent wavelet transformation to allow specific control mechanisms of blood perfusion to be studied (eg, endothelial nitric oxide-independent and -dependent, neurogenic, myogenic, respiratory, and cardiac mechanisms). Results: Skin blood perfusion increased after exercise in all groups (22.3 ± 28.1% with laser speckle contrast imaging and 22.1 ± 52.5% with LDF). Throughout postexercise recovery, the decrease was blunted in those with subclinical peripheral neuropathy and confirmed peripheral neuropathy when compared to the other 3 groups. After exercise, total spectral power increased in all groups. The relative contributions of each endothelial band was lower in those with confirmed peripheral neuropathy than in the healthy controls and those with obesity (nitric oxide-dependent function: 23.6 ± 8.9% vs 35.5 ± 5.8% and 29.3 ± 8.8%, respectively; nitric oxide-independent function: 49.1 ± 23.7% vs 53.3 ± 10.4% and 64.6 ± 11.4%, respectively). The neurogenic contribution decreased less in those with confirmed peripheral neuropathy and in those with type 2 diabetes alone, compared to those with subclinical peripheral neuropathy and those with obesity (-14.5 ± 9.9% and -12.2 ± 6.1% vs -26.5 ± 4.7% and -21.7 ± 9.4%, respectively). Conclusion: Peripheral neuropathy, whatever the stage, altered the microvascular response to exercise via impaired endothelial and neurogenic mechanisms. [ABSTRACT FROM AUTHOR]

Simple Summary: Postural changes induce arteriolar vasoconstriction in response to an increase in venous pressure in the limbs known as the venoarteriolar reflex (VAR). Previous studies reported that skin blood perfusion is impaired during the VAR in persons with type 2 diabetes mellitus (T2DM) with or without peripheral neuropathy, compared to control subjects. The aim of this study is to investigate the underlying mechanisms of the VAR in T2DM, with and without peripheral neuropathy. This study provides evidence that confirmed neuropathy alters the VAR by an alteration of the neurogenic response to leg dependency. The aim of this study is to investigate the underlying mechanisms of the venoarteriolar reflex (VAR) in type 2 diabetes mellitus (T2DM), with and without peripheral neuropathy. Laser Doppler flowmetry (LDF) recordings were performed on the medial malleus and dorsal foot skin, before and during leg dependency in healthy controls, in persons with obesity, in those with T2DM, in those with T2DM and subclinical neuropathy, and in those with T2DM and confirmed neuropathy. LDF recordings were analyzed with the wavelet transform to evaluate the mechanisms controlling the flowmotion (i.e., endothelial nitric oxide-independent and -dependent, neurogenic, myogenic, respiratory and cardiac mechanisms). Skin blood perfusion decreased throughout leg dependency at both sites. The decrease was blunted in persons with confirmed neuropathy compared to those with T2DM alone and the controls. During leg dependency, total spectral power increased in all groups compared to rest. The relative contribution of the endothelial bands increased and of the myogenic band decreased, without differences between groups. Neurogenic contribution decreased in controls, in persons with obesity and in those with T2DM, whereas it increased in subclinical- and confirmed neuropathy. In conclusion, this study provides evidence that confirmed diabetic neuropathy alters the VAR through the neurogenic response to leg dependency. [ABSTRACT FROM AUTHOR]