Concomitant Peripheral Neuropathy and Type 2 Diabetes Impairs Postexercise Cutaneous Perfusion and Flowmotion

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.