Effect Of Postprandial Hyperglycemia On Functional Sympatholysis In Young Non-diabetic Adults

During exercise, increased muscle sympathetic nerve activity induces sympathetic vasoconstriction but is blunted in an active limb (i.e., functional sympatholysis). Functional sympatholysis is crucial in regulating blood flow (BF) distribution during exercise and implicated by endothelial function. Postprandial hyperglycemia decreases brachial flow-mediated dilation (FMD) as an index of endothelial function; however, whether it also reduces functional sympatholysis is unknown. PURPOSE: This study aimed to elucidate whether postprandial hyperglycemia causes further reductions in the vascular conductance (FVC) of the active limb in response to sympathetic stimulation during exercise. METHODS: This study randomly assigned eight non-diabetic adults (5 males and 3 females; 23 ± 1 years, Mean ± SD) into two trials. Five (3 males and 2 females) and three (2 males and 1 female) adults completed trials by consuming a beverage with 75 g glucose (glucose trial) and 75 g fructose (sham trial), respectively. After 42 min of beverage consumption, they performed a 5-min one-hand handgrip exercise at 15% maximal voluntary contraction. After 3 min of exercise initiation, sympathetic stimulation was performed with lower-body negative pressure (LBNP, −20 mmHg) for 2 min. The brachial diameter and velocity of the active limb were measured using Doppler ultrasound, and FMD and BF were then calculated. Mean arterial pressure (MAP) was measured continuously using finger plethysmography, and FVC was calculated as BF divided by MAP. The magnitude reduction of percent change in FVC by LBNP (Δ%FVC) was calculated as [(FVCduring LBNP - FVCpre-LBNP)/FVCpre-LBNP] × 100. FMD tests and venous blood samplings were conducted before and 60 min after beverage consumption. RESULTS: The glucose trial revealed 3 of 5 adults with postprandial hyperglycemia (≧140 mg/dL) and decreased FMD (7.1 ± 3.1% to 5.1 ± 2.5%, P < 0.01). However, the sham trial showed no increase in blood glucose levels in all participants and thus no change in FMD (4.9 ± 0.5% to 5.1 ± 0.8%, P = 0.57). The glucose trial exhibited greater Δ%FVC than the sham trial (−7.2 ± 1.9% vs. 10.4 ± 13.3%, P = 0.04). CONCLUSION: Our findings suggest that postprandial hyperglycemia attenuates functional sympatholysis due to endothelial dysfunction in young non-diabetic adults. JSPS KAKENHI Grant Number 21K11290K